Assignment: Environmental and Genetic Impact on Fetal Development

Both environmental and genetic influences impact fetal development. Some substances (e.g., folic acid, hormones, etc.) have the biggest influence at sensitive periods during gestation. Early in gestation, when neurological development is at its peak, folic acid is most important. Hormones, such as androgen and estrogen, are necessary for external genital differentiation between 9 and 12 weeks of gestation. Prenatal alcohol exposure, however, can impact fetal growth at any time during gestation. On the other hand, environmental influences such as maternal genetics, nutrition, health, and immunization can have a positive impact on fetal development, mitigating the impact of substances and other negative influences. In addition to environmental influences, you must also consider the impact of genetic influences. Genes determine not only an individual’s physical features at birth—they also contribute to hormonal processes throughout the lifespan. The interaction of environmental influences and genetic influences impacts the development of a fetus.

For this Discussion, you will examine environmental and genetic influences on fetal development.

To prepare for this Discussion Assignment: Fetal Development:

· Select one genetic influence and one environmental influence on fetal development and think about how these influences might impact each other.

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By Day 4 of this Assignment: Fetal Development

Post a brief description of the genetic influence and the environmental influence you selected. Then, explain how the environmental influence might positively or negatively affect the development of a fetus with the genetic influence you selected. Be specific and provide examples. Use your Learning Resources to support your post. Use proper APA format and citations.

Berk, L. E. (2014). Development through the lifespan (6th ed.). Upper Saddle River, NJ: Pearson Education.

  • Chapter 2, “Genetic and      Environmental Foundations” (pp. 44–77)
  • Chapter 3, “Prenatal Development, Birth, and      the Newborn Baby” (pp. 78–117)

Charness, M. E., Riley, E. P., & Sowell, E. R. (2016). Drinking during pregnancy and the developing brain: Is any amount safe? Trends in Cognitive Sciences, 20(2), 80–82. doi:10.1016/j.tics.2015.09.011

Note: You will access this article from the Walden Library databases.

Entringer, S., Buss, C., & Wadhwa, P. D. (2015). Prenatal stress, development, health and disease risk: A psychobiological perspective—2015 Curt Richter Award Paper. Psychoneuroendocrinology, 62, 366–375. doi:10.1016/j.psyneuen.2015.08.019

Note: You will access this article from the Walden Library databases.

Tzouma, V., Grepstad, M., Grimaccia, F., & Kanavos, P. (2015). Clinical, ethical, and socioeconomic considerations for prescription drug use during pregnancy in women suffering from chronic diseases. Therapeutic Innovation & Regulatory Science, 49(6), 947–956.


Note: You will access this article from the Walden Library databases.

Prenatal Development Assignment Case Study Paper

Prenatal Development Assignment Case Study Paper



TED Talk and Reflection

Watch the following Ted Talk on the visualization of prenatal development:

Answer the following 2 questions:

1. Describe two things you found interesting and/or surprising.

2. What do you want to learn more about prenatal development?


1. Choose ONE article from the list below. Prenatal Development Assignment Case Study Paper

Answer the following 2 questions:

1. Identify the article you chose from above. Why did you choose that specific article? What made you interested in that subject? Prenatal Development Assignment Case Study Paper

2. Summarize the article. Be thorough. Explain the article as if you were telling someone who had not read it.


TED Talk and Reflection

Watch the following Ted Talk on what we learn before we are born: Prenatal Development Assignment Case Study Paper

Answer the following 2 questions:

1. Describe some of the studies that Annie Murphy Paul discusses. What do they tell us about learning in the womb?

2. What did you learn and/or find interesting about this TED Talk?

Prenatal Development Assignment Case Study Paper

Prenatal Development and Infancy Research Paper – Essay

This sample Prenatal Development and Infancy Research Paper is published for educational and informational purposes only. If you need help writing your assignment, please use our research paper writing service and buy a paper on any topic at affordable price. Also check our tips on how to write a research paper, see the lists of psychology research paper topics, and browse research paper examples.

Birth, of course, does not mark the beginning of human development; rather, development begins at conception. Although much of prenatal development occurs within the physical domain, developments in the cognitive and psychosocial domains also emerge at this time. Moreover, although these developments are driven by genetic and maturational forces, experiential factors also play an influential role during this period. Within this research-paper, we address some major areas of prenatal development: sensory experience, neurobehavioral functioning, and teratogenic risks. Postnatally, the period of life known as infancy traditionally consists of the first two years following birth, and it is during this period that often dramatic and rapid developments take place in all domains. Some of the most important of these phenomena, including brain development, visual and auditory perception, cognitive development, temperament, and attachment, are reviewed in the remainder of this chapter. While discussion of the selected topics provides a glimpse into the array of developments occurring during gestation and infancy, they are necessarily limited in their overview of the vast number of changes and issues that have been studied during these earliest phases of life. The reader is thus strongly encouraged to review additional sources for a discussion of subjects such as fetal programming, prematurity, language, and social cognition that are also germane to prenatal and/or infant development.

Sensory Development

Even though sensory development begins long before birth, it is inherently difficult to observe the responses expressed by the fetus. Early fetal chemosensory experience has been examined largely in animals, whereas most studies with human fetuses have investigated auditory responsiveness in the second half of gestation. Our primary sources for knowledge about sensory development in human fetuses derive from studies of prematurely born infants and research using sophisticated noninvasive techniques. For example, magnetic fields generated by active neurons in fetal brain tissue can be detected and used to examine a fetus’s response to auditory stimulation (Huotilainen, Kujala, & Hotakainen, 2005; Zappasodi, Tecchio, & Pizzella, 2001). Generally speaking, the senses become functional sequentially between 8 and 26 weeks, with touch developing first, then taste and smell, hearing, and finally vision.


Sensitivity to touch or pressure begins early in gestation and develops in a cephalocaudal direction (Field, 1990). By about 8 weeks of gestation, the fetus responds to touch on the area around the lips by moving. By 12 weeks, the fetus responds with a grasping movement when fingers are touched. During early gestation, the fetus typically responds by moving away from the source of stimulation. Later in gestation, the fetus tends to move toward the stimulation. For example, touch stimulation on the cheek of a fetus can elicit rooting-like responses, which later help the infant locate the source for nursing. Overall, the sensory abilities to detect touch, along with body motion, appear to be the most developed at birth (Field, 1990).

Taste and Smell

Scientists conclude that fetuses have gustatory and olfactory detection. However, with the exception of the taste for sweet, there has been no direct evidence for fetal chemo-sensory preferences. Flavors and odors from the mother’s diet do pass into the fetus’s amniotic fluid and bloodstream. Thus, the sensation of taste and smell can occur through the fetus’s nose, mouth, and bloodstream. When the fetus engages in breathing movements (beginning at about 10 weeks of gestation), amniotic fluid not only is swallowed but also passes through the nose after the plugs blocking the nostrils dissolve (James, Pillai, & Smoleniec, 1995; Schaal, Orgeur, & Rognon, 1995). Additionally, through blood circulation to the nose and mouth, the fetus has the opportunity to experience different smells and tastes (Schaal, 2005). Following birth, neonatal detection of a variety of odors and flavors is evident, with preferences emerging quickly (e.g., mother’s scent).


The fetus’s auditory system develops gradually starting at around 6 weeks of gestation, and by 28 weeks it is sufficiently well developed to enable the fetus to reliably respond to sounds, typically with startle responses and increased heart rate (Lecanuet, Granier-Deferre, & Busnel, 1995). Within the uterine environment, the fetus is regularly exposed to its mother’s voice, gastrointestinal sounds, and heartbeat. During the last trimester, a fetus also appears to hear external sounds that pass through the uterine walls (Fernald, 2004).


At about 8 weeks of gestation, the lens, eyelids, and muscles controlling eye movement begin to develop. By 15 weeks, the integration of the optic nerve in each eye is complete. By 28 weeks, the development of the visual cortex in the brain resembles that in the adult. Although the fetus can open and blink its eyes for some time, it receives relatively little visual input before birth because of in utero darkness. However, if the fetus is born prematurely at this time, it can already detect changes in brightness (i.e., light and dark; Slater, 2004). Because the neural structure of the eyes and pathways to the brain are still immature, vision appears to be the least sophisticated of the senses and continues to develop substantially after birth.

Neurobehavioral Development and Functioning

The identification of fetal activity patterns and their underlying neural mechanisms is critical not only for understanding the beginnings of human behavior, but also for monitoring the fetus’s healthy development in the functioning of peripheral and central nervous systems. Most knowledge about neurobehavioral development in the fetus has been generated by real-time ultrasound and Doppler-based electronic fetal monitors (DiPietro, 2005). Four aspects of fetal functioning are typically involved in a multidimensional neurobehavioral assessment: motor activity, heart rate, behavioral state (e.g., from active to inactive), and responsivity to stimulation (DiPietro, 2005).

Motor Activity

Movements first appear between 7 and 16 weeks of gestation. The development of fetal movements shows an increase in repertoire. Movements include both large generalized movements (e.g., startle, stretch, rotation, and breathing) and movements of specific body parts (e.g., head, eyes, fingers, jaw opening, yawn, and hand-face contact). Initially, movements tend to appear scattered in a random fashion, but gradually the occurrences of movements are more coordinated and clustered together into bursts, and finally into longer periods of fluctuating activity (Robinson & Kleven, 2005). Although there are individual differences in the quantity of movements among fetuses, they occur less frequently but with more vigor during the second half of gestation (DiPietro, Hodgson, & Costigan, 1996). Increasingly longer periods of inactivity are common as fetuses mature. Thus, motor inhibition is believed to also be a significant marker for neurological development.

Fetal Heart Rate

The heart rate in healthy fetuses is almost twice that of adults, fluctuating between 120 and 160 beats per minute. Cycles of increased and decreased variability in baseline heart rate can be observed throughout the day. Whereas spontaneous accelerations indicate responsiveness in the sympathetic nervous system, general trends in the rate and variability of fetal cardiac activity reflect the maturation of the nervous system. Overall, heart rate shows a pattern of decrease in rate and increase in variability during the prenatal period. However, decelerations after 28 weeks tend to be markers of pathology. Contrary to some common beliefs, fetuses’ heart rates are not in synchrony with their mothers’ heart rates. In a quiet and resting condition, a mother’s heart rate does not influence fetal heart rate, or vice versa (DiPietro et al., 2006). Furthermore, the presence of heart rate acceleration coupled with fetal movements is viewed as a sign of fetal well-being. Increases in the coordinated coupling between the two different systems indicate the integration of the central nervous system.

Behavioral States

Behavioral states are relatively stable periods characterized by coordinated patterns in the fetus’s eye and motor movements as well as heart rate activity. Beginning at about 28 weeks, the fetus begins to show rest-activity cycles. Four fully developed behavioral states can be detected at around 36 weeks: quiet sleep, active sleep, quiet awake, and active awake (de Vries & Hopkins, 2005). The quiet sleep state features the absence of eye movements and a stable heart rate within a narrow range. The active sleep state is characterized by eye movements, a wider range of heart rate oscillation, and periodic stretches and gross body movements. The state of quiet awake is characterized by the absence of gross body movements, a stable heart rate with a wide range of oscillation, and the absence of heart rate acceleration. The active awake state features the presence of eye movements and continuous, vigorous activities with unstable and large accelerations in heart rate. Compared to neonates, fetuses take a longer time to complete a state change and make fewer transitions between quiet and active sleep states. Because behavioral states are believed to reflect neural functioning, and therefore fetal health, observations of fetal states can be used to discriminate abnormalities in pregnancy and growth retardation.


Fetuses respond to stimulation originating outside of the uterus. Compared to airborne sound stimuli, fetuses respond to vibro-acoustic stimuli (comparable to an electric toothbrush) with greater heart rate accelerations and more body movements. In response to repeated presentation of stimuli, a pattern of decreased response (i.e., habituation) reflects healthy fetuses’ capacity for self-regulation and information processing.


Fetal neurobehavioral development is predictable. Overall, it goes through a transition of rapid changes with decreased heart rate, increased heart rate variability, and increased movement-heart rate coupling between 28 and 32 weeks of gestation, after which the development levels off and a stable pattern is established ( DiPietro, 2005). Because similar patterns of coupling and/or disassociation (e.g., between fetal movement and heart rate) are found among fetuses, it is assumed that these fundamental properties of neurobehavioral development prior to birth are universal (DiPietro et al., 2006). Future research will need to explore the underlying mechanisms and experiential factors that may facilitate or impede fetal development and functioning.


Traditionally, teratology is the study of physical damage in the embryo or fetus caused by prenatal exposure to foreign substances. More recent teratology focuses on the impact to the developing central nervous system and its manifested behavioral consequences (Fried, 2002). The most common teratogenic risk factors linked to children’s negative outcomes have been prenatal exposure to maternal use of tobacco, alcohol, or cocaine. According to the Substance Abuse and Mental Health Services Administration (2005), approximately 18 percent of pregnant women in the United States reported smoking cigarettes, 9.8 percent reported drinking alcohol, and 4 percent reported using at least one illegal drug in the previous month.


Cigarette smoking is known to directly deliver chemical toxins to the fetus through the mother’s bloodstream, and thus may influence the developing brain and cause neurophysiological deficits. Prenatal exposure to maternal smoking is associated with an array of problematic physical and behavioral outcomes in both perinatal and postnatal periods such as reduced fetal growth, disruptive fetal heart rate regulation, preterm delivery, perinatal mortality, and suboptimal neonatal neurobehavioral functioning (e.g., increased tremors and startling and increased distractibility; Zeskind & Gringras, 2006). The negative effects of prenatal smoking often persist into childhood and adolescence. For example, longitudinal studies found that offspring of mothers who smoked during pregnancy show an increased risk for exhibiting oppositional behavior, criminal offending behavior, and smoking behavior (Buka, Shenassa, & Niaura, 2003; Gibson, Piquero, & Tibbetts, 2000; Montreaux, Blacker, & Biederman, 2006).

Even when mothers did not smoke cigarettes during pregnancy but were exposed to environmental tobacco smoke (i.e., secondhand smoke), adverse perinatal effects have been demonstrated. Schuetze and Eiden (2006b) found that infants of both mothers who were exposed to secondhand smoke and mothers who smoked cigarettes had a significantly increased baseline heart rate and decreased heart rate variability compared to infants of mothers who had no exposure to cigarette smoke; these outcomes suggest a compromised nervous system. Moreover, this same study documented a dosage effect of prenatal direct and indirect exposure to cigarette smoking on compromised neonatal neurophysiological functioning.


In 2002, over 50 percent of women in their childbearing years drank alcohol without using birth control, and thus potentially were at risk for pregnancy complicated by teratogenic exposure (Centers for Disease Control and Prevention, 2004). The detrimental effects of prenatal alcohol exposure range along a continuum, downward from fetal alcohol syndrome, the most severe result of exposure, to alcohol-related birth defects, alcohol-related neurodevelopmental disorders, and, finally, specific cognitive and psychosocial deficits. Because impairments are not limited to the most severe form of exposure, even low levels of maternal alcohol use during pregnancy may cause potential harm. Prenatal alcohol exposure is linked to a host of cognitive deficits, including mental delays and problems in attention, memory, learning, problem solving, planning of actions, and state regulation (e.g., Howell, Lynch, Platzman, Smith, & Coles, 2006). Emerging evidence shows that these problems begin as early as infancy and often persist into adulthood (O’Connor & Paley, 2006). Researchers have hypothesized that central nervous system abnormalities caused by prenatal exposure to alcohol result in attentional difficulties, which in turn impact higher-order cognitive processes and subsequently compromise functioning. In addition to cognitive deficits, prenatal alcohol exposure is found to be associated with psychosocial problems, including hyperactivity, aggressive behavior, depression, poor interpersonal skills, and psychiatric disorders (O’Connor & Paley, 2006).


Much of the recent research on the effects of prenatal drug exposure has focused on cocaine. Evidence suggests that detrimental effects of prenatal cocaine exposure are modest but consistent on neurobehavioral functioning, physiological regulation, motor development, frustration reactivity, attention and arousal regulation, and language (Beeghly et al., 2006; Bendersky, Bennett, & Lewis, 2006; Dennis, Bendersky, Ramsay, & Lewis, 2006; Schuetze & Eiden, 2006a). Research also has suggested a dosage effect of prenatal cocaine exposure on particular outcomes. Infants who had higher levels of exposure to cocaine showed smaller birth head size, more compromised physiological regulation, and more negative engagement with their mothers than did infants with less prenatal exposure (Behnke et al., 2006; Schuetze & Eiden, 2006a; Tronick et al., 2005: Prenatal Development Assignment Case Study Paper).

Follow-Up Risk

Prenatal exposure to maternal smoking, alcohol, and/or cocaine use is related to some common long-term neurobehavioral and cognitive outcomes, including attention deficit and hyperactivity disorder, decreased cognitive functioning, and deficits in learning (Huizink & Mulder, 2006). The teratogenic insult of prenatal exposure on long-term impact is usually compounded by developmental risks associated with being reared by a substance-abusing parent. Oftentimes, maternal substance use or abuse is a marker of social and psychological problems in the childrearing environment. In other words, in addition to direct effects of maternal prenatal use of tobacco, alcohol, and/or cocaine on the fetus, adverse outcomes may be due to indirect effects mediated through other, related risk factors such as the mothers’ low socioeconomic background, single parenthood, high stress levels, low social support, and deficits in parenting behaviors. For example, Schuetze, Eiden, and Dombkowski (2006) demonstrated that compared to women who did not smoke cigarettes during the prenatal period, women who smoked during pregnancy were insensitive and less affectionate to their newborn infants. This linkage can be further explained by high levels of anxiety and hostility in mothers who smoke cigarettes during pregnancy (Schuetze et al., 2006). Similarly, Tronick and colleagues (2005) reported that, compared to control dyads, levels of dyadic engagement were lower and more negative for infants and their mothers who used cocaine during pregnancy. This suggests that any impact of teratogenic risk of prenatal exposure to cocaine on offspring may be exacerbated by the poor quality of interaction between child and parent.

The above evidence indicates that a simple explanation of teratogenic risk on subsequent problematic behavior may not be sufficient. More sophisticated research approaches are required to examine the complex relations between prenatal substance exposure and various environmental risk factors. Future research regarding teratogenic effects on child development should focus not only on the type, timing, and amount of substance exposure during pregnancy, but also on the joint contribution with multiple risk factors in the childrearing environment (Bendersky et al., 2006; Mayes, 2002). Moreover, researchers have reported that boys and girls may be differently affected by prenatal substance exposure. For example, compared to female neonates, male newborns’ autonomic regulation is more vulnerable to the negative effect of maternal smoking and secondhand smoke exposure (Schuetze & Eiden, 2006b). Prenatal cocaine exposure appears to have a stronger impact on language development in preschool-age girls (Beeghly et al., 2006), whereas it has a significant influence on boys’ frustration reactivity and aggressive behavior (Bendersky et al., 2006; Dennis et al., 2006). Thus, the effect of child characteristics such as sex and temperament in altering the relations between teratogenic risk factors and child outcomes should be considered. Finally, despite the existence of adverse effects, not all children are negatively impacted by prenatal substance exposure. Some resilient children are able to adapt positively and experience healthy development. In addition to understanding the risk of prenatal exposure to teratogens and their direct and indirect effects on child outcomes, investigating the protective factors in buffering against the risks also deserves research attention (Dennis et al., 2006).


Brain Development

Formation and Growth of the Brain

Brain development begins remarkably early during the prenatal period and involves multiple processes and stages. During the second half of the first month of gestation, the brain begins to form from a neural plate through a process called neural induction. The neural plate then transforms into a tube shape through a process termed neurulation. One end of the neural tube develops into the brain and the other becomes the spinal cord. Problems in neural tube development lead to anatomical abnormalities in the brain and/or spinal cord (Couperus & Nelson, 2006). Once this basic structure of the brain is established, the next stage of development is the production of neurons (i.e., cells that transmit information). The brain houses billions of neurons. The process of proliferation begins in the neural tube at five weeks of gestation, reaches its peak at three to four months of gestation, and is largely complete by the end of the second trimester. At the peak, it is estimated that several hundred thousand new cells are generated each minute. The new cells transform from uncommitted cells to differentiated neurons when they travel to their final location in specific regions of the brain. This process of migration begins at six weeks gestation and continues through four to five months after birth (Nelson, de Haan, & Thomas, 2006).

Once a neuron has migrated into its final location, the cell further differentiates and develops. Each neuron consists of a cell body and two ends—axons and dendrites. The primary function of neurons is to process and communicate information. Axons send out information, while dendrites pick up information from other cells. Whereas the proliferation and migration of neuronal cells occur primarily during the prenatal period, the production and growth of axons and dendrites begin at 15 weeks of gestation and continue after birth. The dendrites in some regions of the brain continue to develop throughout the first two years after birth. Despite massive growth and rapid differentiation, neurons also are eliminated through a normal process of apoptosis (i.e., programmed cell death). It is estimated that 40 percent to 60 percent of all neurons may die naturally during embryonic or fetal development (Buss, Sun, & Oppenheim, 2006; Couperus & Nelson, 2006; Nelson et al., 2006).

The establishment of connections within the brain occurs when axons and dendrites come together to form synapses so that information can be transmitted between neurons. A healthy, functional brain is one with a vast array of connections. The first synapses can be observed by 23 weeks of gestation, with the peak of production (i.e., synaptogenesis) at the end of the first year after birth; production continues until adolescence (Kagan & Herschkowitz, 2005; Nelson et al., 2006). It is estimated that 40 percent more synapses than the final number found in adults are produced (Nelson et al., 2006). Thus, the process of synaptic pruning also takes place to eliminate excessive production in synapses. The occurrence of synaptic pruning appears to vary by brain regions, with some reaching adult numbers of synapses by two years after birth while others do not do so until late adolescence. It is believed that the level of communication among neurons determines the pruning. Active synapses are strengthened, whereas inactive synapses are pruned. The pruning process can occur either quantitatively (i.e., overall reduction in number) or qualitatively (i.e., elimination of incorrect or abnormal connections; Nelson et al., 2006).

The last process of brain development is myelination. Myelin is a fatty substance that surrounds and insulates axons to increase the speed and efficiency in transmitting signals. It first appears during the last trimester of the prenatal period. In some brain regions, this process continues until young adulthood or middle age (Kagan & Herschkowitz, 2005; Nelson et al., 2006).

Plasticity of the Brain

Within a period of seven months, a small group of cells transforms into a complete form of the adult brain, with six layers of cortex. The old belief was that brain development is based on a predetermined genetic process unfolding according to a fixed sequence and timing. New data suggests that even the early stages of brain formation are not determined by genetic factors alone; environmental factors also play an important part in the process. Soon after the anatomical structures are formed and connections are made, the brain begins to interact with itself and the environment. The ability for the brain to adapt to the change in itself and/or the environment is referred to as plasticity. Overall, during the prenatal period, neural connectivity is changed by internal spontaneous activity. After birth, there is a shift to the effect of external environmental inputs. Disease, metabolic disturbances, malnutrition, and trauma can produce maladaptive changes in the brain, whereas practice and learning can lead to adaptive functional changes in the brain. Furthermore, changes in one neural system can also influence the organization of another in the brain. For example, visual cortex areas in individuals who are born blind can be activated by Braille reading (a method of reading text through touch).

Although many neural networks have a preferred connectivity pattern, this connectivity is not ixed because experience can alter the innate pattern. In response to exposure to certain experiences, the resultant changes in the brain may serve to maintain, reorganize, or even lose the initial pattern of connectivity. The newly reorganized brain can then serve as a foundation to facilitate the effect of subsequent experience, which can result in further neural changes. Such effects are referred to as cascading influences. For example, the prenatal experience of listening to speech leads to a preference for the rhythmical properties in native language, which further results in an ability to segment words from continuous speech (Werker & Tees, 2005). Evidence of functional brain reorganization also can be found in infants who are deprived of sensory input. For example, profoundly deaf children who received their cochlear implant (a surgically implanted electronic device that directly stimulates the functioning auditory nerves inside the cochlea with electrical impulses) before age two improved their performance of speech recognition and production more than those who had implantation after age four or five (Geers, 2006; Nicholas & Geers, 2006; Rubinstein, 2002). Clinical evidence for the loss of neural connections in infancy is also available. For example, repeated infections in the middle ear (i.e., otitis media) during infancy, which interfere with sound transmission due to fluid in the ear, can reduce experiential input and lead to deficits in phonetic categorization and difficulties in reading and spelling (see Werker & Tees, 2005). The evidence of plasticity in brain development has implications for early intervention. With the aid of devices such as cochlear implants, maintenance and reorganization of the neural structures is possible. In the case of lost connections, once we understand exactly how brain development is changed by experience in terms of its type, timing, and intensity, intervention strategies can then be designed to prevent deviations from the normal range and to provide the necessary experience to bring infants back to a normal track.

Functional Brain Development

Traditionally, researchers believed that the emergence of changes in sensory, motor, cognitive, and language functioning are a result of the maturation of specific regions or pathways in the brain. More recent research suggests that postnatal brain development, particularly within the cerebral cortex, is likely to be the result of interactions between different cortical regions and pathways when recruited for specific tasks. Over time, through repeated interactions, the functions of different regions become increasingly specialized (Johnson, 2000). Thus, this interactive specialization perspective of functional brain development during the postnatal period suggests that in response to environmental demand (e.g., seeing mother’s face), a recruitment process takes place through which interactions between particular regions or pathways occur repeatedly. As a result, they become selectively responsive to specific environmental stimuli. For example, whereas six-month-olds can discriminate between different human and monkey faces, nine-month-olds can discriminate human faces but not monkey faces (Pascalis, de Haan, & Nelson, 2002).


Recent research has further concluded that although human brains are characterized by prolonged plasticity (i.e., neurons are responsive to experience) during the postnatal period, it is not a process of passive response to environmental input. Rather, it is an activity-dependent process involving dynamic interactions between genes, brain, and behavior (Couperus & Nelson, 2006; Johnson, 2000). In other words, early external environmental factors in combination with genetic makeup shape brain development, which determines the expression of behavior. The behavioral activity then leads to further functional and structural alterations in the brain. Although much is known about the growth and structure of the brain, little is known about how developmental changes in the brain are related to behavior. In addition to laboratory experiments with infants by applying noninvasive neuroimaging techniques such as functional magnetic resonance imaging (e.g., Amso & Casey, 2006), a computational modeling approach (i.e., computer simulation based on statistical modeling) can further analyze interactions between neural structure and behavioral function (e.g., Munakata, 2004) and how these interactions may be linked to behavioral development.

Visual and Auditory Experience

By relying on nonverbal measures, much has been discovered about the perceptual experience of newborns and infants. Resourceful methodologies have ranged from simple (e.g., habituation, preferential looking) to intricate (e.g., anticipatory head-turning to classically conditioned stimuli, high-amplitude sucking control of operant stimuli). Capitalizing on infants’ natural preference for novelty after habituating to a previous stimulus, the widely used strategy of dishabituation (i.e., recovery of attention) conveys that infants discriminate stimuli. A potential limitation of dishabituation is conflict between the novelty and the relative appeal of a follow-up stimulus (e.g., happy face followed by sad face). By contrast, approaches based on differential responsiveness or preferences examine how infants behave toward competing stimuli (e.g., looking more to one source). Results signify that infants not only distinguish but also prefer some experiences to others. However, if no overt differences emerge, nondiscrimination may be erroneously assumed. By examining subtle changes in physiology such as contrasting patterns of electrical brain activity (i.e., evoked potentials), some research avoids this concern.


Visual perception is not adultlike at birth and undergoes marked changes during the first months of life. Neonatal vision has limitations because of structural immaturities in the brain (e.g., optic nerve, visual cortex) and eye (e.g., lens muscles, retinal cones). As a result, initial acuity is strikingly poor (e.g., 20/600) but nears adult levels (e.g., 20/20) by six to eight months (Kellman & Arterberry, 2006; Slater, 2004). Newborns also have difficulty discriminating some colors; however, they do have color vision and by two to three months, infants distinguish a wide spectrum of colors (Kellman & Arterberry, 2006; Schiffman, 2000). Newborns can track slowly moving objects, but they do not estimate three-dimensional space as adults do. Nonetheless, some depth perception is evident in the first weeks and appears extracted from kinetic cues (Nanez & Yonas, 1994). Sensitivity to binocular depth cues appears by three to five months (Birch, 1993) followed by the use of pictorial/monocular cues by seven months (Yonas, Elieff, & Arterberry, 2002).

Because of limitations with acuity and color, many patterns and forms are difficult for newborns to detect unless stimuli are very close and offer high contrast (e.g., light and dark elements) that is not lost due to fine-grained detail. Sensitivity to contrast and moderate complexity may contribute to newborns’ preference for faces; however, recent research suggests it is linked to a bias for configurations with upper-half/top-heavy elements (Macchi Cassia, Turati, & Simion, 2004; Turati, 2004). Initially, newborns’ restricted scanning is primarily on outer contours, but by two months they fixate on internal details and thus soon prefer normal to scrambled faces. A change in scanning produces a shift in focal cues (e.g., head shape vs. features), promoting discrimination and preference for mothers’ face (Pascalis et al., 1995). With improved acuity and scanning, it is not long before infants can discern complex patterns, perceive subtle distinctions between faces (i.e., similar emotions), and even prefer attractive faces (Kellman & Arterberry, 2006; Slater, 2004; Slater & Johnson, 1999). A detailed prototype for human faces based on experience seems to develop over the first nine months and enables ever finer discriminations (Pascalis et al., 2002). Nonetheless, the origins and nature-nurture interplay underlying observed facial preferences are not entirely understood (Slater, 2004).


Auditory development is rather sophisticated by birth (Fernald, 2004). Although newborns appear less sensitive to soft sounds than adults, other abilities are impressive. They can localize sound and readily distinguish characteristics such as frequency/pitch and loudness. Infants are particularly responsive to music and are sensitive to dissonant features, melody, rhythm, tempo, and so on (Trehub & Schellenberg, 1995; Zentner & Kagan, 1996, 1998). They are also highly attentive to the human voice and at birth show preferences, based on exposure, for their mother’s voice, their native language, and even for familiar book passages (DeCasper & Fifer, 1980; DeCasper & Spence, 1986; Moon, Cooper, & Fifer, 1993). Young infants also show remarkable discrimination abilities for a range of qualities in human speech (e.g., prosody, phonemic categories; Aslin, Jusczyk, & Pisoni, 1998). Their capacity to distinguish sounds in any language is initially better than that of adults. Such speech perception skills appear to prime neonates for learning any needed languages. However, at around 8 months, infants begin to specialize in detecting the sounds of their culture’s language, and by 12 months have abilities similar to those of the adults around them (Aslin et al., 1998; Werker & Desjardins, 1995).

Cognitive Development

Piaget’s Viewpoint

The theory that originally inspired psychologists’ understanding of infants’ and children’s thinking is that of Jean Piaget. Piaget’s (1950, 1952, 1964, 1970) constructivist viewpoint (Flavell, 1963) argues that individuals of all ages create knowledge on their own initiative, in response to experiences rather than direct instruction. Piaget proposed that the basic units of knowledge are schemes or mental models created to represent and interpret experiences. Using an existing scheme to interpret experience is known as assimilation, whereas modifying or creating schemes in order to adapt to new experiences is referred to as accommodation (Beilin, 1992). Further, the human tendency to organize knowledge into structures promotes discontinuous developmental stages that represent qualitatively different yet coherent forms of understanding. Although the latter two processes propel cognitive advancement, Piaget’s depiction of the shared features of each stage, as well as their invariant sequencing, suggests that maturation also plays a role in ushering in major developmental shifts.

Piaget described the period between birth and the second birthday as the sensorimotor stage because infants appear reliant on their basic sensory and motor abilities to perceive, explore, and understand the world. Based on observations of infants’ actions during individualized clinical interviews, Piaget proposed that the first cognitive stage consists of six increasingly advanced substages that capture the infant’s transition from an initially reflexive to ultimately reflective individual. At the outset, “thinking” and behavior are fused, because one’s dominant cognitive structures are sensorimotor (i.e., behavioral) schemes. Young infants do not think about objects separate and apart from acting on or perceiving them. This fusion is evidenced in the first three substages:

  1. 0-1 month, reflex activity (use and modification of inborn reflexes);
  2. 1-4 months, primary circular reactions (repetition and integration of more complex actions involving one’s body); and
  3. 4-8 months, secondary circular reactions (repetition and integration of interesting acts on objects).

The crowning achievement of the sensorimotor stage is the shift to symbolic capacity, which is the ability to represent objects, actions, and experiences via mental imagery, words, or gestures. This transition is gradually revealed in substages four to six:

  1. 8-12 months, coordination of secondary schemes (intentional combining of actions to solve simple problems);
  2. 12-18 months, tertiary circular reactions (actively “experimenting” with objects through trial and error to solve problems or explore potential uses); and
  3. 18-24 months, symbolic problem solving (“experiment” mentally rather than through trial and error).

By the end of the sensorimotor stage, infants can mentally represent objects and actions on those objects, and are no longer limited to “thinking-by-doing.” The transition to enduring and flexible symbolic thought is also articulated in Piaget’s depiction of infants’ understanding of the existence of objects. According to Piaget, infants through sub-stage three (4-8 months) lack object permanence, which is the ability to represent objects and know that they exist apart from perceiving or acting on them. It is only beginning in substage four (8-12 months) that infants supposedly can form and hold mental representations of objects. The fragility of these initial representations is purportedly evident in the consistent errors that infants show when searching for hidden objects; such search errors occur until the final substage.

Challenges to Piaget’s theory have been considerable (Lourenco & Machado, 1996; Miller, 2002). As a general criticism, it is unclear what maturational brain changes or kinds of experiences are necessary before children display new competencies or progress from one stage to another. A more specific criticism regarding infant cognition is that Piaget relied solely on search behavior to explore infants’ understanding of objects, and thus underestimated their ability for representational thought. Research pioneered by Renee Baillargeon (1987; Baillargeon & DeVos, 1991: Prenatal Development Assignment Case Study Paper) employed measures of infants’ visual rather than motor behavior (e.g., attention to events that violate expectations). This groundbreaking research suggested that infants may have more understanding of object permanence than Piaget held, and ushered in the first of many research findings that do not reconcile with traditional propositions (Meltzoff, 1999).

Modern Viewpoints

Classical Piagetian theory no longer guides current research; competing theories are presently under debate (see Meltzoff, 1999; Meltzoff & Moore, 1994). The nativist perspective (see Johnson, 2003) captures a range of theorists who believe infants are born with a fair amount of innate knowledge about the physical world and possess symbolic ability from the earliest months of life. In other words, although maturation and experience enable further mastery, not all knowledge has to be constructed; rather, infants are evolutionarily adapted with abilities for cognitive representation that enable basic understanding of objects (permanency, solidity, containment, etc.; e.g., Aguiar & Baillargeon, 1998; Baillargeon, Kotovsky, & Needham, 1995; Spelke, 1991), imitation (e.g., Meltzoff & Moore, 1994), and perhaps rudimentary quantification (e.g., Wynn, 1992). “Theory” theorists, like nativists, also argue that infants are born with some inherent knowledge or theories about how the world works, but propose that these ideas are primitive and are constantly updated as predictions are tested and revised. Although this view holds that infants know more than Piaget asserted, it agrees that even infants “construct” knowledge as they test their innate basic beliefs and modify them to fit experience (Gopnick & Meltzoff, 1997; Meltzoff, 1999). The connectionist view, in contrast, argues against the presence of any domain-specific core knowledge. These researchers depict infants’ thinking as based on computerlike artificial neural networks that have the capacity to learn. Aspects of cognition (e.g., formation of concepts, problem solving) are thought best understood as task competencies that emerge from corrective feedback that alters the strength of connections between basic information-processing units. Internal learning or shifting of connection weights precedes overt behavioral change; thus, stagelike developmental competencies can stem from a few low level skills or constraints (McClelland & Jenkins, 1991). Overall, the above (and other) alternatives to a traditional Piagetian view are stimulating much research scrutiny; nonetheless, no modern perspective has achieved theoretical prominence.


Anyone with firsthand exposure to infants recognizes that even neonates are often quite different from one another in terms of behavior. Temperament refers to relatively consistent and stable individual differences in reactivity and self-regulation that are genetically and biologically based and thus evident from the first months of life (Rothbart & Bates, 1998). Although these differences serve as the underpinning of later personality, researchers have not come to definitive agreement as to how to best describe the initial dimensions of temperament that are present among infants. Measurement of temperamental characteristics is also variable. Moreover, the long-term stability of temperamental dimensions is somewhat ambiguous, as are the specific environmental factors that influence and alter attributes over time.

Alexander Thomas and Stella Chess (1977) proposed the first model by which to classify infant temperament. Their pioneering work, based on in-depth parental interviews, found that certain behavioral and emotional characteristics tended to cluster together into three categories of infants. Those with an “easy” temperament tended to readily adapt to novelty, generally exhibited positive emotions, displayed regularity in their bodily functions, and easily established routines. “Difficult” infants tended to reject new experiences, displayed intense and frequent negative reactions, and exhibited irregularity in their daily patterns. “Slow-to-warm-up” infants responded negatively, but mildly, to novel experiences and adapted very slowly; they also tended to have low activity levels and mood intensities. Although the majority of infants studied by Thomas and Chess could be classified into one of these three types, a large percentage (35 percent) did not fit a particular category. Nonetheless, the identification of parental descriptors and associated patterns offered a first inquiry into the study of temperament and its longitudinal stability (Thomas & Chess, 1986; Thomas, Chess, & Birch, 1968: Prenatal Development Assignment Case Study Paper), and has since inspired numerous investigators to refine our understanding of this early developmental phenomenon.

Contemporary researchers vary in their language and classifications; however, several characteristics appear to capture differences in initial temperament. These include irritable distress (i.e., frustration/anger), fearful distress, positive affect, activity level, attention span and persistence, and rhythmicity (Rothbart & Bates, 1998). Other dimensions identified as informative include sociability (Buss & Plomin, 1984), agreeableness/adaptability and effortful control (Rothbart, 2004); the latter reflects one’s self-regulatory capacity to manage reactivity (i.e., inhibit impulses, control arousal, shift attention). Some dimensions (such as fearful distress, self-regulation) take longer than others (such as irritability) to emerge but are nevertheless thought to be biologically rooted.

Along with variability in defining aspects of temperament, researchers have used a number of approaches to measurement. Verbal reports, particularly from parents, have been widely used because they provide information about infants across a variety of situations. Unfortunately, they can be subject to bias due to factors such as state (e.g., anxiousness, depression), limited points of comparison, and expectations. Laboratory observations of behavioral reactions during particular contexts/tasks also have been employed because they enable objectivity. They also readily allow for physiological measures (e.g., heart rate, cortisol, electroencephalographic brain waves) to complement behavioral observations and better inform us of the biological bases of temperament. Unfortunately, a limitation of laboratory data is that they sample from a restricted range of conditions. Since all approaches have advantages and disadvantages, a multimethod approach is considered the most comprehensive (Rothbart & Bates, 1998).

It is generally agreed that temperamental characteristics show continuity during infancy; however, long-term stability appears low to moderate (Putnam, Sanson, & Rothbart, 2002; Rothbart & Bates, 1998). Some dimensions are seemingly more stable than others, particularly when an infant receives an extreme rating. For example, Jerome Kagan (1998; Kagan & Fox, 2006) has found that extremely fearful and highly reactive infants, whom he has classified as “inhibited,” often remain so during childhood and even into adolescence. To a lesser extent, dimensions such as irritability/frustration, positive affect, activity level, and sociability also have exhibited stability (Rothbart & Bates, 1998). Continuity among individuals is likely promoted by the workings of evocative genotype/environment correlations (Scarr & McCartney, 1983) where one’s behavior triggers relatively consistent reactions from others. For example, an infant who readily expresses interest and responsiveness toward people will likely elicit many positive social experiences and further become sociable. Nevertheless, personality predictions from early temperament in the first two years of life are not highly accurate, as many individuals appear to change (Caspi, 1998), especially those who are not rated at the extremes of any dimension. Because infant temperament does not reliably predict later personality, researchers concur that life experiences can alter as well as intensify its development. Genetic underpinnings are usually depicted as placing biological restrictions on the range of possible behavioral outcomes (Scarr, 1992) that can occur in response to environmental factors such as parenting practices. For example, caregivers who patiently help their inhibited infant and toddler to approach and handle new experiences can thereby reduce their offspring’s tendency toward heightened physiological arousal and behavioral withdrawal; however, such a child is highly unlikely to become fearless. Although the mutual influence between parenting and temperament has long been theoretically acknowledged (i.e., the difficult child may evoke maladaptive responses; anxious parenting may promote infant fearfulness), the precise interplay between environmental features (e.g., socialization practices, day-care) and particular temperamental characteristics awaits continued research. For many dimensions (e.g., effortful control, attention span/persistence), the specific experiences that alter early temperament remain unclear.


Attachment refers to an infant’s psychological bond to a specific figure, typically a primary caregiver. It motivates an infant to seek and maintain proximity to this individual, and ultimately obtain security and comfort from this figure during times of stress (Ainsworth, 1973; Bowlby, 1969). The bond involves a cognitive representation, or “internal working model,” of the attachment figure, the self, and their relations. This internal working model eventually encompasses beliefs, expectations, strategies, and heuristics for interpreting information and organizing memories related to the social world (Bowlby, 1973, 1980; Bretherton, 1996; Bretherton, Ridgeway, & Cassidy, 1990). Ainsworth (1972) documented four phases in the development of attachment, three of which occur during infancy. While in the preattachment phase (birth to two to three months), an infant displays undiscriminating social responsiveness with little evidence of preferring a primary caregiver to strangers. During the phase of attachment in the making (three to six to seven months), an infant shows greater orientation and ease of responsiveness toward familiar caregivers. Finally, in the clear-cut attachment phase (seven months to three years), an infant exhibits active maintenance of proximity to a specific figure as well as evidence of using the figure as a base from which to explore. Two fears typically reveal that an attachment has taken place: separation and stranger anxieties. During the latter half of the first year, an infant will show signs of distress when separated from his or her attachment figure. This reaction tends to peak at around 18 months of age and becomes less intense and frequent through preschool (Weinraub & Lewis, 1977). Additionally, it is common for an infant to exhibit wariness, often combined with interest, toward an unfamiliar person. This reaction declines in intensity over the second year of life (Sroufe, 1977, 1996).

Although infants are biologically predisposed to form an attachment due to its adaptive importance for protection and survival (Bowlby, 1969), there is variability in the quality of attachments that infants form. Researchers have documented four main classifications of attachment style. Infants with a secure style have a belief, and corresponding confidence, in the availability of the attachment figure. Thus, they use their figure as a secure base from which to explore, and security is readily achieved, not merely sought. The three insecure attachment types (avoidant, resistant, disorganized) share a lack of belief and confidence in the availability of their attachment figures. Thus, although the particular conduct of each insecure type varies, these infants do not exhibit secure base behavior, nor is security achieved without difficulty.

Attachment quality traditionally has been assessed during infancy using a lab procedure referred to as the strange situation (Ainsworth, Blehar, Waters, & Wall, 1978), which induces stress via a series of brief separations. It is primarily infants’ reactions during reunion that distinguish their attachment styles. Whereas secure infants tend to greet attachment figures warmly upon their return and welcome physical contact, avoidant infants generally turn away so as to ignore or avoid contact with the caregiver, and resistant infants remain near but are likely to resist affectionate overtures and may display anger (Ainsworth et al., 1978). Finally, disorganized infants may act dazed and freeze or show a confusing and inconsistent pattern of responses (Main & Soloman, 1990).

Theoretically, variation in infants’ quality of attachment emerges because infants adapt to the variation characterizing their caregiving environments. Research has generally supported the view that secure attachments are promoted by a caregiver’s sensitivity and appropriate responsiveness to an infant’s needs, feelings, and corresponding behavioral signals (Ainsworth, 1979; Ainsworth et al., 1978; De Wolff & van IJzendoorn, 1997: Prenatal Development Assignment Case Study Paper). Avoidant styles tend to be the result of caregiver rejection (e.g., unresponsiveness due to unavailability, disinterest, impatience, resentment), and resistant attachments are tied to caregiver inconsistency (e.g., responsiveness that may be irregular and unpredictable; Ainsworth, 1979; Ainsworth et al., 1978; Isabella, 1993). The more recently identified disorganized pattern has been linked to an attachment figure’s frightened and/or frightening behavior (e.g., alarm, neediness, trance-like states, maltreatment/ abuse; Lyons-Ruth, Melnick, Bronfman, Sherry, & Llanas, 2004; Main & Hess, 1990). Because the internal working model is initially flexible and receptive to changes in the caregiving environment, an infant’s cognitive representations will adjust to new information occurring in the social realm. Thus, an infant’s attachment style is quite changeable during the first and second years of life. Nonetheless, repeated confirming experiences render an infant’s attachment style and associated cognitive model less modifiable after infancy. As the internal working model becomes increasingly resistant to change, it will distort attachment-relevant information to its existing structure (Bowlby, 1980). Belsky, Spritz, and Crnic (1996) found that although three-year-olds with varying attachment styles paid equal attention to positive and negative events dramatized in a puppet show, insecurely attached children had better memories for the negative experiences, whereas securely attached children better remembered the positive incidents.

Numerous researchers have suggested that attachment quality during infancy has an impact on young children as they develop. For example, compared to counterparts with insecure primary attachments, securely attached infants display less fear and anger as toddlers and preschoolers (Kochanska, 2001) and have better social skills and relations with their peers during childhood (Rubin, Bukowski, & Parker, 2006; Schneider, Atkinson, & Tardiff, 2001).

Infant attachment quality also appears to have long-term social ramifications. Secure attachment in infancy appears to contribute to healthy romantic relationships in adolescence (Collins, Hennighausen, Schmit, & Sroufe, 1997), and adult romantic attachment styles appear to reflect individuals’ attachment histories (Fraley, 2002). Even care-giving of one’s own offspring appears to be associated with early attachment status. Compared to those with insecure attachment histories as measured by the Adult Attachment Interview (see Main, 1991), parents with secure attachment histories appear to interact more sensitively and promote secure attachments with their children (van IJzendoorn, 1995). Despite these predictive associations to adolescent and adult social functioning, the contribution of early primary attachment status relative to other factors such as subsequent parenting, family circumstances (e.g., parental divorce), and peer relationships remains the subject of further research. Moreover, although an infant often develops multiple attachment relationships within weeks after forming his or her primary attachment (Schaffer & Emerson, 1964), the organization of these internal working models remains unclear (e.g., hierarchical versus integrative or independent), as is their relative influence on long-term social development (Main, 1999).


The period of life from conception to the second birthday reveals a profound amount of developmental change, not only physically but also in multiple domains. Prenatally, shortly after the onset of gestation, the brain forms rapidly and achieves the basic structure found in the adult brain. The proliferation of neurons soon reaches its peak, and we witness the production and growth of axons and dendrites and the establishment of synaptic connections. Along with the brain’s rapid development emerges the capacity of nearly all the senses to function to such a level as to enable assessable responsivity and habituation. By the last trimester, hearing becomes sophisticated enough to promote preferences for familiarity at birth, such as for the sound of the mother’s voice. Researchers also observe the emergence of rest-activity cycles and sleep-wake states that resemble those found in adults. Such rapid prenatal growth and development is not entirely canalized (i.e., genetic restriction to predetermined developmental paths; see Waddington, 1966, for a discussion of canalization). Thus, the fetus is vulnerable to physical, neurological, and ultimately cognitive and behavioral troubles stemming from environmental teratogens that pass through to him or her while in utero. For example, researchers have documented short-term and even long-term problems associated with prenatal exposure to tobacco, alcohol, and cocaine.

The following two years after birth (ages 1 to 3) also usher in a considerable amount of change, arguably more than any other 24-month period that follows. Neurologically, we behold the peak of synaptogenesis and plasticity, including the destruction of inactive neurons and synapses. Infancy also marks the emergence and pervasive use of symbolism that serves as the basis of human thinking and language, and begins to overtly reveal itself through one- and two-word utterances and signs of pretend play. As a result of such developments in the cognitive realm, the two-year-old perhaps shares more in common with an adult, in terms of thinking, than he/she does with a newborn. It is also during infancy that early personality, in the form of temperamental behavioral consistencies, becomes evident. Although aspects of temperament may be altered by experiences, temperamental characteristics likewise influence the transactions one has with other humans and one’s larger society. Finally, it is during infancy that a seemingly asocial being bonds with his or her caregivers and purportedly develops subconscious representations of human relationships. The emergence of these cognitive models for human social interaction is hardly gradual. Although such representations are changeable during this initial life phase, they become increasingly inflexible, with the result having a potentially lasting influence, for better or worse, on one’s social functioning.

In total, the scope and rate of transformations—physical, cognitive, psychosocial—that occur during the prenatal period and infancy are often astounding to caregivers and researchers alike. Nonetheless, the full array of abilities, changes, and associated issues and aberrations during each of these episodes of human life is not wholly documented. Likewise, the underlying mechanisms of change, as well as the alterations to change due to experience, are not precisely understood, nor are the degree and means to which these first months and years of human life ultimately influence the future functioning of the individual as a child and adult. Thus, despite our sizable knowledge base, investigators fascinated with young humans still have plenty of questions that inspire continued research.


  1. Aguiar, A., & Baillargeon, R. (1998). Eight-and-a-half-month-old infants’ reasoning about containment events. Child Development, 69, 636-653.
  2. Ainsworth, M. D. S. (1972). Attachment and dependency: A comparison. In J. L. Gewirtz (Ed.), Attachment and dependency. Washington, DC: V. H. Winston and Sons.
  3. Ainsworth, M. D. S. (1973). The development of infant-mother attachment. In B. M. Caldwell & H. N. Ricciuti (Eds.), Review of child development research (Vol. 3). Chicago: University of Chicago Press.
  4. Ainsworth, M. D. S. (1979). Attachment as related to mother-infant interaction. In J. Rosenblatt, R. Hinde, C. Beer, & M. Busnel (Eds.), Advances in the study of behavior (Vol. 9). New York: Academic Press.
  5. Ainsworth, M. D. S., Blehar, M., Waters, E., & Wall, S. (1978). Patterns of attachment: A psychological study of the strange situation. Hillsdale, NJ: Erlbaum.
  6. Amso, D., & Casey, B. J. (2006). Beyond what develops when neuroimaging may inform how cognition changes with development. Current Directions in Psychological Science, 75, 24-29.
  7. Aslin, R., Jusczyk, P., & Pisoni, D. (1998). Speech and auditory processing during infancy: Constraints on and precursors to language. In W. Damon (Series Ed.), D. Kuhn, & R. Siegler (Vol. Eds.), Handbook of child psychology: Vol. 2. Cognition, perception, and language (5th ed.). New York: Wiley.
  8. Baillargeon, R. (1987). Object permanence in 3 VV- and 4 VV-month-old infants. Developmental Psychology, 23, 655-664.
  9. Baillargeon, R., & DeVos, J. (1991). Object permanence in young infants: Further evidence. Child Development, 62, 1227-1246.
  10. Baillargeon, R., Kotovsky, L., & Needham, A. (1995). The acquisition of physical knowledge in infancy. In G. Lewis, D. Premack, & D. Sperber (Eds.), Causal understandings in cognition and culture. Oxford, UK: Oxford University Press.
  11. Beeghly, M., Martin, B., Rose-Jacobs, R., Cabral, H., Heeren, T., Augustyn, M., et al. (2006). Prenatal cocaine exposure and children’s language functioning at 6 and 9.5 years: Moderating effects of child age, birthweight, and gender. Journal of Pediatric Psychology, 37, 98-115.
  12. Behnke, M., Eyler, F. D., Warner, T. D., Garvan, C. W., Hou, W., & Wobie, K. (2006). Outcome from a prospective, longitudinal study of prenatal cocaine use: Preschool development at 3 years of age. Journal of Pediatric Psychology, 37, 41-49.
  13. Beilin, H. (1992). Piaget’s enduring contribution to developmental psychology. Developmental Psychology, 28, 191-204.
  14. Belsky, J., Spritz, B., & Crnic, K. (1996). Infant attachment security and affective-cognitive information processing at age 3. Psychological Science, 7, 111-114.
  15. Bendersky, M., Bennett, D., & Lewis, M. (2006). Aggression at age 5 as a function of prenatal exposure to cocaine, gender, and environmental risk. Journal of Pediatric Psychology, 37, 71-84.
  16. Birch, E. (1993). Stereopsis in infants and its developmental relation to visual acuity. In K. Simons (Ed.), Early visual development: Normal and abnormal (pp. 224-236). New York: Oxford University Press.
  17. Bowlby, J. (1969). Attachment and loss: Vol. I. Attachment. New York: Basic Books.
  18. Bowlby, J. (1973). Attachment and loss: Vol. 2. Separation. New York: Basic Books.
  19. Bowlby, J. (1980). Attachment and loss: Vol. 3. Loss, sadness, and depression. New York: Basic Books.
  20. Bretherton, I. (1996). Internal working models of attachment relationships as related to resilient coping. In G. G. Noam & K. W. Fischer (Eds.), Development and vulnerability in close relationships. Mahwah, NJ: Erlbaum.
  21. Bretherton, I., Ridgeway, D., & Cassidy, J. (1990). The role of internal working models in the attachment relationship: Theoretical, empirical, and developmental considerations. In M. Greenberg, D. Cicchetti, & E. M. Cummings (Eds.), Attachment in the preschool years: Theory, research, and intervention. Chicago: University of Chicago Press.
  22. Buka, S. L., Shenassa, E. D., & Niaura, R. (2003). Elevated risk of tobacco dependence among offspring of mothers who smoked during pregnancy: A 30-year prospective study. American Journal of Psychiatry, 160(11), 1978-1984.
  23. Buss, A., & Plomin, R. (1984). Temperament: Early developing personality traits. Hillsdale, NJ: Erlbaum.
  24. Buss, R. R., Sun, W., & Oppenheim, R. W. (2006). Adaptive roles of programmed cell death during nervous system development. Annual review of neuroscience, 29, 1-35.
  25. Caspi, A. (1998). Personality development across the life course. In W. Damon (Series Ed.), N. Eisenberg (Vol. Ed.), Handbook of child psychology: Vol. 3. Social, emotional, and personality development (5th ed.) New York: Wiley.
  26. Centers for Disease Control and Prevention. (2004). Alcohol consumption among women who are pregnant or who might become pregnant—United States, 2002. MMWR (Morbidity and Mortality Weekly Report), 53(50), 1178-1181.
  27. Collins, W. A., Hennighausen, K., Schmit, D., & Sroufe, L. A. (1997). Developmental precursors of romantic relation-ships: A longitudinal analysis. In S. Shulman & W. A. Collins (Eds.), Romantic relationships in adolescence: Developmental perspectives (pp. 69-84). San Francisco: Jossey-Bass.
  28. Couperus, J. W., & Nelson, C. A. (2006). Early brain development and plasticity. In K. McCartney & D. Phillips (Eds.), Blackwell handbook of early childhood development (pp. 85-105). Malden, MA: Blackwell.
  29. DeCasper, A., & Fifer, W. (1980). Of human bonding: Newborns prefer their mothers’ voices. Science, 208, 1174-1176.
  30. DeCasper, A., & Spence, M. (1986). Prenatal maternal speech influences newborns’ perception of speech sounds. Infant Behavior and Development, 9, 133-150.
  31. Dennis, T., Bendersky, M., Ramsay, D., & Lewis, M. (2006). Reactivity and regulation in children prenatally exposed to cocaine. Developmental Psychology, 42, 688-697.
  32. de Vries, J. I. P., & Hopkins, B. (2005). Fetal movements and postures: What do they mean for postnatal development? In B. Hopkins & S. P. Johnson (Eds.), Prenatal development of postnatal functions (pp. 177-219). Westport, CT: Praeger.
  33. De Wolff, M., & van IJzendoorn, M. (1997). Sensitivity and attachment: A meta-analysis on parental antecedents of infant attachment. Child Development, 66, 571-591.
  34. DiPietro, J. A. (2005). Neurobehavioral assessment before birth. Mental Retardation and Developmental Disabilities Research Reviews, 11, 4-13.
  35. DiPietro, J. A., Caulfield, L. E., Irizarry, R. A., Chen, P., Merialdi, M., & Zavaleta, N. (2006). Prenatal development of intrafetal and maternal-fetal synchrony. Behavioral Neuroscience, 120, 687-701.
  36. DiPietro, J. A., Hodgson, D. M., & Costigan, K. A. (1996). Fetal neurobehavioral development. Child Development, 67, 2553-2567.
  37. Fernald, A. (2004). Auditory development in infancy. In G. Bremner & A. Fogel (Eds.), Blackwell handbook of infant development (pp. 35-70). Malden, MA: Blackwell.
  38. Field, T. M. (1990). Infancy. Cambridge, MA: Harvard University Press.
  39. Flavell, J. H. (1963). The developmental psychology of Jean Piaget. New York: Van Nostrand Reinhold.
  40. Fraley, R. (2002). Attachment stability from infancy to adulthood: Meta-analysis and dynamic modeling of developmental mechanisms. Personality and Social Psychology Review, 6, 123-151.
  41. Fried, P. A. (2002). Conceptual issues in behavioral teratology and their application in determining long-term sequelae of prenatal marihuana exposure. Journal of Child Psychology and Psychiatry, 43, 81-102.
  42. Gibson, C. L., Piquero, A. R., & Tibbetts, S. G. (2000). Assessing the relationship between maternal cigarette smoking during pregnancy and age at first police contact. Justice Quarterly, 77, 519-541.
  43. Gopnick, A., & Meltzoff, A. (1997). Words, thoughts, and theories. Cambridge, MA: MIT Press.
  44. Howell, K. K., Lynch, M. E., Platzman, K. A., Smith, G. H., & Coles, C. D. (2006). Prenatal alcohol exposure and ability, academic achievement, and school functioning in adolescence: A longitudinal follow-up. Journal of Pediatric Psychology, 37, 116-126.
  45. Huizink, A. C., & Mulder, E. J. H. (2006). Maternal smoking, drinking or cannabis use during pregnancy and neurobe-havioral and cognitive functioning in human offspring. Neuroscience & Biobehavioral Reviews, 30, 24-U.
  46. Huotilainen, M., Kujala, A., & Hotakainen, M. (2005). Short-term memory functions of the human fetus recorded with magnetoencephalography. Neuroreport, 76, 81-84.
  47. Jacobson, S. W., & Jacobson, J. L. (2001). Alcohol and drug-related effects of development: A new emphasis on contextual factors. Infant Mental Health Journal, 22, 416-430.
  48. Isabella, R. (1993). Origins of attachment: Maternal interactive behavior across the first year. Child Development, 64, 605-621.
  49. James, D., Pillai, M., & Smoleniec, J. (1995). Neurobehavioral development in the human fetus. In J. Lecanuet, W. P. Fifter, M. A. Krasnegor, & W. P. Smotherman (Eds.), Fetal development: A psychobiological perspective (pp. 101-128). Hillsdale, NJ: Erlbaum.
  50. Johnson, M. H. (2000). Functional brain development in infants: Elements of an integrative specialization framework. Child Development, 77, 75-81.
  51. Johnson, S. P. (2003). The nature of cognitive development. Trends in Cognitive Sciences, 7, 102-114.
  52. Kagan, J. (1998). Biology and the child. In W. Damon (Series Ed.) & N. Eisenberg (Vol. Ed.), Handbook of child psychology: Vol. 3. Social, emotional, and personality development (5th ed.). New York: Wiley.
  53. Kagan, J., & Fox, N. (2006). Biology, culture, and temperamental biases. In W. Damon, R. Lerner (Series Eds.) & N. Eisenberg (Vol. Ed.), Handbook of child psychology: Vol. 3. Social, emotional, and personality development (6th ed.). New York: Wiley.
  54. Kagan, J., & Herschkowitz, N. (2005). A young mind in a growing brain. Mahwah, NJ: Erlbaum.
  55. Kellman, P., & Arterberry, M. (2006). Infant visual perception. In W. Damon, R. Lerner (Series Eds.), D. Kuhn, & R. Siegler (Vol. Eds.), Handbook of child psychology: Vol. 2. Cognition, perception, and language (6th ed.). New York: Wiley.
  56. Kochanska, G. (2001). Emotional development in children with different attachment histories: The first three years. Child Development, 72, 474—490.
  57. Lecanuet, J. P., Granier-Deferre, C., & Busnel, M. C. (1995). Human fetal auditory perception. In J. Lecanuet, W. P. Fifter, M. A. Krasnegor, & W. P. Smotherman (Eds.), Fetal development: A psychobiologicalperspective (pp. 239-262). Hillsdale, NJ: Erlbaum.
  58. Lourenco, O., & Machado, A. (1996). In defense of Piaget’s theory: A reply to 10 common criticisms. Psychological Review, 103, 143-164.
  59. Lyons-Ruth, K., Melnick, S., Bronfman, E., Sherry, S., & Llanas, L. (2004). Hostile-helpless relational models and disorganized attachment patterns between parents and their young children: Review of research and implications for clinical work. In L. Atkinson & S. Goldberg (Eds.), Attachment issues in psychopathology and intervention. Mahwah, NJ: Erlbaum.
  60. Macchi Cassia, V., Turati, C., & Simion, F. (2004). Can a nonspecific bias toward top-heavy patterns explain newborns’ face preference? Psychological Science, 15(6), 379-383.
  61. Main, M. (1991). Metacognitive knowledge, metacognitive monitoring, and singular (coherent) versus multiple (incoherent) models of attachment. Findings and directions for future research. In C. Parkes, J. Stevenson-Hinde, & P. Marris (Eds.), Attachment across the life cycle (pp. 127-159). London: Routledge.
  62. Main, M. (1999). Attachment theory: Eighteen points with suggestions for future studies. In J. Cassidy & P. Shaver (Eds.), Handbook of attachment (pp. 845-887). New York: Guilford Press.
  63. Main, M., & Hess, E. (1990). Parents’ unresolved traumatic experiences are related to infant disorganized attachment status: Is frightened or frightening behavior the linking mechanism? In M. Greenberg, D. Cicchetti, & E. M. Cummings (Eds.), Attachment in the preschool years: Theory, research, and intervention. Chicago: University of Chicago Press.
  64. Main, M., & Soloman, J. (1990). Procedures for identifying infants as disorganized/disoriented during the Ainsworth Strange Situation. In M. Greenberg, D. Cicchetti, & E. M. Cummings (Eds.), Attachment in the preschool years: Theory, research, and intervention. Chicago: University of Chicago Press.
  65. Mayes, L. C. (2002). A behavioral teratogenic model of the impact of prenatal cocaine exposure on arousal regulatory systems. Neurotoxicology and Teratology, 24, 385-395.
  66. McClelland, J. L., & Jenkins, E. (1991). Nature, nurture, and connections: Implications of connectionist models for cognitive development. In K. VanLehn (Ed.), Architectures for intelligence: The twenty-second Carnegie Mellon symposium on cognition (pp. 41-73). Hillsdale, NJ: Erlbaum.
  67. Miller, P. H. (2002). Theories of developmental psychology (4th). New York: Worth.
  68. Meltzoff, A. (1999). Origins of theory of mind, cognition and communication. Journal of Communication Disorders, 32, 251-269.
  69. Meltzoff, A., & Moore, M. (1994). Imitation, memory, and the representations of persons. Infant Behavior and Development, 17, 83-89.
  70. Montreaux, M. C., Blacker, D., & Biederman, J. (2006). Maternal smoking during pregnancy and offspring overt and covert conduct problems: a longitudinal study. Journal of Child Psychology and Psychiatry, 47, 883-890.
  71. Moon, C., Cooper, R. P., & Fifer, W. (1993). Two-day-old infants prefer their native language. Infant Behavior and Development, 16, 495-500.
  72. Munakata, Y. (2004). Computational cognitive neuroscience of early memory development. Developmental Review, 24,133-153.
  73. Nanez, J., & Yonas, A. (1994). Effects of luminance and texture motion on infant defensive reactions to optical collision. Infant Behavior and Development, 17, 165-174.
  74. Nelson, C. A. (1999). Neural plasticity and human development. Current Directions in Psychological Science, 8, 42-45.
  75. Nelson, C. A., de Haan, M., & Thomas, K. M. (2006). Neuroscience of cognitive development: The role of experience and the developing brain. Hoboken, NJ: John Wiley.
  76. O’Connor, M. J., & Paley, B. (2006). The relationship of prenatal alcohol exposure and the postnatal environment to child depressive symptoms. Journal of Pediatric Psychology, 31, 50-64.
  77. Pascalis, O., de Haan, M., & Nelson, C. A. (2002). Is face processing species-specific during the first year of life? Science, 296, 1321-1323.
  78. Pascalis, O., DeSchonen, S., Morton, J., Deruelle, C., & Fabregrenet, M. (1995). Mother’s face recognition by neonate: A replication and extension. Infant Behavior and Development, 18, 79-85.
  79. Piaget, J. (1950). The psychology of intelligence. New York: Harcourt Brace.
  80. Piaget, J. (1952). The origins of intelligence in children. New York: International Universities Press.
  81. Piaget, J. (1964). Development and learning. In R. Ripple & V. Rockcastle (Eds.), Piaget rediscovered. Ithaca, NY: Cornell University Press.
  82. Piaget, J. (1970). Piaget’s theory. In P. H. Mussen (Ed.), Carmichael’s manual of child psychology (Vol. 1, pp. 703-732). New York: Wiley.
  83. Putnam, S. P., Sanson, A. V., & Rothbart, M. K. (2002). Child temperament and parenting. In M. Bornstein (Ed.), Handbook of parenting: Vol. 1. Children and parenting (2nd ed.).
  84. Mahwah, NJ: Erlbaum. Robinson, S. R., & Kleven, G. A. (2005). Learning to move before birth. In B. Hopkins & S. P. Johnson (Eds.), Prenatal development of postnatal functions (pp. 131-176). Westport, CT: Praeger.
  85. Rothbart, M. K. (2004). Temperament and the pursuit of an integrated developmental psychology. Merrill-Palmer Quarterly, 50, 492-505.
  86. Rothbart, M. K., Ahadi, S., & Evans, D. (2000). Temperament and personality: Origins and outcomes. Journal of Personality and Social Psychology, 78, 122-135.
  87. Rothbart, M. K., & Bates, J. E. (1998). Temperament. In W. Damon (Series Ed.) & N. Eisenberg (Vol. Ed.), Handbook of child psychology: Vol. 3. Social, emotional, and personality development (5th ed.). New York: Wiley.
  88. Rubin, K., Bukowski, W., & Parker, J. (2006). Peer interactions, relationships, and groups. In W. Damon, R. Lerner (Series Eds.) & N. Eisenberg (Vol. Ed.), Handbook of child psychology: Vol. 3. Social, emotional, and personality development (6th ed.). New York: Wiley.
  89. Scarr, S. (1992). Developmental theories for the 1990s: Development and individual differences. Child Development, 63, 1-19.
  90. Scarr, S., & McCartney, K. (1983). How people make their own environments: A theory of genotype/environment effects. Child Development, 54, 424-135.
  91. Schaal, B. (2005). From amnion to colostrums to milk: Odor bridging in early developmental transitions. In B. Hopkins & S. P. Johnson (Eds.), Prenatal development of postnatal functions (pp. 51-102). Westport, CT: Praeger.
  92. Schaal, B., Orgeur, P., & Rognon, C. (1995). Odor sensing in the human fetus: Anatomical functional, and chemoecological bases. In J. Lecanuet, W. P. Fifter, M. A. Krasnegor, & W. P. Smotherman (Eds.), Fetal development: A psychobiological perspective (pp. 205-237). Hillsdale, NJ: Erlbaum.
  93. Schaffer, R., & Emerson, P. (1964). The development of social attachments in infancy. Monographs of the Society for Research in Child Development, 29(3, Serial No. 94).
  94. Schiffman, H. R. (2000). Sensation and perception (5th ed.). New York: Wiley.
  95. Schneider, B., Atkinson, L., & Tardiff, C. (2001). Child-parent attachment and children’s peer relations: A quantitative review. Developmental Psychology, 37, 86-100.
  96. Schuetze, P., & Eiden, R. D. (2006a). The association between maternal cocaine use during pregnancy and physiological regulation in 4- to 8-week-old infants: An examination of possible mediators and moderators. Journal of Pediatric Psychology, 31, 15-26.
  97. Schuetze, P., & Eiden, R. D. (2006b). The association between maternal smoking and secondhand exposure and autonomic functioning at 2-4 weeks of age. Infant Behavior and Development, 29, 32-43.
  98. Schuetze, P., Eiden, R. D., & Dombkowski, L. (2006). The association between cigarette smoking during pregnancy and maternal behavior during the neonatal period. Infancy, 10, 267-288.
  99. Slater, A. (2004). Visual perception. In G. Bremner & A. Fogel (Eds.), Blackwell handbook of infant development (pp. 5-34). Malden, MA: Blackwell.
  100. Slater, A., & Johnson, S. (1999). Visual sensory and perceptual abilities of the newborn: Beyond the blooming, bussing confusion. In A. Slater & S. Johnson (Eds.), The development of sensory, motor and cognitive capacities in early infancy (pp. 121-141). Hove, UK: Sussex Press.
  101. Spelke, E. (1991). Physical knowledge in infancy: Reflections on Piaget’s theory. In S. Carey & R. Gelman (Eds.), Epigenesis of mind: Essays in biology and knowledge. Hillsdale, NJ: Erlbaum.
  102. Sroufe, L. A. (1977). Wariness of strangers and the study of infant development. Child Development, 48, 1184-1199.
  103. Sroufe, L. A. (1996). Emotional development: The organization of emotional life in the early years. Cambridge, UK: Cambridge University Press.
  104. Substance Abuse and Mental Health Services Administration. (2005). Substance use during pregnancy: 2002 and 2003 update. Rockville, MD: Author.
  105. Thomas, A., & Chess, S. (1977). Temperament and development. New York: Brunner/Mazel.
  106. Thomas, A., & Chess, S. (1986). The New York longitudinal study: From infancy to early adult life. In R. Plomin & J. Dunn (Eds.), The study of temperament: Changes, continuities, and challenges. Hillsdale, NJ: Erlbaum.
  107. Thomas, A., Chess, S., & Birch, H. G. (1968). Temperament and behavior disorders in children. New York: New York University Press.
  108. Thompson, R., & Raikes, H. (2003). Toward the next quarter-century: Conceptual and methodological challenges for attachment theory. Development and Psychopathology, 15, 691-718.
  109. Trehub, S., & Schellenberg, E. (1995). Music: Its relevance to infants. Annals of Child Development, 11, 1-24.
  110. Tronick, E. Z., Messinger, D. S., Weinberg, M. K., Lester, B. M., LaGasse, L., Seifer, R., et al. (2005). Cocaine exposure is associated with subtle compromises of infants’ and mothers’ social-emotional behavior and dyadic features of their interaction in the face-to-face still-face paradigm. Developmental Psychology, 41, 711-722.
  111. Turati, C. (2004). Why faces are not special to newborns: An alternative account of the face preference. Current Directions in Psychological Science, 13, 5-8.
  112. van IJzendoorn, M. (1995). Adult attachment representations, parental responsiveness, and infant attachment: A meta-analysis on the predictive validity of the adult attachment interview. Psychological Bulletin, 117, 387-103.
  113. Waddington, C. (1966). Principles of development and differentiation. New York: Macmillan.
  114. Weinraub, M., & Lewis, M. (1977). The determinants of children’s responses to separation. Monographs of the Society for Research in Child Development, 42(4, Serial No. 172).
  115. Werker, J., & Desjardins, R. (1995). Listening to speech in the first year of life: Experiential influences on phoneme perception. Current Directions in Psychological Science, 4, 76-81.
  116. Werker, J. F., & Tees, R. C. (2005). Speech perception as a window for understanding plasticity and commitment in language systems of the brain. Developmental Psychobiology, 46, 233-251.
  117. Wynn, K. (1992). Addition and subtraction by human infants. Nature, 358, 749-750.
  118. Yonas, A., Elieff, C., & Arterberry, M. (2002). Emergence of sensitivity to pictorial depth cues: Charting development in individual infants. Infant Behavior and Development, 25, 495-514.
  119. Zappasodi, F., Tecchio, F., & Pizzella, V. (2001). Detection of fetal auditory evoked responses by means of magnetoen-cephalography. Brain Research, 917, 167-173.
  120. Zentner, M., & Kagan, J. (1996). Perception of music by infants. Nature, 383, 29.
  121. Zentner, M., & Kagan, J. (1998). Infants’ perception of consonance and dissonance in music. Infant Behavior and Development, 21, 483-492.
  122. Zeskind, P. S., & Gingras, J. L. (2006). Maternal cigarette-smoking during pregnancy disrupts rhythms in fetal heart rate. Journal of Pediatric Psychology, 31, 5-14.

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