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Review
. 2006 Nov;48(7):583-602.
doi: 10.1002/dev.20170.

The International Society for Developmental Psychobiology annual meeting symposium: Impact of early life experiences on brain and behavioral development

Affiliations
Review

The International Society for Developmental Psychobiology annual meeting symposium: Impact of early life experiences on brain and behavioral development

Regina Sullivan et al. Dev Psychobiol. 2006 Nov.

Abstract

Decades of research in the area of developmental psychobiology have shown that early life experience alters behavioral and brain development, which canalizes development to suit different environments. Recent methodological advances have begun to identify the mechanisms by which early life experiences cause these diverse adult outcomes. Here we present four different research programs that demonstrate the intricacies of early environmental influences on behavioral and brain development in both pathological and normal development. First, an animal model of schizophrenia is presented that suggests prenatal immune stimulation influences the postpubertal emergence of psychosis-related behavior in mice. Second, we describe a research program on infant rats that demonstrates how early odor learning has unique characteristics due to the unique functioning of the infant limbic system. Third, we present work on the rodent Octodon degus, which shows that early paternal and/or maternal deprivation alters development of limbic system synaptic density that corresponds to heightened emotionality. Fourth, a juvenile model of stress is presented that suggests this developmental period is important in determining adulthood emotional well being. The approach of each research program is strikingly different, yet all succeed in delineating a specific aspect of early development and its effects on infant and adult outcome that expands our understanding of the developmental impact of infant experiences on emotional and limbic system development. Together, these research programs suggest that the developing organism's developmental trajectory is influenced by environmental factors beginning in the fetus and extending through adolescence, although the specific timing and nature of the environmental influence has unique impact on adult mental health.

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Figures

FIGURE 1
FIGURE 1
The diagram illustrates the hypothesized early prenatal and postnatal factors involved in the precipitation of brain and behavioral pathology following prenatal immune challenge. Exposure to viral and bacterial pathogens rapidly results in the production of pro-(●) and anti-inflammatory (▲) cytokines in the maternal host. The specificity of the pathogen-induced cytokine production is critically influenced by the genetic background (not shown) as well as the gestational stage. Immunological stimulation is also strongly associated with the activation of the stress response axes such as the hypothalamic-pituitary-adrenal (HPA) axis. Trans-placental transfer of maternally produced cytokines and/or production of cytokines at the maternal-fetal interface lead to an elevation of these molecules in the fetal environment, including the fetal brain. The fetal system at late but not early/mid gestation contributes to this process by endogenously synthesizing and secreting specific cytokines following maternal immune activation. Once in the fetal brain, cytokines affect ongoing neurodevelopmental processes depending on the fetal developmental stage and cytokine specificity. Disturbance of normal fetal brain development by cytokine-associated inflammatory events results in altered neonatal brain maturation and ultimately leads to the emergence of adult psychopathology. The precise pattern of brain and behavioral pathology emerging in adulthood is also critically determined by the time of prenatal immune challenge, that is, prenatal immune activation at early/mid gestation precipitates behavioral dysfunctions associated with (but not limited to) the positive symptoms of schizophrenia, whereas prenatal immune activation at late gestation triggers behavioral pathology associated with the negative symptoms of the disease. Immunologically induced stress (e.g., via activation of the HPA axis).
FIGURE 2
FIGURE 2
Gray-scale images of odor-evoked local field potential (LFP) oscillatory activity in the basolateral amygdala of immature and adult rats. Light gray and white regions represent high power in an FFT analysis of LFP activity within specific frequency bands. In young rats, odor stimulation evokes strong, low frequency activity with minimal high-frequency components. In contrast, odors evoke strong high-frequency activity (low gamma/high beta) in adults. These results are similar to those observed in olfactory bulb and piriform cortex (Fletcher et al., 2005), and could have an important impact on local circuit processing of odors and their associations (see text).

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