Date of Graduation

1999

Document Type

Thesis

Abstract

Research points to a combination of genetic, physiological, and environmental factors in the origin of anxiety and depressive disorders. These factors are adversely impacted by stress and can be influenced by both the prenatal and postnatal environments. Our research shows that offspring of mothers stressed during the last week of gestation appear to be normal in basal behavioral states. However, upon the presentation of stressful stimuli in the forms of anxiogenic drugs (e.g. yohimbine and idazoxan), prenatally stressed offspring respond differentially in comparison with control (normal) offspring. Doses of yohimbine and idazoxan that increased acoustic startle in control animals were ineffective at increasing acoustic startle responses in prenatally stressed animals. These findings suggested physiological alterations in the stress responsive systems of the body and their associated neurotransmitter systems. This hypothesis is supported by the observation that prenatally stressed animals had significantly elevated levels of basal plasma corticosterone, suggesting a state of chronic stress. This contention is further supported by alterations in the content of the neurotransmitter corticotropin releasing factor (CRF), a key mediator of the hypothalamic and extra-hypothalamic responses to stress. In prenatally stressed offspring, there were age-dependent increases in CRF content in several nuclei (e.g. amygdala, PVN, and LC/PBN) critically involved in eliciting, coordinating, and producing the body's response to stress. From these studies it can be concluded that the prenatal stress syndrome produces functional changes in rats in the form of physiological, neurochemical, and behavioral differences. These changes persist well into adulthood, suggesting their permanence.

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