| dc.description.abstract | Exposure to stress early in development can have lifelong effects on an organism's physiological and psychological health. Prior research suggests that prenatal stress exposure, among other effects, can lead to hyper-reactivity of the offspring's HPA axis and alterations in immune function. These stress-induced changes have been linked to a greater propensity to develop depression or an anxiety disorder in both human and non-human animals. Furthermore, prenatally stressed offspring have been found to be more susceptible to certain diseases, relative to non-stressed controls. The immune alterations induced by prenatal stress exposure may disrupt the normal communication between the immune system, endocrine system, and central nervous system, potentially making prenatally stressed individuals more vulnerable to the negative aspects of immune activation, namely cytokine-induced cognitive deficits and increased anxiety.^The present study investigated whether prenatal stress exposure would exaggerate these detrimental effects of immune activation.Specifically, we hypothesized that prenatally stressed subjects would be hypersensitive to endotoxin administration and would therefore show exaggerated learning deficits, increased anxiety-like behavior, and increased peripheral and central interleukin-1b production. The observed results only partially supported our hypotheses, as prenatally stressed subjects showed evidence, albeit modest, of increased anxiety-like behavior following endotoxin administration relative to non-stressed controls. However, the data failed to support the primary hypothesis that prenatally stressed subjects would show exaggerated cognitive deficits, engendered via enhanced peripheral and central IL-1b production, following immune activation.^Collectively, these data suggest that while prenatal stress exposure may lead to increases in anxiety-like behavior following a subthreshold dose of endotoxin, it does not appear to produce greater susceptibility to LPS-induced cognitive decline or elevations in proinflammatory cytokine production. | |
