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Journal of Neuroscience, Vol 15, 376-384, Copyright © 1995 by Society for Neuroscience
Neonatal endotoxin exposure alters the development of the hypothalamic- pituitary-adrenal axis: early illness and later responsivity to stress
N Shanks, S Larocque and MJ Meaney
Douglas Hospital Research Centre, Department of Psychiatry, McGill University, Montreal, Canada.
The long-term consequences of neonatal endotoxin exposure on
hypothalamic-pituitary-adrenal axis (HPA) function were assessed in adult
female and male Long-Evans rats. At 3 and 5 d of age, pups were
administered endotoxin (Salmonella enteritidis, 0.05 mg/kg, i.p.) at a dose
that provokes a rapid and sustained physiological response, but with no
mortality. As adults, neonatally endotoxin-treated animals exhibited
significantly greater adrenocorticotrophic hormone (ACTH) and
corticosterone responses to restraint stress than controls. In addition,
dexamethasone pretreatment was less effective in suppressing ACTH responses
to restraint stress in endotoxin-treated animals than in controls,
suggesting decreased negative-feedback sensitivity to glucocorticoids.
Neonatal endotoxin treatment elevated resting-state median eminence levels
of corticotropin-releasing hormone (CRH) and arginine vasopressin in adult
male animals, and arginine vasopressin in both adult males and females.
Neonatal exposure to endotoxin also increased CRH mRNA expression in the
paraventricular nucleus of the hypothalamus of adult males, with no
difference in females. Finally, glucocorticoid receptor density was reduced
across a wide range of brain regions in the neonatal endotoxin-treated,
adult animals. These data illustrate the interactive nature of immune and
endocrine systems during development. It appears that endotoxin exposure
during critical stages of development decreases glucocorticoid
negative-feedback inhibition of ACTH secretagogue synthesis, thus
increasing HPA responsiveness to stress. The implication of these findings
is that exposure to gram-negative LPS in early life can alter the
development of neural systems which govern endocrine responses to stress
and may thereby predispose individuals to stress-related pathology.
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