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Abstract
Retrospective studies in humans suggest that chronic maternal stress during pregnancy,
associated with raised plasma levels of CRH, ACTH and cortisol may increase the likelihood
of preterm birth, developmental delays and behavioural abnormalities in the children.
In adulthood, it may contribute to the significant association between the incidence
of schizophrenia, increased left or mixed handedness, reduction in cerebral asymmetry
and anomalies in brain morphology. Our studies and others have shown that prenatal
stress in rats can mimic these developmental and behavioural alterations. These rats
show a reduced propensity for social interaction, increased anxiety in intimidating
or novel situations and a reduction in cerebral asymmetry and dopamine turnover, consistent
with those in schizophrenic humans. Prenatally-stressed (PS) rats also show behaviour
consistent with depression, including a phase-shift in their circadian rhythm for
corticosterone, sleep abnormalities, a hedonic deficit and greater acquisition of
learned helplessness under appropriate conditions. These behavioural abnormalities
are associated with impaired regulation of the hypothalamic-pituitary-adrenal axis
response to stress and increased CRH activity. PS males may show demasculinisation
and feminisation of their sexual behaviour. The developmental and behavioural abnormalities
in PS offspring could occur through sensitisation of the foetal brain by maternal
stress hormones to the action of glucocorticoid and CRH and to neurotransmitters affected
by them. This may have long-lasting consequences and could explain the precipitation
of depressive symptoms or schizophrenia by psychosocial stress in later life. The
character of the behavioural abnormalities probably depends on the timing of the maternal
stress in relation to development of the particular neuronal systems.