PLASTICITY IN THE STRESS-REGULATING CIRCUIT - DECREASED INPUT FROM THE BED NUCLEUS OF THE STRIA TERMINALIS TO THE HYPOTHALAMIC PARAVENTRICULAR NUCLEUS IN WISTAR RATS FOLLOWING ADRENALECTOMY

The bed nucleus of the stria terminalis is involved in the stress-regu lating circuit by funnelling limbic information to the hypothalamic pa raventricular nucleus. Since adrenalectomy influences both limbic stru ctures (by inducing cell death in the hippocampus) and the hypothalami c paraventricular nucleus (by increased corticotrophin-releasing hormo ne synthesis), we investigated whether the bed nucleus of the stria te rminalis is also influenced by adrenalectomy. For this purpose, we ana lysed and compared the projections from the bed nucleus of the stria t erminalis to the hypothalamic paraventricular nucleus in normal and ad renalectomized rats by anterograde tracer injections in the bed nucleu s of the stria terminalis. Quantitative analysis of the fibre pattern in the hypothalamic paraventricular nucleus of normal rats revealed a homogeneous distribution of fibres of the bed nucleus of the stria ter minalis over the different subdivisions of the hypothalamic paraventri cular nucleus. In adrenalectomized rats, the absolute fibre density wa s significantly lower in the whole hypothalamic paraventricular nucleu s (1.17 +/- 0.27 10(-3) mu m/mu m(3) in adrenalectomized rats versus 2 .59 +/- 0.24 10(-3) mu m/mu m(3) in normal rats; P < 0.01) and all its subdivisions. The largest decrease of fibre density was found in the corticotrophin-releasing hormone-rich part of the hypothalamic paraven tricular nucleus (relative fibre density; adrenalectomized rats: 0.602 +/- 0.106, versus 1.095 +/- 0.019 in normal rats, P < 0.01). These re sults show a loss of input from the bed nucleus of the stria terminali s to the hypothalamic paraventricular nucleus, and particularly to the corticotrophin-releasing hormone neurons, following adrenalectomy. Th e data suggest that this pathway within the stress-regulating circuit is functionally affected by corticosteroids in adult rats and may impl y that human disorders associated with corticosteroid imbalance are al lied to a changed circuitry in the brain.