SHORT STRESSOR INDUCED LONG-LASTING INCREASES OF VASOPRESSIN STORES IN HYPOTHALAMIC CORTICOTROPIN-RELEASING HORMONE (CRH) NEURONS IN ADULT-RATS

Recently, we demonstrated that single administration of interleukin-1 beta (IL-I) to adult rats induces a long-lasting (weeks) increase of v asopressin (AVP) stores in terminals of CRH neurons in the external zo ne of the median eminence (ZEME), This is accompanied by hypersecretio n of AVP into the pituitary portal circulation and long-lasting hyperr esponsiveness of the hypothalamo-pituitary-adrenal (HPA) axis to stres sors, Here, we determine whether this form of plasticity of hypothalam ic CRH neurons is specific for IL-l or represents a general response t o a stressor, Single exposure of rats to lipopolysaccharide (LPS), IL- l, brain surgery or electric footshocks increases the AVP stores in th e ZEME 7 and II days later. Exposure to insulin or ether does not affe ct the AVP stores, The stressors have little or no effect on the CRH s tores in the ZEME. The amplitude of the increase in AVP as measured 7- 11 days after stimulation correlates with the overall ACTH response to the stressor (area under curve, r=0.89, P<0.0001), with the peak ACTH levels (r=0,52, P<0.05), but not with the duration of the ACTH respon se nor with any parameter of the corticosterone response. Administrati on of ACTH or corticosterone at doses that mimic stress-induced plasma levels does not increase AVP stores 7 days later, We conclude that lo ng-lasting increases of AVP stores in CRH terminals in the ZEME can be induced by various stressors and postulate that the amplitude of such increases depends on the degree of activation of the CRH neurons by t he stressor.