Stress-induced oxytocin release in the rat after lesion of the paraventricular nuclei; possible deficiency of corticotrophin-releasing factor.

Abstract Oxytocin is released under stressful conditions and corticotrophin-releasing factor (CRF) is known to be involved in mediating general 'stress responses'. We therefore examined whether CRF neurons in the paraventricular nucleus participate in the stress-induced oxytocin release in the rat. CRF (0.02 to 2 nmol) injected into the third ventricle produced a dose-dependent rise in the plasma oxytocin concentration. The oxytocin release induced by CRF occurred without a change in blood pressure, and was not affected by dexamethasone pretreatment, which prevents adrenocorticotrophin release following CRF injection. Lesioning of the paraventricular nucleus reduced oxytocin release by immobilization stress, but did not alter the release of oxytocin in response to osmotic stimulation induced by intraperitoneal injection of hypertonic saline. Anti-CRF serum injection into the third ventricle reduced delayed oxytocin response to immobilization stress. These results are consistent with the hypothesis that CRF neurons in the paraventricular nucleus are involved in the oxytocin release during immobilization stress in the rat.