Abstract

Electrolytic lesions of tissue surrounding the preoptic recess (AV3V region) appear to cause loss of stimulatory input to the supraoptic nuclei from angiotensin receptors and osmoreceptors. To investigate the pathways affected by AV3V lesions, we observed the ultrastructural effects of coronal cuts in a plane caudal to the organum vasculosum lamina terminalis upon supraoptic nuclei and neural lobes of rats. Like AV3V lesions, these cuts caused degeneration of axons and terminals in the supraoptic nuclei. Degenerating terminals lay in axodendritic synapses and in axosomatic synapses on neurosecretory cells. Unlike AV3V lesions, the cuts did not result in an appearance of decreased secretory activity in the supraoptic nuclei or decreased release of hormone from the neural lobe. On the contrary, terminals in the neural lobe tended to be depleted of neurosecretory material, and glial cell processes tended to be withdrawn from the secretory interface at the basal lamina surrounding fenestrated capillaries; both are changes which have been associated with enhanced hormone release. We suggest that inhibitory input to the supraoptic nuclei is lost as a result of these cuts.

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