Long term effects on the supraoptic nuclei and neural lobe produced by ablation of the tissue surrounding the preoptic recess (AV3V)

Abstract

In previous investigations, lesions of the AV3V region surrounding the preoptic recess in the rat caused acute loss of the antidiuretic response to severe dehydration. Ultrastructural study of the supraoptic nuclei and neural lobes following several days of adipsia revealed a lack of response in neurosecretory cell bodies, which would normally show hypertrophy, and engorgement of axon terminals in the neural lobe with unreleased hormone, which would normally be depleted. When rats with such lesions were sustained through the acute phase, they regained their ability to concentrate their urine maximally in response to water deprivation, but their antidiuretic responses to angiotensin II or centrally injected hypertonic saline were still impaired. In this study we compared the fine structure of supraoptic nuclei and neural lobes of rats with AV3V lesions and rats with sham lesions after a recovery period of 5 weeks. We also compared responses to 5 days of water deprivation in lesioned and sham lesioned rats. Neurosecretory cell bodies in lesioned rats were smaller and contained fewer neurosecretory granulated vesicles, and axon terminals in the neural lobe contained more neurosecretory granulated vesicles compared to controls. In addition, the basal lamina surrounding fenestrated capillaries was covered to a greater degree by pituicyte processes in neural lobes of lesioned rats. Lesioned rats deprived of water for 5 days had changes in supraoptic nuclei and neural lobes which in general were qualitatively similar to those of controls. However, AV3V lesions blocked the increase in neurosecretory granulated vesicles in cell bodies in supraoptic nuclei and significantly inhibited depletion of neurosecretory granulated vesicles from axon terminals in the neural lobe of water deprived rats. We conclude that after 5 weeks of recovery the neurosecretory system had regained its ability to respond to dehydration, but the response was chronically affected by AV3V lesions.