| Abstract: | Small lesions of the tissue surrounding the anterior ventral third ventricle (AV3V) cause adipsia, but there is no compensatory antidiuretic response. Therefore, the fine structure of the supraoptic nucleus and neural lobe, the major sites of synthesis and release of antidiuretic hormone (ADH), were compared in rats rendered adipsic by AV3V lesions 3 days earlier, rats deprived of water for 3 days and rats drinking normally.In sham-lesioned rats which were deprived of water, neuronal somas in the supraoptic nucleus show signs of stimulated secretory activity. However, the neuronal somas of supraoptic nuclei of rats which did not drink because they were made adipsic by AV3V lesions resemble those of normally hydrated controls. Neural lobes of water-deprived animals contain a sharply reduced number of neurosecretory granulated vesicles and reduced apposition of glial processes with the perivascular connective tissue compared to those of normally hydrated rats. In contrast, neural lobes of rats with AV3V lesions contain large accumulations of densely packed neurosecretory vesicles, as well as abundant dense bodies and multilamellar bodies which may be evidence of increased crinophagy, and they have increased interposition of glial processes between axon endings and the perivascular connective tissue.In rats with AV3V lesions the severe dehydration due to adipsia was unable to stimulate release of ADH. The accumulation of neurosecretory vesicles in the neural lobe indicates that transport of ADH to the neural lobe was not impaired in this time period, but that exocytosis of ADH-containing neurosecretory vesicles in the neural lobe was blocked. |
