| Literature DB >> 7059805 |
Abstract
The uptake and intracellular distribution of intravenously injected horseradish peroxidase were studied at various time intervals to trace the fate of endocytotic vacuoles formed at axon terminals in the neurohypophyses of normal and water deprived rats. Up to 4 h after tracer administration, enzymatic reaction product was limited to the cytoplasm of the neurohypophysial axons sequestered mainly in large vacuoles and cup-shaped organelles; with increasing time, it was also present in multivesicular bodies. Four hours after tracer injection, profiles labeled with peroxidase also appeared within neurosecretory perikarya in the supraoptic nucleus of the hypothalamus. Perikaryal organelles containing reaction product included vacuoles of various size, tubular profiles, multivesicular bodies and residual bodies. Morphometric analysis indicated that the accumulation of peroxidase-labeled profiles, both in the neurohypophysial axons and in the supraoptic perikarya, is closely related to secretion, for there was a highly significant augmentation in the relative volume occupied by such organelles in preparations from dehydrated animals, at 4 and 8 h after tracer injection, as compared to their corresponding controls. The analysis demonstrates moreover, that with increasing time, the mean volume density of peroxidase-labeled organelles in the supraoptic perikarya increased, whilst that in the neurohypophysial axons diminished. In the perikarya, reaction product progressively accumulated in the lysosomal multivesicular and residual bodies. These observations suggest that material internalized by compensatory endocytosis at the neurosecretory terminals after the release of hormone by exocytosis is subsequently removed by retrograde axonal transport to their perikarya in the hypothalamus where it gradually becomes sequestered in lysosomes. Whether all the material retrieved at the terminals, especially the membrane, is ultimately degraded remains to be determined.Entities:
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Year: 1982 PMID: 7059805 DOI: 10.1016/0006-8993(82)90925-8
Source DB: PubMed Journal: Brain Res ISSN: 0006-8993 Impact factor: 3.252