Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Regeneration and functional recovery of the hypothalamoneurohypophysial system (HNS) in neurohypophysectomized rats treated with either saline or vasopressin (VP) were analyzed utilizing specific immunohistochemical and physiological measures. Neural lobe ablation combined with VP administration precipitated a profound diabetes insipidus (following cessation of VP delivery) that persisted for the duration of the experiment. Diabetes insipidus was correlated with a drastic reduction in the number of VP-positive neurons in magnocellular hypothalamic nuclei. In contrast, large numbers of oxytocin (OT)-positive neurons survived neurohypophysectomy in VP-treated neurohypophysectomized rats; OT neurons accounted for the vast majority of magnocellular profiles observed in Nissl-counterstained sections. VP-immunoreactive fibers could be observed in limited quantities in the external lamina of the median eminence of VP-treated neurohypophysectomized rats, with little staining evident in the internal lamina. Saline-treated neurohypophysectomized rats exhibited the recovery of antidiuretic function characteristically seen following this lesion, with evidence of survival of considerable numbers of VP and OT neurons and median eminence hypertrophy. Both the internal and external laminae of the median eminence were densely innervated by large-caliber VP and OT fibers. Sham-operated animals receiving VP treatment did not show any long-term deficit in water metabolism, changes in the complement of VP or OT perikarya in hypothalamus, or changes in the innervation of the median eminence. Results indicate that VP treatment following neurohypophysectomy results in extensive retrograde degeneration of magnocellular VP neurons without affecting the survival of OT cells.
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PMID:Selective cell death of magnocellular vasopressin neurons in neurohypophysectomized rats following chronic administration of vasopressin. 330 29

A compelling body of evidence indicates that the suprachiasmatic nucleus (SCN) of the hypothalamus is a pacemaker in the rodent circadian timing system. Two important components of this evidence are studies showing that SCN lesions abolish circadian rhythms and others demonstrating restoration of circadian activity rhythms after transplantation of fetal SCN into the brains of arrhythmic hosts. In the present study, we evaluated what has remained a persisting issue in this transplant literature, the extent to which the exact localization and organization of the transplants is critical to their capacity to restore circadian function in the hamster. The data obtained indicate that the location of the graft in the ventricular system is not crucial to outcome. Grafts in the lateral ventricle, dorsal third ventricle, interventricular foramen, and caudal third ventricle are as capable of restoring circadian function as ones placed in the ventral third ventricle in the vicinity of the lesion. Restoration of rhythmicity does require that the grafts contain a minimum volume of SCN-like tissue as defined by cytoarchitecture and the presence of vasopressin--and vasoactive intestinal polypeptide (VIP)--immunoreactive cells and fibers. There is also an indication that VIP-immunoreactive elements are the component critical to functional recovery. Connections between graft and host are evident in the immunohistochemical material but are quite variable in extent and often very limited. Thus, the data obtained in this study are consistent with the view that restoration of circadian function by fetal grafts requires the presence of SCN, and probably VIP-containing neurons, but does not depend upon the exact location of the graft or the presence of specific connections between graft and host.
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PMID:Morphological correlates of circadian rhythm restoration induced by transplantation of the suprachiasmatic nucleus in hamsters. 786 54