ArticleThe Journal of physiology2004
Vasopressin-induced taurine efflux from rat pituicytes: a potential negative feedback for hormone secretion.
Article in The Journal of physiology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 41 citations in OpenAlex.
- Taurine and Astrocytes: A Homeostatic and Neuroprotective Relationship.Frontiers in molecular neuroscience · 2022Review
- The signaling role for chloride in the bidirectional communication between neurons and astrocytes.Neuroscience letters · 2019Review
- Cell Volume Control in Healthy Brain and Neuropathologies.Current topics in membranes · 2018Review
- Volume-regulated anion channel--a frenemy within the brain.Pflugers Archiv : European journal of physiology · 2016Review
- The maternal brain: an organ with peripartal plasticity.Neural plasticity · 2014Review
- Inner capillary diameter of hypothalamic paraventricular nucleus of female rat increases during lactation.BMC neuroscience · 2013Article
- Cellular and subcellular aquaporin-4 distribution in the mouse neurohypophysis and the effects of osmotic stimulation.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2011Article
- Receptor regulation of osmolyte homeostasis in neural cells.The Journal of physiology · 2010Review
- Chronic vs. acute interactions between supraoptic oxytocin neurons and astrocytes during lactation: role of glial fibrillary acidic protein plasticity.TheScientificWorldJournal · 2009Review
- Metabolism and synthesis of arginine vasopressin in conscious newborn sheep.American journal of physiology. Endocrinology and metabolism · 2008Article
- Volume-dependent osmolyte efflux from neural tissues: regulation by G-protein-coupled receptors.Journal of neurochemistry · 2008Review
- Two conventional protein kinase C isoforms, alpha and beta I, are involved in the ATP-induced activation of volume-regulated anion channel and glutamate release in cultured astrocytes.Journal of neurochemistry · 2008Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Previous work on the whole neurohypophysis has shown that hypotonic conditions increase release of taurine from neurohypophysial astrocytes (pituicytes). The present work confirms that taurine is present in cultured pituicytes, and that its specific release increases in response to a hypotonic shock. We next show that vasopressin (VP) and oxytocin (OT) also specifically release taurine from pituicytes. With an EC(50) of approximately 2 nm, VP is much more potent than OT, and the effects of both hormones are blocked by SR 49059, a V(1a) receptor antagonist. This pharmacological profile matches the one for VP- and OT-evoked calcium signals in pituicytes, consistent with the fact that VP-induced taurine efflux is blocked by BAPTA-AM. However, BAPTA-AM also blocks the taurine efflux induced by a 270 mosmol l(-1) challenge, which per se does not evoke any calcium signal, suggesting a permissive role for calcium in this case. Nevertheless, the fact that structurally unrelated calcium-mobilizing agents and ionomycin are able to induce taurine efflux suggests that calcium may also play a signalling role in this event. It is widely accepted that in hypotonic conditions taurine exits cells through anionic channels. Antagonism by the chloride channel inhibitors 4,4'-diisothiocyanatostilbene-2,2'-disulphonic acid (DIDS) and 5-nitro-2-(3-phenylpropylamino)-benzoic acid (NPPB) suggests the same pathway for VP-induced taurine efflux, which is also blocked in hypertonic conditions (330 mosmol l(-1)). Moreover, it is likely that the osmosensitivity of the taurine channel is up-regulated by calcium. These results, together with our in situ experiments showing stimulation of taurine release by endogenous VP, strengthen the concept of a glial control of neurohormone output.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.