Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P01178 (oxytocin)
 15,767 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

For over four decades steroids have been regarded first as facilitators of enzymic reactions and subsequently as activators of genomic activity. The brain, long studied in terms of its bioelectric properties and anatomical connectivity, has now been recognized as a complex target tissue for genomic effects of steroid hormones, which bring about long-lasting alterations in brain structure and neurochemistry as well as changes in behaviour and neuroendocrine function. Studies of steroid effects on brain bioelectric activity have also shown rapid effects which are difficult to explain by a strictly genomic mechanism. One way to distinguish between genomic and non-genomic effects is by the time course, with extremely rapid effects being non-genomic and delayed effects being genomic. Effects with onset latencies of minutes to an hour may be due to either mechanism. Examples illustrating genomic actions include delayed effects of oestrogen which alter oxytocin and GABAA receptors and induce spines on dendrites and delayed glucocorticoid effects on neuronal survival. There are also examples of apparent genomic effects of oestradiol which interact with rapid and apparently non-genomic effects of progesterone: progesterone rapidly promotes spread of oestrogen-induced oxytocin receptors in ventromedial hypothalamus and rapidly modifies oestrogen-regulated GABAA receptor density in hypothalamus. The former effect is one produced by progesterone itself whereas the latter effect may be related to the ability of progesterone metabolites to interact with the chloride channel of the GABAA-benzodiazepine receptor complex.
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PMID:Steroid effects on neuronal activity: when is the genome involved? 198 52

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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PMID:Vasopressin-induced taurine efflux from rat pituicytes: a potential negative feedback for hormone secretion. 1461 76