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Journal ArticleDOI

Physiological Pathways Regulating the Activity of Magnocellular Neurosecretory Cells

Gareth Leng, +2 more
- 01 Apr 1999 - 
- Vol. 57, Iss: 6, pp 625-655
TLDR
This review considers the rôle played by particular afferent pathways in the regulation of the activity of oxytocin and vasopressin cells.
About
This article is published in Progress in Neurobiology.The article was published on 1999-04-01. It has received 307 citations till now. The article focuses on the topics: Vasopressin & Oxytocin.

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Citations
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Journal ArticleDOI

The Oxytocin Receptor System: Structure, Function, and Regulation

TL;DR: The regulation by gonadal and adrenal steroids is one of the most remarkable features of the OT system and is, unfortunately, the least understood.
Journal ArticleDOI

Vasopressin and oxytocin release within the brain: a dynamic concept of multiple and variable modes of neuropeptide communication

TL;DR: This concept considers neuropeptides in the extracellular fluid of the brain rather than those in the cerebrospinal fluid or plasma as primary signals, triggering a variety of receptor-mediated effects, including those underlying behavioral and neuroendocrine regulation and psychopathology.
Journal ArticleDOI

Dendritic peptide release and peptide-dependent behaviours

TL;DR: The recently demonstrated ability of neuropeptides to prime vesicle stores for activity-dependent release could lead to a temporary functional reorganization of neuronal networks harbouring specific peptide receptors, providing a substrate for long-lasting effects.
Journal ArticleDOI

Physiology of Vasopressin Relevant to Management of Septic Shock

TL;DR: Clinical use of vasopressin should await a randomized controlled trial of its effects on clinical outcomes such as organ failure and mortality, because clinical studies have been relatively small, focused on physiologic end points, and because of potential adverse effects of vasipressin.
Journal ArticleDOI

The hypothalamic-neurohypophysial system regulates the hypothalamic-pituitary-adrenal axis under stress: an old concept revisited.

TL;DR: Data supporting the concept of HNS effects on HPA axis activity is presented and their possible impact on some aspects of behavioural regulation and psychopathology is outlined.
References
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Journal ArticleDOI

Histamine mediates fast synaptic inhibition of rat supraoptic oxytocin neurons via chloride conductance activation.

TL;DR: It is concluded that histaminergic neurons monosynaptically contact both oxytocin and vasopressin cells of the supraoptic nucleus and inhibit the former via activation of chloride channels which can be blocked by the histamine receptor subtype 2 antagonists, famotidine and cimetidine.
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Cellular localization and differential distribution of GABAA receptor subunit proteins and messenger RNAs within hypothalamic magnocellular neurons

TL;DR: Results show that all oxytocin and vasopressin neurons located in the supraoptic nucleus synthesize and express alpha 1, alpha 2 and beta 2 subunits of the GABAA receptor while those in the paraventricular nucleus are only immunoreactive for the alpha 2 subunit.
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Depolarizing effect of noradrenaline on neurons of the rat supraoptic nucleus in vitro.

TL;DR: It is concluded that NA depolarized and increased the firing rate of both vasopressin- and oxytocin-containing neurons through an action on alpha-adrenergic receptors.
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Extracellular potassium changes in the rat neurohypophysis during activation of the magnocellular neurosecretory system.

TL;DR: In this article, the extracellular [K+] in the isolated rat neurohypophysis maintained in vitro was measured using potassium-sensitive microelectrodes, and it was shown that the extacellular [k+] increase was largely independent of events subsequent to evoked release of hormone and transmitters.
Journal ArticleDOI

Histamine-induced prolonged depolarization in rat supraoptic neurons: G-protein-mediated, Ca2+-independent suppression of K+ leakage conductance

TL;DR: It is suggested that histamine depolarizes supraoptic neurons, at least in part, by inhibiting a K+ leakage current mediated by H1 receptors linked to GTP-binding proteins and Ca(2+)-independent pathways.
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