Osmosensation in vasopressin neurons: changing actin density to optimize function.

Abstract:

:The proportional relation between circulating vasopressin concentration and plasma osmolality is fundamental for body fluid homeostasis. Although changes in the sensitivity of this relation are associated with pathophysiological conditions, central mechanisms modulating osmoregulatory gain are unknown. Here, we review recent data that sheds important light on this process. The cell autonomous osmosensitivity of vasopressin neurons depends on cation channels comprising a variant of the transient receptor potential vanilloid 1 (TRPV1) channel. Hyperosmotic activation is mediated by a mechanical process where sensitivity increases in proportion with actin filament density. Moreover, angiotensin II amplifies osmotic activation by a rapid stimulation of actin polymerization, suggesting that neurotransmitter-induced changes in cytoskeletal organization in osmosensory neurons can mediate central changes in osmoregulatory gain.

journal_name

Trends Neurosci

journal_title

Trends in neurosciences

authors

Prager-Khoutorsky M,Bourque CW

doi

10.1016/j.tins.2009.11.004

subject

Has Abstract

pub_date

2010-02-01 00:00:00

pages

76-83

issue

2

eissn

0166-2236

issn

1878-108X

pii

S0166-2236(09)00196-9

journal_volume

33

pub_type

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