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 Neuroscijournal_title
Trends in neurosciencesauthors
Prager-Khoutorsky M,Bourque CWdoi
10.1016/j.tins.2009.11.004subject
Has Abstractpub_date
2010-02-01 00:00:00pages
76-83issue
2eissn
0166-2236issn
1878-108Xpii
S0166-2236(09)00196-9journal_volume
33pub_type
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