Osmosensation in vasopressin neurons: changing actin density to optimize function.
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.
Prager-Khoutorsky
Masha
M
Center for Research in Neuroscience, Research Institute of the McGill University Health Center, Montreal General Hospital, 1650 Cedar Avenue, Montreal, Canada.
Bourque
Charles W
CW
D000199:Actins / Q000502:physiology*; D000804:Angiotensin II; D000818:Animals; D001826:Body Fluids / Q000502:physiology; D003599:Cytoskeleton / Q000502:physiology; D006706:Homeostasis / Q000502:physiology; D006801:Humans; D009474:Neurons / Q000502:physiology*; D015398:Signal Transduction / Q000502:physiology; D050916:TRPV Cation Channels / Q000378:metabolism; D014667:Vasopressins / Q000378:metabolism*; D014882:Water-Electrolyte Balance / Q000502:physiology*
D000199:Actins; D050916:TRPV Cation Channels; C494484:TRPV1 receptor; D014667:Vasopressins; D000804:Angiotensin II