An N-terminal variant of Trpv1 channel is required for osmosensory transduction.
Nat Neurosci
; 9(1): 93-8, 2006 Jan.
Article
em En
| MEDLINE
| ID: mdl-16327782
ABSTRACT
Body fluid homeostasis requires the release of arginine-vasopressin (AVP, an antidiuretic hormone) from the neurohypophysis. This release is controlled by specific and highly sensitive 'osmoreceptors' in the hypothalamus. Indeed, AVP-releasing neurons in the supraoptic nucleus (SON) are directly osmosensitive, and this osmosensitivity is mediated by stretch-inhibited cation channels. However, the molecular nature of these channels remains unknown. Here we show that SON neurons express an N-terminal splice variant of the transient receptor potential vanilloid type-1 (Trpv1), also known as the capsaicin receptor, but not full-length Trpv1. Unlike their wild-type counterparts, SON neurons in Trpv1 knockout (Trpv1(-/-)) mice could not generate ruthenium red-sensitive increases in membrane conductance and depolarizing potentials in response to hyperosmotic stimulation. Moreover, Trpv1(-/-) mice showed a pronounced serum hyperosmolality under basal conditions and severely compromised AVP responses to osmotic stimulation in vivo. These results suggest that the Trpv1 gene may encode a central component of the osmoreceptor.
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Base de dados:
MEDLINE
Assunto principal:
Sensação
/
Equilíbrio Hidroeletrolítico
/
Transdução de Sinais
/
Canais de Cátion TRPV
/
Neurônios
Idioma:
En
Ano de publicação:
2006
Tipo de documento:
Article
País de afiliação:
Canadá