| First Author | Sharif Naeini R | Year | 2006 |
| Journal | Nat Neurosci | Volume | 9 |
| Issue | 1 | Pages | 93-8 |
| PubMed ID | 16327782 | Mgi Jnum | J:105254 |
| Mgi Id | MGI:3614581 | Doi | 10.1038/nn1614 |
| Citation | Naeini RS, et al. (2006) An N-terminal variant of Trpv1 channel is required for osmosensory transduction. Nat Neurosci 9(1):93-8 |
| abstractText | 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. |
