| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 4356212 | Hearing Research | 2007 | 12 Pages |
Abstract
These results suggest that hyposmotic stimulation can induce NO production by the [Ca2+]i increase, which is presumably mediated by the activation of TRPV4 in OHCs. NO conversely inhibits the Ca2+ response via the NO-cGMP-PKG pathway by a feedback mechanism.
Keywords
eNOSIHCsOHCsPKGDAF-2DAnNOSTRPV44α-PDDODQ[K+]iNOSEGTADAF-2 DAPSS4,5-diaminofluorescein diacetateDMSOl-NAMEl-NG-Nitroarginine methyl esterROIsethylene glycol-bis(β-aminoethyl ether)N,N,N′,N′-tetraacetic acidCochleaDimethylsulfoxideouter hair cellOuter hair cellsinner hair cellsendothelial nitric oxide synthaseneuronal nitric oxide synthaseSNAPRegions Of InterestNitric oxidenitric oxide synthaseTransient receptor potential vanilloid 4cGMP-dependent protein kinase
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Authors
Hiroko Takeda-Nakazawa, Narinobu Harada, Jing Shen, Nobuo Kubo, Hans-Peter Zenner, Toshio Yamashita,