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A recent study demonstrated that an N-terminal splice variant of the transient receptor potential vanilloid type 1 (TRPV1) is essential for osmosensory transduction in the SON. In the present study, we examined the effects of mannitol and angiotensin II on miniature EPSCs (mEPSCs) in the supraoptic MNCs using whole-cell patch-clamp recording in<jats:italic>in vitro<\/jats:italic>slice preparation. Mannitol (60 m<jats:sc>m<\/jats:sc>) and angiotensin II (0.1 \u03bc<jats:sc>m<\/jats:sc>) increased the frequency of mEPSCs without affecting the amplitude. These effects were attenuated by pre-exposure to a nonspecific TRPV channel blocker, ruthenium red (10 \u03bc<jats:sc>m<\/jats:sc>) and enhanced by pre-exposure to cannabinoid type1 receptor antagonist, AM251 (2 \u03bc<jats:sc>m<\/jats:sc>). Mannitol-induced potentiation of mEPSCs was not attenuated by angiotensin II receptor antagonist, losartan (10 \u03bc<jats:sc>m<\/jats:sc>), indicating independent pathways of mannitol and angiotensin II to the TRPV channels. The potentiation of mEPSCs by mannitol was not mimicked by a TRPV1 agonist, capsaicin, and also not attenuated by TRPV1 blockers, capsazepine (10 \u03bc<jats:sc>m<\/jats:sc>). PKC was involved in angiotensin II-induced potentiation of mEPSCs. The effects of mannitol and angiotensin II on the supraoptic MNCs in<jats:italic>trpv1<\/jats:italic>knock-out mice were significantly attenuated compared with those in wild-type mice counterparts. The results suggest that hyperosmotic stimulation and angiotensin II independently modulate mEPSCs through capsaicin-insensitive TRPV1 channel in the presynaptic terminals of the SON.<\/jats:p>","DOI":"10.1523\/jneurosci.2986-09.2010","type":"journal-article","created":{"date-parts":[[2010,1,20]],"date-time":"2010-01-20T20:23:27Z","timestamp":1264019007000},"page":"876-884","source":"Crossref","is-referenced-by-count":17,"title":["TRPV1 Gene Deficiency Attenuates Miniature EPSC Potentiation Induced by Mannitol and Angiotensin II in Supraoptic Magnocellular 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