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- W2039742541 abstract "CaV2.3 channels and neurokinin receptors type-1 (NK1R) participate in pain signaling transmission. Recently, we have shown that CaV2.3 channels, heterologously expressed in HEK293 cells, were inhibited by NK1R through Gq/11 proteins mediated signaling (Meza et al., 2007; Mol Pharmacol 71:284-293). Here, we report that such inhibitory signaling was attenuated by the treatment of HEK293 cells with the cholesterol scavenger agent methyl-beta-cyclodextrin (MbCD). Our results show that MbCD treatment (15 mM/15 min) significantly reduced (47%) inhibition of CaV2.3 channels by NKA (1 microM), a natural agonist of NK1R. Interestingly, MbCD treatment diminished also the membrane capacitance (35%), but it did not affect the CaV2.3 current density. The analysis of macroscopic current biophysical properties (i.e., steady state voltage dependent activation and inactivation, and activation and inactivation kinetics) did not show important modifications induced by MbCD treatment. Our results suggest that MbCD treatment could attenuate the NK1R signaling pathway by depleting membrane cholesterol and, according with the rafts domain hypothesis, by disrupting the signaling complex involved in the inhibitory modulation of CaV2.3 channels by NK1R." @default.
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- W2039742541 date "2009-02-01" @default.
- W2039742541 modified "2023-09-29" @default.
- W2039742541 title "Methyl-beta-cyclodextrin Attenuates CaV2.3 Channels Modulation By NK1 Receptors" @default.
- W2039742541 doi "https://doi.org/10.1016/j.bpj.2008.12.875" @default.
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