Abstract

Striatal cholinergic interneurons exhibit tonic firing and more positive membrane potentials, however, the mechanism is unclear. In the present study, we found that intracellular perfusion of TRPC3 antibody induced outward current in striatal cholinergic interneurons identified by electrophysiological characteristics. The TRPC3 channel blocker flufenamic acid induced hyperpolarization, and reduced firing rate and outward current which was similar to the effect of TRPC3 channel antibody. Furthermore, by using single-cell RT-PCR we confirmed the co-existence of TRPC3 channel and D5 receptor mRNA in striatal cholinergic interneurons identified by electrophysiological characteristics and expression of choline acetyltransferase (Chat) mRNA. These results implied that the TRPC3 channel is involved in modulating the depolarization of cholinergic interneurons.

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