Activity of T-type calcium channels is independent of CRMP2 in sensory neurons
AffiliationUniv Arizona Hlth Sci, Coll Med, Dept Pharmacol
MetadataShow full item record
PublisherTAYLOR & FRANCIS INC
CitationCai, S., Shan, Z., Zhang, Z., Moutal, A., & Khanna, R. (2019). Activity of T-type calcium channels is independent of CRMP2 in sensory neurons. Channels, 13(1), 147-152.
RightsCopyright © 2019 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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AbstractAmongst the regulators of voltage-gated ion channels is the collapsin response mediator protein 2 (CRMP2). CRMP2 regulation of the activity and trafficking of NaV1.7 voltage-gated sodium channels as well as the N-type (CaV2.2) voltage-gated calcium channel (VGCC) has been reported. On the other hand, CRMP2 does not appear to regulate L- (CaV1.x), P/Q- (CaV2.1), and R- (CaV2.3) type high VGCCs. Whether CRMP2 regulates low VGCCs remains an open question. Here, we asked if CRMP2 could regulate the low voltage-gated (T-type/CaV3.x) channels in sensory neurons. Reducing CRMP2 protein levels with short interfering RNAs yielded no change in macroscopic currents carried by T-type channels. No change in biophysical properties of the T-type currents was noted. Future studies pursuing CRMP2 druggability in neuropathic pain will benefit from the findings that CRMP2 regulates only the N-type (CaV2.2) calcium channels.
NoteOpen access journal
VersionFinal published version
SponsorsGuangdong Medical Research Foundation [A2017047]; National Institute of Neurological Disorders and Stroke [R01NS098772]; National Institute on Drug Abuse [R01DA042852]
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