Drosophila CaV2 channels harboring human migraine mutations cause synapse hyperexcitability that can be suppressed by inhibition of a Ca2+ store release pathway.

Drosophila CaV2 channels harboring human migraine mutations cause synapse hyperexcitability that can be suppressed by inhibition of a Ca2+ store release pathway.

Gain-of-function mutations in the human CaV2.1 gene CACNA1A cause familial hemiplegic migraine type 1 (FHM1). To characterize cellular problems potentially triggered by CaV2.1 gains of function, we engineered mutations encoding FHM1 amino-acid substitutions S218L (SL) and R192Q (RQ) into transgenes...

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Bibliographic Details
Main Authors: Douglas J Brusich, Ashlyn M Spring, Thomas D James, Catherine J Yeates, Timothy H Helms, C Andrew Frank
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2018-08-01
Series:PLoS Genetics
Online Access:http://europepmc.org/articles/PMC6095605?pdf=render

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http://europepmc.org/articles/PMC6095605?pdf=render

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