Nature Neuroscience
2, 407 - 415 (1999)
doi:10.1038/8070
Splicing of  1A subunit gene generates phenotypic variants
of P- and Q-type calcium channelsEmmanuel Bourinet1, 5, Tuck W. Soong2, 4, 5, Kathy Sutton2, Sarah Slaymaker2, Eleanor Mathews2, Arnaud Monteil1, Gerald W. Zamponi3, Joel Nargeot1
& Terry P. Snutch21
Physiopathologie des Canaux Ioniques, IGH, CNRS UPR
1142, Montpellier, France
2
Biotechnology Laboratory, University of British Columbia,
Vancouver, British Columbia, Canada
3
Department of Pharmacology, University of Calgary,
Calgary, Alberta, Canada
4
Present Address: Institute of Molecular and Cell Biology,
30 Medical Drive, University of Singapore, Singapore
5
The first two authors contributed equally to this work
Correspondence should be addressed to Terry P. Snutch snutch@zoology.ubc.caP-type and Q-type calcium channels mediate neurotransmitter release at
many synapses in the mammalian nervous system. The  1A calcium
channel has been implicated in the etiologies of conditions such as episodic
ataxia, epilepsy and familial migraine, and shares several properties with
native P- and Q-type channels. However, the exact relationship between
1A and P- and Q-type channels is unknown. Here we report that alternative
splicing of the 1A subunit gene results in channels with
distinct kinetic, pharmacological and modulatory properties. Overall, the
results indicate that alternative splicing of the 1A gene
generates P-type and Q-type channels as well as multiple phenotypic variants.
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