P/Q-type calcium channels mediate the activity-dependent feedback of syntaxin-1A

Kathy G. Sutton, John E. McRory, Heather Guthrie, Timothy H. Murphy and Terrance P. Snutch ()
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Kathy G. Sutton: Biotechnology Laboratory and Dept Psychiatry University of British Columbia
John E. McRory: Biotechnology Laboratory and Dept Psychiatry University of British Columbia
Heather Guthrie: Biotechnology Laboratory and Dept Psychiatry University of British Columbia
Timothy H. Murphy: Kinsmen Laboratory of Neurological Research, Dept Psychiatry University of British Columbia
Terrance P. Snutch: Biotechnology Laboratory and Dept Psychiatry University of British Columbia

Nature, 1999, vol. 401, issue 6755, 800-804

Abstract: Abstract Spatial and temporal changes in intracellular calcium concentrations are critical for controlling gene expression in neurons1,2,3,4,5. In many neurons, activity-dependent calcium influx through L-type channels stimulates transcription that depends on the transcription factor CREB by activating a calmodulin-dependent pathway6,7,8,9,10,11. Here we show that selective influx of calcium through P/Q-type channels12,13,14 is responsible for activating expression of syntaxin-1A, a presynaptic protein that mediates vesicle docking, fusion and neurotransmitter release. The initial P/Q-type calcium signal is amplified by release of calcium from intracellular stores and acts through phosphorylation that is dependent on the calmodulin-dependent kinase CaM K II/IV, protein kinase A and mitogen-activated protein kinase kinase. Initiation of syntaxin-1A expression is rapid and short-lived, with syntaxin-1A ultimately interacting with the P/Q-type calcium channel to decrease channel availability. Our results define an activity-dependent feedback pathway that may regulate synaptic efficacy and function in the nervous system.

Date: 1999
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DOI: 10.1038/44586

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