SNAP-25 modulation of calcium dynamics underlies differences in GABAergic and glutamatergic responsiveness to depolarization.

Authors: Verderio, C  Pozzi, D  Pravettoni, E  Inverardi, F  Schenk, U  Coco, S  Proux-Gillardeaux, V  Galli, T  Rossetto, O  Frassoni, C  Matteoli, M 
Citation: Verderio C, etal., Neuron. 2004 Feb 19;41(4):599-610.
Pubmed: (View Article at PubMed) PMID:14980208

SNAP-25 is a component of the SNARE complex implicated in synaptic vesicle exocytosis. In this study, we demonstrate that hippocampal GABAergic synapses, both in culture and in brain, lack SNAP-25 and are resistant to the action of botulinum toxins type A and E, which cleave this SNARE protein. Relative to glutamatergic neurons, which express SNAP-25, GABAergic cells were characterized by a higher calcium responsiveness to depolarization. Exogenous expression of SNAP-25 in GABAergic interneurons lowered calcium responsiveness, and SNAP-25 silencing in glutamatergic neurons increased calcium elevations evoked by depolarization. Expression of SNAP-25(1-197) but not of SNAP-25(1-180) inhibited calcium responsiveness, pointing to the involvement of the 180-197 residues in the observed function. These data indicate that SNAP-25 is crucial for the regulation of intracellular calcium dynamics and, possibly, of network excitability. SNAP-25 is therefore a multifunctional protein that participates in exocytotic function both at the mechanistic and at the regulatory level.

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CRRD ID: 1581082
Created: 2006-09-14
Species: All species
Last Modified: 2006-09-14
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RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.