ArticleBMC neuroscience2008
The role of the t-SNARE SNAP-25 in action potential-dependent calcium signaling and expression in GABAergic and glutamatergic neurons.
Article in BMC neuroscience, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 25 citations in OpenAlex.
- Targeting LncRNA-Vof16: A Novel Therapeutic Strategy for Neuropathic Pain Relief.CNS neuroscience & therapeutics · 2025Article
- The role of snare proteins in cortical development.Developmental neurobiology · 2022Review
- FOXC1 modulates MYOC secretion through regulation of the exocytic proteins RAB3GAP1, RAB3GAP2 and SNAP25.PloS one · 2017Article
- Regulation of Ca2+ channels by SNAP-25 via recruitment of syntaxin-1 from plasma membrane clusters.Molecular biology of the cell · 2016Article
- SNAP-25a/b Isoform Levels in Human Brain Dorsolateral Prefrontal Cortex and Anterior Cingulate Cortex.Molecular neuropsychiatry · 2015Article
- Accelerated intoxication of GABAergic synapses by botulinum neurotoxin A disinhibits stem cell-derived neuron networks prior to network silencing.Frontiers in cellular neuroscience · 2015Article
- Article
- Expression of synaptosomal-associated protein-25 in the rat brain after subarachnoid hemorrhage.Neural regeneration research · 2013Article
- Article
- Regulation of intracellular membrane trafficking and cell dynamics by syntaxin-6.Bioscience reports · 2012Review
- Release, neuronal effects and removal of extracellular β-nicotinamide adenine dinucleotide (β-NAD⁺) in the rat brain.The European journal of neuroscience · 2012Article
- Presynaptic residual calcium and synaptic facilitation at hippocampal synapses of mice with altered expression of SNAP-25.Brain research · 2012Article
- VAMP-2, SNAP-25A/B and syntaxin-1 in glutamatergic and GABAergic synapses of the rat cerebellar cortex.BMC neuroscience · 2011Article
- SNAP25 expression in mammalian retinal horizontal cells.The Journal of comparative neurology · 2011Article
- Endogenous SNAP-25 regulates native voltage-gated calcium channels in glutamatergic neurons.The Journal of biological chemistry · 2010Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundThe soluble N-ethylmaleimide-sensitive factor attachment protein receptor (SNARE) complex, comprised of SNAP-25, syntaxin 1A, and VAMP-2, has been shown to be responsible for action potential (AP)-dependent, calcium-triggered release of several neurotransmitters. However, this basic fusogenic protein complex may be further specialized to suit the requirements for different neurotransmitter systems, as exemplified by neurons and neuroendocrine cells. In this study, we investigate the effects of SNAP-25 ablation on spontaneous neuronal activity and the expression of functionally distinct isoforms of this t-SNARE in GABAergic and glutamatergic neurons of the adult brain.
resultsWe found that neurons cultured from Snap25 homozygous null mutant (Snap25-/-) mice failed to develop synchronous network activity seen as spontaneous AP-dependent calcium oscillations and were unable to trigger glial transients following depolarization. Voltage-gated calcium channel (VGCC) mediated calcium transients evoked by depolarization, nevertheless, did not differ between soma of SNAP-25 deficient and control neurons. Furthermore, we observed that although the expression of SNAP-25 RNA transcripts varied among neuronal populations in adult brain, the relative ratio of the transcripts encoding alternatively spliced SNAP-25 variant isoforms was not different in GABAergic and glutamatergic neurons.
conclusionWe propose that the SNAP-25b isoform is predominantly expressed by both mature glutamatergic and GABAergic neurons and serves as a fundamental component of SNARE complex used for fast synaptic communication in excitatory and inhibitory circuits required for brain function. Moreover, SNAP-25 is required for neurons to establish AP-evoked synchronous network activity, as measured by calcium transients, whereas the loss of this t-SNARE does not affect voltage-dependent calcium entry.
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