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Updated: Aug 26, 2026

Visualizing Shifts on Neuron-Glia Circuit with the Calcium Imaging Technique
Published on: April 8, 2022
SNAP-25 modulation of calcium dynamics underlies differences in GABAergic and glutamatergic responsiveness to
Claudia Verderio1, Davide Pozzi, Elena Pravettoni
1Department of Medical Pharmacology, CNR Institute of Neuroscience, Center of Excellence for Neurodegenerative Diseases, University of Milano, Via vanvitelli 32, Milano 20129, Italy.
Abstract:
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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