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Synapsin I Synchronizes GABA Release in Distinct Interneuron Subpopulations.
N Forte1,2, F Binda1,2, A Contestabile3
1Center for Synaptic Neuroscience and Technology, Istituto Italiano di Tecnologia, Largo Rosanna Benzi 10, 16132 Genova, Italy.
Cerebral Cortex (New York, N.Y. : 1991)
|September 11, 2019
Summary
Synapsins (Syns) regulate neurotransmitter release. Lacking Synapsin I impairs synchronous GABA release and boosts asynchronous release, impacting brain excitation/inhibition balance.
Area of Science:
- Neuroscience
- Molecular Biology
- Cell Biology
Background:
- Synapsins (Syns) are crucial phosphoproteins regulating synaptic vesicle (SV) release.
- Synaptic transmission involves synchronous and asynchronous neurotransmitter release.
- Dysregulation of excitation/inhibition balance, often linked to GABAergic signaling, can lead to epilepsy.
Purpose of the Study:
- To investigate the specific role of Synapsin I (SynI) in regulating the dynamics of gamma-aminobutyric acid (GABA) release.
- To determine how SynI deficiency affects synchronous versus asynchronous GABA release in the hippocampus.
- To identify the specific interneuron populations and calcium channel types involved in SynI-mediated GABA release regulation.
Main Methods:
- Patch-clamp electrophysiology in hippocampal slices to record GABA release.
- Synapsin I knockout (KO) mouse model.
- In situ hybridization to assess SynI expression in interneuron subtypes.
- Optogenetic stimulation of specific interneuron populations (parvalbumin and SOM).
- Pharmacological manipulation using ω-AgatoxinIVA to probe calcium channel involvement.
Main Results:
- SynI knockout impairs synchronous GABA release by reducing readily releasable SVs.
- SynI deficiency leads to a parallel increase in asynchronous GABA release.
- The impairment of synchronous release in SynI KO mice is mediated by P/Q-type Ca2+ channels.
- SynI shows differential expression in hippocampal interneurons, being higher in parvalbumin (PV) interneurons (synchronous release) than cholecystokinin or SOM interneurons (asynchronous release).
- Optogenetic activation confirmed reduced synchronous release in PV/SynIKO interneurons and increased asynchronous release in SOM/SynIKO interneurons.
Conclusions:
- Synapsin I plays a critical role in balancing synchronous and asynchronous GABA release.
- SynI differentially regulates GABA release dynamics depending on the interneuron subtype.
- SynI is essential for maintaining the precise timing and physiological balance of inhibitory neurotransmission in the hippocampus.
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