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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
PubMed
Summary

Synapsins (Syns) regulate neurotransmitter release. Lacking Synapsin I impairs synchronous GABA release and boosts asynchronous release, impacting brain excitation/inhibition balance.

Keywords:
GABA interneuronsSynapsin Ihippocampusparvalbuminsomatostatin

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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.