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Surface-accessible GABA supports tonic and quantal synaptic transmission.
J Vautrin1, D Maric, M Sukhareva
1Laboratory of Neurophysiology, National Institute of Neurological Disorders and Stroke, NIH, Bethesda, MD 20892, USA. vautrin@codon.nih.gov
Synapse (New York, N.Y.)
|June 8, 2000
Summary
This study reveals that the neurotransmitter GABA is stored in a matrix within neurons, not freely in vesicles. This matrix-bound GABA is released directly from the neuronal surface, challenging traditional exocytosis models for synaptic transmission.
Area of Science:
- Neuroscience
- Cell Biology
- Synaptic Transmission
Background:
- Exocytosis is the established model for fast synaptic transmission.
- Variability in miniature postsynaptic signals challenges the all-or-none exocytosis model.
- Endocrine studies suggest hormone release can be independent of exocytosis due to matrix trapping.
Purpose of the Study:
- To investigate if the neurotransmitter GABA is also trapped in a matrix before release.
- To challenge the exclusive role of exocytosis in fast synaptic transmission.
- To explore alternative mechanisms of GABA release from neurons.
Main Methods:
- Confocal microscopy and flow cytometry on embryonic rat hippocampal neurons.
- Utilized tetanus toxin fragment C (TTFC) binding to identify GT1b-containing membrane sites.
- Employed liposome experiments to mimic GABA binding and release.
Main Results:
- GABA immunoreaction was observed on the surface of live neurons and growth cones, correlating with TTFC binding.
- GT1b-containing liposomes showed similar GABA and TTFC surface binding patterns.
- Neurons exhibited tonic and transient postsynaptic signals mediated by GABA(A) receptors, rapidly suppressed by saline and transformable by isoguvacine.
Conclusions:
- Synaptic GABA may be stored in a matrix and released from the neuronal surface, not solely via exocytosis.
- Findings support an immediately releasable pool of transmitter accessible from the presynaptic surface.
- This challenges the conventional view of exocytosis as the sole mechanism for quantal synaptic transmission.