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Whole-cell Currents Induced by Puff Application of GABA in Brain Slices

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Kainate modulates presynaptic GABA release from two vesicle pools.

Seena S Mathew¹, Lucas Pozzo-Miller, John J Hablitz

¹Department of Neurobiology and Evelyn F. McKnight Brain Institute, University of Alabama at Birmingham, Birmingham, Alabama 35294, USA.

The Journal of Neuroscience : the Official Journal of the Society for Neuroscience

|January 18, 2008

Summary

Kainate receptor activation enhances GABA release from presynaptic terminals in the rat prefrontal cortex. This study reveals kainate modulates two distinct pools of GABA vesicles involved in spontaneous and activity-dependent recycling.

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Quantitative Analysis of Synaptic Vesicle Pool Replenishment in Cultured Cerebellar Granule Neurons using FM Dyes

Quantitative Analysis of Synaptic Vesicle Pool Replenishment in Cultured Cerebellar Granule Neurons using FM Dyes

Published on: November 11, 2011

Area of Science:

Neuroscience
Cellular Neuroscience
Synaptic Plasticity

Background:

Inhibitory control by local neuronal circuits is vital for prefrontal cortex function.
Mechanisms underlying neuromodulator effects on inhibitory circuits, particularly synaptic vesicle recycling, remain poorly understood.
The existence of distinct vesicle pools for spontaneous versus activity-dependent recycling is debated.

Purpose of the Study:

To investigate the impact of kainate receptor activation on GABA release in the rat prefrontal neocortex.
To clarify the presynaptic mechanisms involved in neuromodulation of inhibitory neurotransmission.
To determine if different vesicle pools are involved in spontaneous and activity-dependent GABA release.

Main Methods:

Electrophysiological recordings of miniature inhibitory postsynaptic currents (IPSCs) in acute neocortical slices.
Styryl dye imaging and multiphoton excitation microscopy to visualize vesicular release.
Utilized spontaneous and evoked activity protocols for dye loading and vesicle recycling analysis.

Main Results:

Kainate receptor activation significantly increased the frequency of miniature IPSCs, indicating a presynaptic effect on GABA release.
Direct visualization confirmed kainate facilitates GABA release from inhibitory presynaptic terminals.
Evidence suggests the presence of two distinct pools of GABA-containing vesicles.
Kainate's modulation of these vesicle pools is dependent on the matching of dye loading protocols (spontaneous or evoked activity) with vesicle endocytosis and exocytosis.

Conclusions:

Kainate receptor activation enhances GABA release through presynaptic mechanisms in the prefrontal cortex.
The findings support the existence of at least two functionally distinct pools of GABA vesicles within inhibitory terminals.
The modulation of these vesicle pools by kainate is dependent on the specific activity patterns governing their recycling, highlighting a nuanced mechanism of synaptic regulation.