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Related Experiment Videos

Presynaptic GABA(B) receptors on glutamatergic terminals of CA1 pyramidal cells decrease in efficacy after partial

Nick Poon1, Fabian Kloosterman, Chiping Wu

  • 1Department of Physiology-Pharmacology, University of Western Ontario, London, Ontario, Canada.

Synapse (New York, N.Y.)
|December 13, 2005
PubMed
Summary

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Partial hippocampal kindling reduces the effectiveness of presynaptic GABA(B) receptors on glutamate release. This decreased receptor efficacy enhances glutamate release and increases seizure susceptibility following repeated neural activity.

Area of Science:

  • Neuroscience
  • Epilepsy Research
  • Synaptic Plasticity

Background:

  • Presynaptic GABA(B) receptors modulate neurotransmitter release.
  • Hippocampal kindling is a model for studying epilepsy and synaptic changes.
  • The role of GABA(B) heterosynaptic receptors in kindling is not fully understood.

Purpose of the Study:

  • To investigate the hypothesis that presynaptic GABA(B) receptor efficacy decreases after partial hippocampal kindling.
  • To determine the functional consequences of altered GABA(B) receptor function on glutamate release and seizure susceptibility.

Main Methods:

  • Partial hippocampal kindling was induced in rats via high-frequency electrical stimulation.
  • Excitatory postsynaptic potentials (EPSPs) were recorded in hippocampal slices in vitro.

Related Experiment Videos

  • The effects of GABA(B) receptor agonists (baclofen) and A1 receptor agonists (cyclopentyladenosine) on synaptic transmission were assessed.

    • Main Results:

    • GABA(B) receptor agonist-induced suppression of field EPSPs and intracellular EPSPs was significantly reduced in kindled rats compared to controls.
    • The suppression of EPSPs by GABA(B) heteroreceptors was diminished at 1 and 21 days post-kindling.
    • A1 receptor-mediated suppression of EPSPs was not different between groups, indicating specificity of GABA(B) receptor changes.

    Conclusions:

    • Partial hippocampal kindling leads to a reduced efficacy of presynaptic GABA(B) heterosynaptic receptors on glutamatergic terminals.
    • This reduction in GABA(B) receptor function likely contributes to increased glutamate release and heightened seizure susceptibility.
    • Findings suggest a novel mechanism contributing to epileptogenesis in the hippocampus.