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Decrease in GABAergic function induced by pentylenetetrazol kindling in rats: antagonism by MK-801.

M G Corda1, M Orlandi, D Lecca

  • 1Department of Experimental Biology, University of Cagliari, Italy.

The Journal of Pharmacology and Experimental Therapeutics
|August 1, 1992
PubMed
Summary
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Pentylenetetrazol (PTZ) kindling in rats reduced gamma-aminobutyric acid (GABA) inhibition and increased seizure susceptibility. NMDA receptor antagonist MK-801 prevented PTZ-induced kindling and heightened sensitivity to GABA inhibitors.

Area of Science:

  • Neuroscience
  • Pharmacology
  • Epilepsy Research

Background:

  • The pentylenetetrazol (PTZ) kindling model is used to study epilepsy.
  • Gamma-aminobutyric acid (GABA) and N-methyl-D-aspartate (NMDA) receptors play critical roles in neuronal excitability and seizure development.

Purpose of the Study:

  • To investigate the involvement of GABA-A and NMDA receptors in the PTZ kindling model.
  • To assess the effects of NMDA receptor antagonism on PTZ-induced kindling and associated neurochemical changes.

Main Methods:

  • Rats were subjected to repeated administration of subconvulsant PTZ doses to induce chemical kindling.
  • GABA receptor function was assessed by measuring [3H]GABA binding, 35S-t-butylbicyclophosphorothionate binding, and 36Cl- uptake.
  • Sensitivity to GABA function inhibitors was tested.

Related Experiment Videos

  • The NMDA receptor antagonist MK-801 was administered before PTZ injections.

    • Main Results:

    • PTZ kindling was successfully induced in 80% of rats.
    • PTZ kindling was associated with decreased GABAergic inhibition in the cerebral cortex.
    • Kindled rats exhibited increased sensitivity to convulsant effects of GABA function inhibitors.
    • MK-801 pretreatment dose-dependently prevented kindling development and the increased sensitivity to GABA inhibitors.

    Conclusions:

    • GABA-A receptor dysfunction contributes to the development of PTZ-induced kindling.
    • NMDA receptor antagonism effectively inhibits the development of chemical kindling and associated GABAergic deficits.