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Related Experiment Videos

GABA(B) receptor activation and limbic network ictogenesis.

Massimo Avoli1, Ruba Benini, Philip de Guzman

  • 1Departments of Neurology and Neurosurgery, and of Physiology, Montreal Neurological Institute, McGill University, Montreal, QC, Canada H3A 2B4. toula.papadopoulos@mcgill.ca

Neuropharmacology
|December 5, 2003
PubMed
Summary

GABA(B) receptor activation in rat brain slices alters epilepsy-like activity by shifting seizure origin from the entorhinal cortex to the hippocampus, suggesting a role in limbic system ictogenesis.

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Area of Science:

  • Neuroscience
  • Epileptology
  • Pharmacology

Background:

  • The hippocampus and entorhinal cortex (EC) are interconnected brain regions involved in epilepsy.
  • 4-aminopyridine induces interictal and ictal discharges in rat brain slices.
  • N-methyl-D-aspartic (NMDA) and non-NMDA glutamatergic receptors play roles in epileptiform activity.

Purpose of the Study:

  • To investigate the effects of GABA(B) receptor activation on ictogenesis in hippocampus-entorhinal cortex slices.
  • To determine how GABA(B) receptor modulation influences the origin and propagation of epileptiform discharges.
  • To explore the potential role of GABA(B) receptor modulation in mesial temporal lobe epilepsy.

Main Methods:

  • Experiments were conducted on rat brain slices containing the hippocampus and entorhinal cortex.

Related Experiment Videos

  • 4-aminopyridine was used to induce epileptiform activity.
  • Baclofen (a GABA(B) receptor agonist) and CGP 35348 (a GABA(B) receptor antagonist) were applied.
  • Schaffer collaterals were cut to isolate network activity.
  • Dose-response curves were generated to determine IC50 values for baclofen in different regions.

    • Main Results:

    • 4-aminopyridine induced CA3-driven interictal discharges propagating to the EC and NMDA receptor-dependent ictal events originating in the EC.
    • GABA(B) receptor activation by baclofen depressed CA3 activity and unmasked non-NMDA glutamatergic receptor-dependent ictal discharges originating in the CA3 region.
    • Baclofen showed a lower IC50 in the EC (0.6 microM) compared to the CA3 region (2.5 microM), indicating greater sensitivity of the EC to GABA(B) receptor activation.
    • These effects were reversible by the GABA(B) receptor antagonist CGP 35348.

    Conclusions:

    • Entorhinal cortex ictogenesis is dependent on NMDA receptor function and CA3 output under control conditions.
    • GABA(B) receptor activation shifts ictogenesis from the EC to the CA3 region by differentially depressing EC excitability.
    • GABA(B) receptor modulation is proposed as a key mechanism regulating the site of seizure initiation, propagation, and receptor dependency in the limbic system.