Spontaneous paroxysmal activity induced by zero magnesium and bicuculline: suppression by NMDA antagonists and GABA mimetics.
Slices of rat cerebral cortex developed spontaneous paroxysmal discharges when superfused with Krebs medium containing zero Mg2+ or 50 microM bicuculline. In both situations, the N-methyl-D-aspartate (NMDA) antagonists APV, 100 microM, and ketamine, 100 microM substantially reduced the frequency of the paroxysmal events, the reduction being greater in zero Mg2+. gamma-Aminobutyric acid (GABA) 1 mM, the GABA-A agonist muscimol 2 microM and the GABA-B receptor agonist baclofen 10 microM, each reduced the frequency of events in zero Mg2+ while muscimol and GABA also reduced the amplitude of the events. GABA and baclofen were similarly effective against bicuculline-induced events but the muscimol concentration required was 5-10-fold higher. These results suggest that, under our vitro conditions, neocortical cells are normally restrained from paroxysmal discharges by Mg2+. Inhibition by GABA through GABA-A receptors and inhibition by GABA through GABA-B receptors, may also contribute to this restraint.
D000818:Animals; D001224:Aspartic Acid / Q000031:analogs & derivatives / Q000037:antagonists & inhibitors; D001418:Baclofen / Q000494:pharmacology; D001640:Bicuculline / Q000494:pharmacology*; D003337:Corpus Callosum / Q000502:physiology; D066298:In Vitro Techniques; D008274:Magnesium / Q000502:physiology*; D016202:N-Methylaspartate; D009467:Neuromuscular Depolarizing Agents; D051381:Rats; D011919:Rats, Inbred Strains; D005680:gamma-Aminobutyric Acid / Q000502:physiology*
D009467:Neuromuscular Depolarizing Agents; D001224:Aspartic Acid; D005680:gamma-Aminobutyric Acid; D016202:N-Methylaspartate; D001418:Baclofen; D008274:Magnesium; D001640:Bicuculline