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Biomedical subjects

C Frank

Publications and source records attributed to C Frank.

202 records · Page 12Linked to original sources

Antiepileptic effects of the excitatory amino acid antagonist cis-2,3 piperidine-dicarboxylic acid depend on non-N-methyl-d-aspartate receptors.

The effects of the broad spectrum antagonist of the excitatory amino acid neurotransmission, the cis-2,3 piperidine-dicarboxylic acid (cis-2,3 PDA) were investigated on the epileptiform activity induced in vitro by different treatments on rat hippocampal slices. The drug reduced the bursting duration by 45% and the occurrence of the additional population spikes by 50% compared with controls using 1 microM kainic acid to induce epileptiform bursting. At the same concentrations (50-100 microM) cis-2,3 PDA did not significantly affect the magnesium free-induced epileptiform activity. At higher concentrations (200-400 microM), the drug was able to reduce by 25% the bursting duration and the occurrence of the additional population spikes using 1 mM penicillin to induce epileptiform bursting. Our data indicate that the broad spectrum antagonist of the excitatory amino acid transmission, cis-2,3 PDA, presents a low antiepileptic activity that could be related to an influence on "non N-methyl-d-aspartate" (NMDA) receptors.

Animals↗

Influence of adenosinergic drugs on the epileptiform and neurotoxic effects of N-methyl-d-aspartate: comparison with the effects of MK801.

In the present paper, the influence of the adenosine receptor agonist N6-(l-2-phenylisopropyl)adenosine (L-PIA) and of the adenosine receptor antagonist caffeine on the epileptiform and neurotoxic effects of N-methyl-d-aspartate (NMDA) has been tested in rat hippocampal slices. Slice superfusion with 1 microM NMDA changed within 30 min the control CA1 field potentials into an epileptiform bursting in all experiments. Slice superfusion with 0.5-1 microM L-PIA or 50-100 microM caffeine plus 1 microM NMDA inhibited or potentiated, respectively, the CA1 epileptiform bursting duration with respect to a slice superfusion with 1 microM NMDA alone. Slice superfusion with 50-100 microM NMDA induced within a few minutes the appearance of short-lived (1-2 min) additional epileptiform population spikes, followed by an irreversible disappearance of the CA1 population spike. Slice superfusion with 50 microM of the NMDA antagonist dizocilpine (MK801) plus 50-100 microM NMDA prevented in all experiments the irreversible disappearance of the CA1 population spike with respect to a slice superfusion with 50-100 microM alone. Neither in a slice superfusion with 0.5-1 microM L-PIA plus 50-100 microM NMDA nor in a slice superfusion with 50-100 microM caffeine plus 50-100 microM NMDA did this effect occur. The results demonstrate that adenosine receptor ligands modulate the epileptiform but not the neurotoxic effects of NMDA.

Action Potentials↗