Postsynaptic actions of baclofen associated with its antagonism of bicuculline-induced epileptogenesis in hippocampus.
The effect of baclofen on bicuculline-induced epileptogenesis was investigated in the CA3 region of hippocampal slices taken from rats 9 days to 8 weeks of age. Bath application of baclofen blocked all spontaneous epileptiform activity and raised the stimulus strength required for orthodromic induction of epileptiform discharges. Baclofen was equally effective in antagonizing depolarization shift generation in mature and immature rat slices. The duration of afterdischarges recorded in immature hippocampus was unaltered, yet these events were eliminated when the proceeding depolarization shift was blocked. Baclofen hyperpolarized all CA3 pyramidal cells studied with an associated decrease in membrane resistance. These effects were produced by a direct postsynaptic action.
D000818:Animals; D001418:Baclofen / Q000494:pharmacology* / Q000627:therapeutic use; D001640:Bicuculline / Q000037:antagonists & inhibitors*; D004827:Epilepsy / Q000139:chemically induced* / Q000188:drug therapy; D066298:In Vitro Techniques; D008564:Membrane Potentials / Q000187:drug effects; D009431:Neural Conduction / Q000187:drug effects; D051381:Rats; D009435:Synaptic Transmission / Q000187:drug effects
D001418:Baclofen; D001640:Bicuculline