Afterpotentials of penicillin-induced epileptiform neuronal discharges in the motor cortex of the rat in vivo.
Interictal spikes and sharp waves in the EEG are followed by intervals in which the excitability of the brain seems to be normal or decreased. Often interictal spikes even appear in rhythmical patterns with intervals in the order of 0.5-2 s. These observations suggest that intrinsic and synaptic inhibitory and excitatory processes are activated which outlast the duration of the interictal discharge. In the present study such afterpotentials were analyzed in penicillin foci of the rat motor cortex in vivo using intracellular recording techniques. Paroxysmal depolarizations (PDS) of neurons within the focus were followed by afterpotentials comprising several components. Fast afterpotentials with a duration of 640 ms were associated with a sevenfold increase in membrane conductance. The fast afterpotentials were depolarizing in the majority of recordings and had an average equilibrium potential of -62 mV. This equilibrium potential was Cl(-)-dependent and was not affected by intracellular EGTA or Cs+. It is suggested that these afterpotentials represent GABAA responses. In 38% of the neurons slow afterhyperpolarizations with a twofold increase in membrane conductance and a duration of 2 s were observed. These afterhyperpolarizations had a reversal potential of -79 mV, were blocked by intracellular Cs+, were reduced in duration and amplitude by intracellular EGTA, and are suggested to present a combination of a GABAB response and a calcium-dependent potassium current. In addition, slow afterdepolarizations with a duration of about 1900 ms were registered in 16% of the recordings. It is concluded that afterpotentials with several intrinsic and synaptic components follow penicillin-induced PDS. Among these are giant Cl(-)-dependent potentials which probably represent GABAA responses, GABAB responses and a slow calcium-dependent potassium current. It is suggested that the depolarizing equilibrium potential of the Cl(-)-dependent component is due to intracellular Cl- accumulation which might favor transition to ictal discharges.
Witte
O W
OW
Neurologische Klinik der Heinrich Heine Universität, Düsseldorf, Germany.
D000200:Action Potentials / Q000502:physiology; D000818:Animals; D002118:Calcium / Q000502:physiology; D002712:Chlorides / Q000494:pharmacology; D004827:Epilepsy / Q000139:chemically induced / Q000503:physiopathology*; D005071:Evoked Potentials / Q000502:physiology; D008297:Male; D008839:Microelectrodes; D009044:Motor Cortex / Q000503:physiopathology*; D009474:Neurons / Q000502:physiology*; D010406:Penicillins; D015221:Potassium Channels / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D011963:Receptors, GABA-A / Q000187:drug effects; D018080:Receptors, GABA-B / Q000187:drug effects; D013569:Synapses / Q000187:drug effects / Q000502:physiology
D002712:Chlorides; D010406:Penicillins; D015221:Potassium Channels; D011963:Receptors, GABA-A; D018080:Receptors, GABA-B; D002118:Calcium