Mechanism of aminopyridine-induced ictal seizure activity in the cat neocortex.
Intracellular recordings were obtained from neurons in the motor cortex of anesthetized cats in order to examine membrane and synaptic processes involved in aminopyridine (AP)-induced ictal seizure activity. Depolarizing and hyperpolarizing membrane potential sequences which behaved as large, synchronized excitatory and inhibitory postsynaptic potentials, were found to accompany the ictal seizure potentials. After several repetitions of the seizure attack, partial responses, bursts and depolarizing plateaus with spike inactivation occurred. In layers IV and V we found non-pyramidal tract neurons showing endogenous bursting ability activated by AP. These neurons seemed to be the initiators of the rhythmic synchronous activity of the epileptic neuron population. Our results suggest that AP-induced epileptogenesis represents an adequate model of ictal events in the neocortex.
D000200:Action Potentials / Q000187:drug effects; D000631:Aminopyridines / Q000494:pharmacology*; D000818:Animals; D002415:Cats; D008564:Membrane Potentials / Q000187:drug effects; D009044:Motor Cortex / Q000187:drug effects* / Q000503:physiopathology; D012640:Seizures / Q000139:chemically induced* / Q000503:physiopathology
D000631:Aminopyridines; C031283:3-aminopyridine