Mechanisms underlying epileptiform burst discharge.
Studies of hyperexcitable cells in alumina-gel and penicillin epileptogenic foci suggest that epileptid or triggered by a number of extrinsic factors which disrupt the normal depolarizing-hyperpolarizing balance. This paper presents the hypothesis that the most important influence for burst discharge is influx of calcium ions. This excitatory effect is modulated by synaptic inputs, hyperpolarizing conductances, cell morphology and membrane characteristics, and the extracellular milieu. The hypothesis incorporates findings from both penicillin and alumina models of epilepsy and provides experimentally testable concepts for further investigation.
D000200:Action Potentials; D000537:Aluminum Oxide; D000818:Animals; D001253:Astrocytes; D002118:Calcium / Q000378:metabolism*; D002540:Cerebral Cortex / Q000378:metabolism* / Q000473:pathology; D004195:Disease Models, Animal; D004594:Electrophysiology; D000882:Haplorhini; D007473:Ion Channels / Q000378:metabolism*; D008564:Membrane Potentials; D010406:Penicillins; D011188:Potassium / Q000378:metabolism; D012640:Seizures / Q000139:chemically induced / Q000378:metabolism* / Q000473:pathology
D007473:Ion Channels; D010406:Penicillins; D000537:Aluminum Oxide; D011188:Potassium; D002118:Calcium