Membrane electrophysiology of epileptiform activity in the hippocampus.
Several different types of Na+ and Ca++ channels in the membrane of neurones provide the driving force for excitation. Whilst some of these may be activated by the transmembrane voltage or ionic concentrations, others are mediated by neurotransmitters and neuromodulators. The role of these ionic mechanisms in epileptiform activity are discussed, with particular reference to the involvement of the NMDA receptor mediated channel. Multiple K+ and Cl- mediated mechanisms provide the stabilizing influence on the electrophysiological behavior of the cells. Loss or reduction in activity of one or more of these conductances may lead to the expression of epileptiform activity. The role of the extracellular concentration of K+ in burst firing of populations of cells is discussed. The examples are primarily chosen from studies of the hippocampus in animal models of epilepsy, however wherever possible experiments on human tissue have been discussed. These studies on the membrane and synaptic mechanisms that contribute to epileptiform activity provide us with the necessary insights to allow the development of new methods for controlling such activity.
Wheal
H V
HV
Department of Neurophysiology, University of Southampton, U.K.
D000818:Animals; D002118:Calcium / Q000502:physiology; D002712:Chlorides / Q000502:physiology; D004828:Epilepsies, Partial / Q000503:physiopathology*; D006624:Hippocampus / Q000503:physiopathology*; D006801:Humans; D007473:Ion Channels / Q000502:physiology*; D008564:Membrane Potentials / Q000502:physiology; D011188:Potassium / Q000502:physiology; D016194:Receptors, N-Methyl-D-Aspartate / Q000502:physiology
D002712:Chlorides; D007473:Ion Channels; D016194:Receptors, N-Methyl-D-Aspartate; D011188:Potassium; D002118:Calcium