Experimental neurobiology of epilepsies.
Epileptic discharges are a pathological extreme of neuronal synchrony. Experimental models of both focal and primary generalized epilepsies reveal the importance of the interaction of intrinsic (membrane current) properties of neurons and the synaptic networks which connect them. Focal epilepsies depend on excitatory networks within individual cortical structures, but full seizures may require widely dispersed neuronal networks. Absence seizures are generated by the thalamocortical system, and depend on inhibitory postsynaptic potentials, Ca2(+)-activated K+ currents and low threshold "T" currents. Other forms of synchronization can occur under particular circumstances, including field effects and gap junctions, but at the moment appear to be less generally involved in epileptogenesis. The cellular and network mechanisms of chronic experimental epilepsies are more complex and involve synaptic reorganization, and functional disconnection of inhibitory neurons.
Jefferys
J G
JG
Department of Physiology and Biophysics, St. Mary's Hospital Medical School, Imperial College, University of London, UK.
D000818:Animals; D001921:Brain / Q000503:physiopathology; D004195:Disease Models, Animal; D004827:Epilepsy / Q000503:physiopathology*; D006801:Humans; D007473:Ion Channels / Q000502:physiology; D008564:Membrane Potentials / Q000502:physiology; D009415:Nerve Net / Q000503:physiopathology; D009433:Neural Inhibition / Q000502:physiology; D009474:Neurons / Q000502:physiology; D009435:Synaptic Transmission / Q000502:physiology
D007473:Ion Channels