Physiological mechanisms of focal epileptogenesis.
The key elements in the development of epileptogenesis appear to be the capacity of membranes in some (pacemaker) neurons to develop intrinsic burst discharges, the presence of disinhibition, and the proper excitatory synaptic circuitry. It is likely that the relative role of each of these processes will differ at different sites in the central nervous system which are prone to epileptogenesis. Synchronization of neuronal populations is a vital element in the development of focal discharge and a variety of mechanisms, including those dependent upon excitatory postsynaptic potentials, and other interactions are possible. Pathological processes may alter some or all of these regulatory mechanisms. However, different pathological entities presumably produce epileptogenesis through different combinations of pathogenetic mechanisms.
D000109:Acetylcholine / Q000378:metabolism / Q000502:physiology; D000200:Action Potentials; D000818:Animals; D001921:Brain / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D002540:Cerebral Cortex / Q000378:metabolism / Q000503:physiopathology; D003344:Cortical Synchronization; D004298:Dopamine / Q000378:metabolism / Q000502:physiology; D004828:Epilepsies, Partial / Q000209:etiology / Q000473:pathology / Q000503:physiopathology*; D000882:Haplorhini; D006624:Hippocampus / Q000378:metabolism / Q000503:physiopathology; D006801:Humans; D009431:Neural Conduction; D009473:Neuronal Plasticity; D009474:Neurons / Q000378:metabolism / Q000473:pathology / Q000502:physiology; D012640:Seizures / Q000209:etiology / Q000503:physiopathology; D012701:Serotonin / Q000378:metabolism / Q000502:physiology; D013569:Synapses / Q000502:physiology
D012701:Serotonin; D000109:Acetylcholine; D004298:Dopamine