Intrinsic neuronal electroresponsiveness and its possible role in epileptogenesis.
An increased neuronal excitability is one of the most important factors involved in the physiopathology of epileptic states. It may occur via two major routes: an increase in cation inflow, a decreasing cation outflow. The recent discovery that Na+ and Ca2+ inflow may occur through channels that do not inactivate (close) rapidly and that can therefore produce plateau action potentials of great duration, make these conductances quite significant in the generation and maintenance of epilepsy. The presence of excitatory neurotransmitters released either by presynaptic terminal or by glial elements must also be considered. As for the mechanisms that operate by reducing outward cationic flow, a reduction in K+ conductance is mainly involved in membrane depolarization. Other ionic conductances of importance in epileptogenesis will relate most significantly to the reduction in synaptic inhibitory mechanisms, i.e. a reduction of GABAergic or glutaminergic synapses.
D000200:Action Potentials; D000818:Animals; D002118:Calcium / Q000502:physiology*; D004827:Epilepsy / Q000503:physiopathology*; D006168:Guinea Pigs; D007473:Ion Channels / Q000502:physiology*; D011689:Purkinje Cells / Q000503:physiopathology*; D012964:Sodium / Q000502:physiology*
D007473:Ion Channels; D012964:Sodium; D002118:Calcium