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Instituto Nacional de Neurología y Neurocirugía

2011, Number 4

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Arch Neurocien 2011; 16 (4)

K+ channels its velathionship to type my chanelo pathy in epileptogenesis

Solís H, López-Hernández E

Language: Spanish
References: 98
Page: 200-208
PDF size: 122.71 Kb.


ABSTRACT

M-type potassium channel: channelopathie and role in epileptogenesis. Progress in the study of ion channels has made it possible to analyze the effects of human neurological disease-causing channel mutations at the level of the single channel, the subcellular domain, the neuronal network, and the behaving organism. Improper voltage-gated ion channels integration could cause several types of epilepsy. Neuronal KCNQ channels, voltage-dependent potassium channels that activate slowly but show no inactivation, correspond to the M channels that exert crucial influence over neuronal excitability. This review covers recent studies of the M-current (IM) and its participation over epileptogenesis. M-channels are now known to be composed of subunits of the Kv7 (KCNQ) K+ channel family. In humans, mutations in the Kv7.2 (KCNQ2) or Kv7.3 (KCNQ3) potassium-channel genes are associated with a form of juvenile epilepsy called benign familial neonatal convulsions (BNFC). Transgenic mice that conditionally express dominant-negative KCNQ2 subunits in brain, are associated with spontaneous seizures, behavioral hyperactivity and morphological changes in the hippocampus. It has been recently recognized that channelopathies can also include aberrant ion channel function that is acquired after an insult or injury to the brain. These acquired alterations are being investigated in animal models of temporal lobe epilepsy, where studies have shown functional changes in voltage-gated ion channels that lead to increases in excitability. These excitability changes could be related with IM inhibition. Therefore, epileptic hippocampal neurons may have altered the IM regulation.


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