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Voltage-gated ion-channels in epilepsies: circuit dysfunctions and treatments
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International audience. Voltage-gated ion channels are key players in neuronal excitability, synaptic transmission and neuronal synchrony, and represent one of the major sources of abnormal function of neuronal circuits occurring during epilepsy.
Epilepsy does not solely result from the imbalance between excitatory and inhibitory ion channels but loss-of-function in excitatory channels or gain-of-function in inhibitory channels are also reported in epileptic encephalopathies.
Synaptic inhibition triggers focal epilepsies possibly through the facilitation of excitatory synaptic transmission due to the de-inactivation of axonal sodium channels.
Neural synchrony and its transmission within neural micro-circuits is controlled by voltage-gated ion channels located in the axon, the dendrites and the cell body.
New molecules targeting excitatory and inhibitory ion channels need to be identified and tested in in vitro and in vivo models of epileptic encephalopathies.
Epileptic encephalopathies are generally considered to be functional disruptions in the balance between neural excitation and inhibition. Excitatory and inhibitory voltage-gated ion channels are key targets of antiepileptic drugs, playing a critical role in regulating neuronal excitation and synaptic transmission. Recent research has highlighted the significance of ion channels in various aspects of epilepsy, including presynaptic neurotransmitter release, intrinsic neuronal excitability and neural synchrony. Genetic alterations in excitatory and inhibitory ion channels within principal neurons and in inhibitory interneurons have also been identified as key contributors to the development of epilepsies. We review these recent studies, shed light on the bidirectional relationship between epilepsy and neuronal excitability, and the latest advancements in pharmacological therapeutics targeting ion channels for epilepsy treatment.
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