Seizing control of KCC2: a new therapeutic target for epilepsy
Trends in neurosciences, 2017•cell.com
Deficits in GABAergic inhibition result in the abnormal neuronal activation and
synchronization that underlies seizures. However, the molecular mechanisms responsible
for transforming a normal brain into an epileptic one remain largely unknown.
Hyperpolarizing inhibition mediated by type A GABA (GABA A) receptors is dependent on
chloride extrusion by the neuron-specific type 2K+–Cl− cotransporter (KCC2). Loss-of-
function mutations in KCC2 are a known cause of infantile epilepsy in humans and KCC2 …
synchronization that underlies seizures. However, the molecular mechanisms responsible
for transforming a normal brain into an epileptic one remain largely unknown.
Hyperpolarizing inhibition mediated by type A GABA (GABA A) receptors is dependent on
chloride extrusion by the neuron-specific type 2K+–Cl− cotransporter (KCC2). Loss-of-
function mutations in KCC2 are a known cause of infantile epilepsy in humans and KCC2 …
Deficits in GABAergic inhibition result in the abnormal neuronal activation and synchronization that underlies seizures. However, the molecular mechanisms responsible for transforming a normal brain into an epileptic one remain largely unknown. Hyperpolarizing inhibition mediated by type A GABA (GABAA) receptors is dependent on chloride extrusion by the neuron-specific type 2K+–Cl− cotransporter (KCC2). Loss-of-function mutations in KCC2 are a known cause of infantile epilepsy in humans and KCC2 dysfunction is present in patients with both idiopathic and acquired epilepsy. Here we discuss the growing evidence that KCC2 dysfunction has a central role in the development and severity of the epilepsies.
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