Abstract
Compounds that stimulate or inhibit M-channels (ie, voltage-gated potassium channels formed by KCNQ2, KCNQ3 and KCNQ5) have been evaluated in clinical trials for epilepsy, stroke and Alzheimer's disease. The importance of M-channel function in reducing neuronal excitability is underscored by the finding that KCNQ2/3 mutations causing mild reduction of M-channel activity are linked to neonatal epilepsy. M-channel openers decrease the hyperexcitability responsible for epileptic seizures, neuropathic pain and migraine. Conversely, M-channel blockers may enhance cognitive functions. The M-channel has thus emerged as a promising target for treating epilepsy, stroke, migraine, pain, dementia, anxiety and bipolar disorder.
MeSH terms
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Animals
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Carbamates / chemistry
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Carbamates / pharmacology
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Carbamates / therapeutic use
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Central Nervous System Agents / chemistry
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Central Nervous System Agents / pharmacology
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Central Nervous System Agents / therapeutic use*
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Clinical Trials as Topic
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Humans
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Indoles / chemistry
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Indoles / pharmacology
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Indoles / therapeutic use
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Molecular Structure
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Phenylenediamines / chemistry
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Phenylenediamines / pharmacology
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Phenylenediamines / therapeutic use
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Potassium Channels, Voltage-Gated / agonists
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Potassium Channels, Voltage-Gated / antagonists & inhibitors
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Potassium Channels, Voltage-Gated / physiology*
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Pyridines / chemistry
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Pyridines / pharmacology
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Pyridines / therapeutic use
Substances
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Carbamates
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Central Nervous System Agents
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Indoles
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Phenylenediamines
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Potassium Channels, Voltage-Gated
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Pyridines
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ezogabine
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linopirdine