Редактирование: KCNQ3

Potassium voltage-gated channel subfamily KQT member 3 (KQT-like 3) (Potassium channel subunit alpha KvLQT3) (Voltage-gated potassium channel subunit Kv7.3)

==Publications==

{{medline-entry
|title=Age-dependent modulation of hippocampal excitability by KCNQ-channels.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/12576170
|abstract=Recently, mutations of [[KCNQ2]] or [[KCNQ3]], members of the KCNQ-related K( )-channel (KCNQ-channel) family, were identified as cause of benign familial neonatal convulsions (BFNC). However, the exact pathogenic mechanisms of age-dependent development and spontaneous remission of BFNC remain to be elucidated. To clarify the age-dependent etiology of BFNC, we determined age-dependent functional switching of KCNQ-channels, GABAergic- and glutamatergic-transmission in rat hippocampus. The effects of inhibitors of KCNQ-channel, GABA- and glutamate-receptors on propagation of neuronal-excitability and neurotransmitter release were determined by 64-channel multielectrode-dish (MED64), whole-cell recording, in vitro release technique and in vivo microdialysis biosensor, using rat hippocampus from day of birth (P0) to postnatal-day 56 (P56). Inhibition of KCNQ-channels enhanced depolarization-induced glutamate and GABA releases during P0-P7, but not during P14-P28. Inhibition of KCNQ-channels magnified neuronal-excitability propagation from P0 to P14: maximal at P3, but this effect disappeared by P28. GABA(A)-receptor inhibition surprisingly reduced neuronal-excitability propagation during P0-P3, but not at P7. AMPA/glutamate-receptors inhibition reduced propagation of neuronal-excitability throughout the study period. KCNQ-channels inhibition shortened spike-frequency adaptation, but this stimulation was more predominant during P<7 than P>14. During the first week of life, KCNQ-channels performed as a predominant inhibitory system, whereas after this period GABAergic-transmission switched from excitatory to inhibitory function. Contrary, glutamatergic-transmission has acquired as excitatory function from P0. These findings suggest that the pathogenic mechanisms of age-dependent development and spontaneous remission of BFNC are, at least partially, associated with the interaction between age-dependent reduction of inhibitory KCNQ-channel activity and age-dependent functional switching of the GABAergic-system from excitatory to inhibitory action in neonatal CNS.
|mesh-terms=* Aging
* Animals
* Biosensing Techniques
* Cortical Spreading Depression
* Epilepsy, Benign Neonatal
* Glutamic Acid
* Hippocampus
* Male
* Membrane Potentials
* Microdialysis
* Neurons
* Neurotransmitter Agents
* Potassium
* Potassium Channels
* Rats
* Rats, Wistar
* Remission, Spontaneous
* Synaptic Transmission
* gamma-Aminobutyric Acid

|full-text-url=https://sci-hub.do/10.1016/s0920-1211(02)00249-8
}}
{{medline-entry
|title=The [[KCNQ2]] potassium channel: splice variants, functional and developmental expression. Brain localization and comparison with [[KCNQ3]].
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/9827540
|abstract=Benign familial neonatal convulsions, an autosomal dominant epilepsy of newborns, are linked to mutations affecting two six-transmembrane potassium channels, [[KCNQ2]] and [[KCNQ3]]. We isolated four splice variants of [[KCNQ2]] in human brain. Two forms generate, after transient expression in COS cells, a potassium-selective current similar to the [[KCNQ1]] current. L-735,821, a benzodiazepine molecule which inhibits the [[KCNQ1]] channel activity (EC50 = 0.08 microM), also blocks [[KCNQ2]] currents (EC50 = 1.5 microM). Using in situ hybridization, [[KCNQ2]] and [[KCNQ3]] have been localized within the central nervous system, in which they are expressed in the same areas, mainly in the hippocampus, the neocortex and the cerebellar cortex. During brain development, [[KCNQ3]] is expressed later than [[KCNQ2]].
|mesh-terms=* Aging
* Alternative Splicing
* Amino Acid Sequence
* Animals
* Benzodiazepines
* Brain
* COS Cells
* Gene Expression Regulation
* Gene Expression Regulation, Developmental
* Genetic Variation
* Humans
* In Situ Hybridization
* KCNQ2 Potassium Channel
* KCNQ3 Potassium Channel
* Mice
* Molecular Sequence Data
* Organ Specificity
* Potassium Channels
* Potassium Channels, Voltage-Gated
* RNA, Messenger
* Recombinant Proteins
* Transcription, Genetic
* Transfection

|full-text-url=https://sci-hub.do/10.1016/s0014-5793(98)01296-4
}}