https://transhumanist.ru/index.php?action=history&feed=atom&title=KCNQ3 2026-06-23T13:00:49Z История изменений этой страницы в вики MediaWiki 1.43.6 https://transhumanist.ru/index.php?title=KCNQ3&diff=5067&oldid=prev 2021-05-12T13:27:46Z

<p>Новая страница: «Potassium voltage-gated channel subfamily KQT member 3 (KQT-like 3) (Potassium channel subunit alpha KvLQT3) (Voltage-gated potassium channel subunit Kv7.3) ==Pu...»</p> <p><b>Новая страница</b></p><div>Potassium voltage-gated channel subfamily KQT member 3 (KQT-like 3) (Potassium channel subunit alpha KvLQT3) (Voltage-gated potassium channel subunit Kv7.3)<br /> <br /> ==Publications==<br /> <br /> {{medline-entry<br /> |title=Age-dependent modulation of hippocampal excitability by KCNQ-channels.<br /> |pubmed-url=https://pubmed.ncbi.nlm.nih.gov/12576170<br /> |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&lt;7 than P&gt;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.<br /> |mesh-terms=* Aging<br /> * Animals<br /> * Biosensing Techniques<br /> * Cortical Spreading Depression<br /> * Epilepsy, Benign Neonatal<br /> * Glutamic Acid<br /> * Hippocampus<br /> * Male<br /> * Membrane Potentials<br /> * Microdialysis<br /> * Neurons<br /> * Neurotransmitter Agents<br /> * Potassium<br /> * Potassium Channels<br /> * Rats<br /> * Rats, Wistar<br /> * Remission, Spontaneous<br /> * Synaptic Transmission<br /> * gamma-Aminobutyric Acid<br /> <br /> |full-text-url=https://sci-hub.do/10.1016/s0920-1211(02)00249-8<br /> }}<br /> {{medline-entry<br /> |title=The [[KCNQ2]] potassium channel: splice variants, functional and developmental expression. Brain localization and comparison with [[KCNQ3]].<br /> |pubmed-url=https://pubmed.ncbi.nlm.nih.gov/9827540<br /> |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]].<br /> |mesh-terms=* Aging<br /> * Alternative Splicing<br /> * Amino Acid Sequence<br /> * Animals<br /> * Benzodiazepines<br /> * Brain<br /> * COS Cells<br /> * Gene Expression Regulation<br /> * Gene Expression Regulation, Developmental<br /> * Genetic Variation<br /> * Humans<br /> * In Situ Hybridization<br /> * KCNQ2 Potassium Channel<br /> * KCNQ3 Potassium Channel<br /> * Mice<br /> * Molecular Sequence Data<br /> * Organ Specificity<br /> * Potassium Channels<br /> * Potassium Channels, Voltage-Gated<br /> * RNA, Messenger<br /> * Recombinant Proteins<br /> * Transcription, Genetic<br /> * Transfection<br /> <br /> |full-text-url=https://sci-hub.do/10.1016/s0014-5793(98)01296-4<br /> }}</div>

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