Protein kinase C bound with A-kinase anchoring protein is involved in muscarinic receptor-activated modulation of M-type KCNQ potassium channels

Haruhiro Higashida, Naoto Hoshi, Jia Sheng Zhang, Shigeru Yokoyama, Minako Hashii, Duo Jin, Mami Noda, Jon Robbins

研究成果: Contribution to journalArticle

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The second messenger for closure of M/KCNQ potassium channels in post-ganglionic neurons and central neurons had remained as a 'mystery in the neuroscience field' for over 25 years. However, recently the details of the pathway leading from muscarinic acetylcholine receptor (mAChR)-stimulation to suppression of the M/KCNQ-current were discovered. A key molecule is A-kinase anchoring protein (AKAP; AKAP79 in human, or its rat homolog, AKAP150) which forms a trimeric complex with protein kinase C (PKC) and KCNQ channels. AKAP79 or 150 serves as an adapter that brings the anchored C-kinase to the substrate KCNQ channel to permit the rapid and 'definitive' phosphorylation of serine residues, resulting in avoidance of signal dispersion. Thus, these findings suggest that mAChR-induced short-term modulation (or memory) does occur within the already well-integrated molecular complex, without accompanying Hebbian synapse plasticity. However, before this identity is confirmed, many other modulators which affect M-currents remain to be addressed as intriguing issues.

元の言語英語
ページ(範囲)231-234
ページ数4
ジャーナルNeuroscience Research
51
発行部数3
DOI
出版物ステータス出版済み - 3 2005

All Science Journal Classification (ASJC) codes

  • Neuroscience(all)

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