フクシマ ヤスヒロ   Fukushima Yasuhiro
  福島 康弘
   所属   川崎医療福祉大学  医療福祉学部 医療福祉学科
   職種   准教授
論文種別 原著
言語種別 英語
査読の有無 査読あり
表題 The effect of coactivation of muscarinic and nicotinic acetylcholine receptors on LTD in the hippocampal CA1 network.
掲載誌名 正式名:Brain research
略  称:Brain Res
ISSNコード:00068993
巻・号・頁 1649,44-52頁
著者・共著者 Sugisaki Eriko, Fukushima Yasuhiro, Fujii Satoshi, Yamazaki Yoshihiko, Aihara Takeshi
発行年月 2016/10
概要 The neuromodulator acetylcholine (ACh) is considered to have a crucial effect on sensory inputs in the process of learning and memory, and ACh activates muscarinic (mAChR) and nicotinic (nAChR) acetylcholine receptors. Meanwhile in a hippocampal CA1 network including inhibitory connections, long-term potentiation (LTP) or long-term depression (LTD) is induced by the application of positive timing of the spike timing-dependent plasticity (STDP) protocol, while LTD is induced by negative timing protocol. In the previous study, the influence of ACh on LTD induced by the negative timing protocol application in the interneuron-blocked CA1 network was reported. However, the responsibility of mAChR and nAChR on pyramidal neuron and interneuron on STDP induction is still unclear. In order to clarify the role of AChRs in LTD, positive or negative timing protocol was applied in the interneuron-activated CA1 network in the presence of eserine. Consequently, the LTD induced by the positive timing protocol was switched to LTP, and the LTD by negative timing protocol was shifted toward potentiation when ACh was effective. The STDP facilitation was more effectively brought by mAChR activation on pyramidal neuron than nAChR, while mAChR on interneuron had a potential to down regulate the facilitation. These findings suggest that the direction (LTD/LTP) of STDP is determined by the activation of mAChR not only on pyramidal neuron but also on interneuron, and the magnitude of STDP is sensitively fine-tuned by nAChR. Therefore, the modulation of synaptic plasticity induced by the coactivation of mAChR and nAChR might be an important stage in integrating ACh and sensory inputs in the hippocampal CA1 network.