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The Journal of Neuroscience, November 30, 2005, 25(48):11194-11200; doi:10.1523/JNEUROSCI.2338-05.2005

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Cellular/Molecular
Modulation of Synaptic Plasticity by Physiological Activation of M₁ Muscarinic Acetylcholine Receptors in the Mouse Hippocampus

Toru Shinoe,^1,2 Minoru Matsui,¹ Makoto M. Taketo,³ and Toshiya Manabe^1,2,4

¹Division of Neuronal Network, Department of Basic Medical Sciences, Institute of Medical Science, University of Tokyo, Minato-ku, Tokyo, 108-8639, Japan, ²Division of Cell Biology and Neurophysiology, Department of Neuroscience, Faculty of Medicine, Kobe University, Chuo-ku, Kobe, 650-0017, Japan, ³Department of Pharmacology, Graduate School of Medicine, Kyoto University, Sakyo-ku, Kyoto, 606-8501, Japan, and ⁴Core Research for Evolutional Science and Technology and Research Institute of Science and Technology for Society, Japan Science and Technology Agency, Kawaguchi, 332-0012, Japan

The muscarinic acetylcholine receptor (mAChR) has been considered one of the neurotransmitter receptors regulating hippocampal synaptic plasticity, which likely plays a critical role in learning and memory. In previous studies, however, muscarinic agonists were used at relatively high concentrations, and the subtype selectivity of muscarinic antagonists was not satisfactory. Thus, it remains to be answered whether physiological levels of ACh are involved in the regulation of synaptic plasticity and which mAChR subtypes are responsible for such effects. We found in this study that a low concentration (50 nM) of carbachol enhanced long-term potentiation (LTP) of excitatory synaptic transmission in mouse hippocampal slices. Notably, this enhancing effect was abolished in M₁ mAChR knock-out (KO) but not in M₃ mAChR KO mice, although LTP itself was intact in both mutant mice. Furthermore, we found that repetitive stimulation in the stratum oriens, which presumably triggered the release of endogenous ACh from cholinergic terminals, could enhance LTP in wild-type mice but not in M₁ mAChR KO mice. These results suggest that physiologically released ACh from cholinergic fibers modulates hippocampal synaptic plasticity through the postsynaptic M₁ mAChR activation.

Key words: synaptic transmission; long-term potentiation; LTP; acetylcholine; muscarinic receptor; knock-out mouse; learning

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Received Jan 7, 2005; revised October 18, 2005; accepted October 18, 2005.

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