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Synaptic plasticity

Breaking the learning barrier with ACh

Nature Reviews Neuroscience volume 12, pages 62–63 (2011)Cite this article

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Both studies investigated how glutamatergic transmission is modulated by muscarinic activation. In the first study, Buchanan et al. used a selective agonist of muscarinic M1 receptors to show that M1 receptor activation facilitates LTP in the hippocampus. The authors showed in current-clamped cells that M1 activation specifically enhanced the NMDA receptor-mediated component of the postsynaptic potential and, using voltage-clamping, revealed that M1 activation did not act directly on NMDA receptors.

In the second paper, Giessel and Sabatini found that activation of muscarinic receptors by the muscarinic agonist oxotremorine-M increased Ca2+ transients and synaptic potentials induced by two-photon laser uncaging of glutamate onto individual dendritic spines. The M1 antagonist Mtx-7 prevented this effect, indicating that M1 receptors were responsible. By measuring currents in voltage-clamped neurons, the authors showed that the numbers and properties of NMDA and AMPA glutamate receptors were not altered by activation of muscarinic receptors.

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ORIGINAL RESEARCH PAPERS

  1. Buchanan, K. A. et al. Facilitation of long-term potentiation by muscarinic M1 receptors is mediated by inhibition of SK channels. Neuron 68, 948–963 (2010)

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  2. Giessel, A. J. & Sabatini, B. L. M1 muscarinic receptors boost synaptic potentials and calcium influx in dendritic spines by inhibiting postynaptic SK channels. Neuron 68, 936–947 (2010)

    Article  CAS  Google Scholar 

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  1. Rachel Jones
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Jones, R. Breaking the learning barrier with ACh. Nat Rev Neurosci 12, 62–63 (2011). https://doi.org/10.1038/nrn2986

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