ArticleNeurochemical research2019
Muscarinic Receptor Modulation of the Cerebellar Interpositus Nucleus In Vitro.
Article in Neurochemical research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 5 citations in OpenAlex.
- Bidirectional Modulation of Beam Traversal Performance by Acetylcholine in the Cerebellar Nuclei.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026Article
- Inhibiting cholinergic signalling in the cerebellar interpositus nucleus impairs motor behaviour.The European journal of neuroscience · 2024Article
- Peptidergic modulation of motor neuron output via CART signaling at C bouton synapses.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Neuromodulatory control of complex adaptive dynamics in the brain.Interface focus · 2023Review
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
How the cerebellum carries out its functions is not clear, even for its established roles in motor control. In particular, little is known about how the cerebellar nuclei (CN) integrate their synaptic and neuromodulatory inputs to generate cerebellar output. CN neurons receive inhibitory inputs from Purkinje cells, excitatory inputs from mossy fibre and climbing fibre collaterals, as well as a variety of neuromodulatory inputs, including cholinergic inputs. In this study we tested how activation of acetylcholine receptors modulated firing rate, intrinsic properties and synaptic transmission in the CN. Using in vitro whole-cell patch clamp recordings from neurons in the interpositus nucleus, the acetylcholine receptor agonist carbachol was shown to induce a short-term increase in firing rate, increase holding current and decrease input resistance of interpositus CN neurons. Carbachol also induced long-term depression of evoked inhibitory postsynaptic currents and a short-term depression of evoked excitatory postsynaptic currents. All effects were shown to be dependent upon muscarinic acetylcholine receptor activation. Overall, the present study has identified muscarinic receptor activation as a modulator of CN activity.
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Registered trials
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