Gating of long-term potentiation by nicotinic acetylcholine receptors at the cerebellum input stage.

The brain needs mechanisms able to correlate plastic changes with local circuit activity and internal functional states. At the cerebellum input stage, uncontrolled induction of long-term potentiation or depression (LTP or LTD) between mossy fibres and granule cells can saturate synaptic capacity an...

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Autores principales: Francesca Prestori, Claudia Bonardi, Lisa Mapelli, Paola Lombardo, Rianne Goselink, Maria Egle De Stefano, Daniela Gandolfi, Jonathan Mapelli, Daniel Bertrand, Martijn Schonewille, Chris De Zeeuw, Egidio D'Angelo
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Publicado: Public Library of Science (PLoS) 2013
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Acceso en línea:https://doaj.org/article/0ab6acb13183473b9f8a1f8e1dff3502
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spelling oai:doaj.org-article:0ab6acb13183473b9f8a1f8e1dff35022021-11-18T07:43:32ZGating of long-term potentiation by nicotinic acetylcholine receptors at the cerebellum input stage.1932-620310.1371/journal.pone.0064828https://doaj.org/article/0ab6acb13183473b9f8a1f8e1dff35022013-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/23741401/?tool=EBIhttps://doaj.org/toc/1932-6203The brain needs mechanisms able to correlate plastic changes with local circuit activity and internal functional states. At the cerebellum input stage, uncontrolled induction of long-term potentiation or depression (LTP or LTD) between mossy fibres and granule cells can saturate synaptic capacity and impair cerebellar functioning, which suggests that neuromodulators are required to gate plasticity processes. Cholinergic systems innervating the cerebellum are thought to enhance procedural learning and memory. Here we show that a specific subtype of acetylcholine receptors, the α7-nAChRs, are distributed both in cerebellar mossy fibre terminals and granule cell dendrites and contribute substantially to synaptic regulation. Selective α7-nAChR activation enhances the postsynaptic calcium increase, allowing weak mossy fibre bursts, which would otherwise cause LTD, to generate robust LTP. The local microperfusion of α7-nAChR agonists could also lead to in vivo switching of LTD to LTP following sensory stimulation of the whisker pad. In the cerebellar flocculus, α7-nAChR pharmacological activation impaired vestibulo-ocular-reflex adaptation, probably because LTP was saturated, preventing the fine adjustment of synaptic weights. These results show that gating mechanisms mediated by specific subtypes of nicotinic receptors are required to control the LTD/LTP balance at the mossy fibre-granule cell relay in order to regulate cerebellar plasticity and behavioural adaptation.Francesca PrestoriClaudia BonardiLisa MapelliPaola LombardoRianne GoselinkMaria Egle De StefanoDaniela GandolfiJonathan MapelliDaniel BertrandMartijn SchonewilleChris De ZeeuwEgidio D'AngeloPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 8, Iss 5, p e64828 (2013)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
Francesca Prestori
Claudia Bonardi
Lisa Mapelli
Paola Lombardo
Rianne Goselink
Maria Egle De Stefano
Daniela Gandolfi
Jonathan Mapelli
Daniel Bertrand
Martijn Schonewille
Chris De Zeeuw
Egidio D'Angelo
Gating of long-term potentiation by nicotinic acetylcholine receptors at the cerebellum input stage.
description The brain needs mechanisms able to correlate plastic changes with local circuit activity and internal functional states. At the cerebellum input stage, uncontrolled induction of long-term potentiation or depression (LTP or LTD) between mossy fibres and granule cells can saturate synaptic capacity and impair cerebellar functioning, which suggests that neuromodulators are required to gate plasticity processes. Cholinergic systems innervating the cerebellum are thought to enhance procedural learning and memory. Here we show that a specific subtype of acetylcholine receptors, the α7-nAChRs, are distributed both in cerebellar mossy fibre terminals and granule cell dendrites and contribute substantially to synaptic regulation. Selective α7-nAChR activation enhances the postsynaptic calcium increase, allowing weak mossy fibre bursts, which would otherwise cause LTD, to generate robust LTP. The local microperfusion of α7-nAChR agonists could also lead to in vivo switching of LTD to LTP following sensory stimulation of the whisker pad. In the cerebellar flocculus, α7-nAChR pharmacological activation impaired vestibulo-ocular-reflex adaptation, probably because LTP was saturated, preventing the fine adjustment of synaptic weights. These results show that gating mechanisms mediated by specific subtypes of nicotinic receptors are required to control the LTD/LTP balance at the mossy fibre-granule cell relay in order to regulate cerebellar plasticity and behavioural adaptation.
format article
author Francesca Prestori
Claudia Bonardi
Lisa Mapelli
Paola Lombardo
Rianne Goselink
Maria Egle De Stefano
Daniela Gandolfi
Jonathan Mapelli
Daniel Bertrand
Martijn Schonewille
Chris De Zeeuw
Egidio D'Angelo
author_facet Francesca Prestori
Claudia Bonardi
Lisa Mapelli
Paola Lombardo
Rianne Goselink
Maria Egle De Stefano
Daniela Gandolfi
Jonathan Mapelli
Daniel Bertrand
Martijn Schonewille
Chris De Zeeuw
Egidio D'Angelo
author_sort Francesca Prestori
title Gating of long-term potentiation by nicotinic acetylcholine receptors at the cerebellum input stage.
title_short Gating of long-term potentiation by nicotinic acetylcholine receptors at the cerebellum input stage.
title_full Gating of long-term potentiation by nicotinic acetylcholine receptors at the cerebellum input stage.
title_fullStr Gating of long-term potentiation by nicotinic acetylcholine receptors at the cerebellum input stage.
title_full_unstemmed Gating of long-term potentiation by nicotinic acetylcholine receptors at the cerebellum input stage.
title_sort gating of long-term potentiation by nicotinic acetylcholine receptors at the cerebellum input stage.
publisher Public Library of Science (PLoS)
publishDate 2013
url https://doaj.org/article/0ab6acb13183473b9f8a1f8e1dff3502
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