Cholinergic midbrain afferents modulate striatal circuits and shape encoding of action strategies.


Journal

Nature communications
ISSN: 2041-1723
Titre abrégé: Nat Commun
Pays: England
ID NLM: 101528555

Informations de publication

Date de publication:
08 04 2020
Historique:
received: 26 12 2019
accepted: 13 03 2020
entrez: 10 4 2020
pubmed: 10 4 2020
medline: 28 7 2020
Statut: epublish

Résumé

Assimilation of novel strategies into a consolidated action repertoire is a crucial function for behavioral adaptation and cognitive flexibility. Acetylcholine in the striatum plays a pivotal role in such adaptation, and its release has been causally associated with the activity of cholinergic interneurons. Here we show that the midbrain, a previously unknown source of acetylcholine in the striatum, is a major contributor to cholinergic transmission in the striatal complex. Neurons of the pedunculopontine and laterodorsal tegmental nuclei synapse with striatal cholinergic interneurons and give rise to excitatory responses. Furthermore, they produce uniform inhibition of spiny projection neurons. Inhibition of acetylcholine release from midbrain terminals in the striatum impairs the association of contingencies and the formation of habits in an instrumental task, and mimics the effects observed following inhibition of acetylcholine release from striatal cholinergic interneurons. These results suggest the existence of two hierarchically-organized modes of cholinergic transmission in the striatum, where cholinergic interneurons are modulated by cholinergic neurons of the midbrain.

Identifiants

pubmed: 32269213
doi: 10.1038/s41467-020-15514-3
pii: 10.1038/s41467-020-15514-3
pmc: PMC7142106
doi:

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, Non-P.H.S.

Langues

eng

Sous-ensembles de citation

IM

Pagination

1739

Subventions

Organisme : NINDS NIH HHS
ID : R01 NS100824
Pays : United States

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Auteurs

Daniel Dautan (D)

Center for Molecular and Behavioral Neuroscience, Rutgers University, Newark, NJ, USA. daniel.dautan@iit.it.
Department of Neuroscience, Physiology and Behavior, University of Leicester, Leicester, LE1 9HN, UK. daniel.dautan@iit.it.
MRC Anatomical Neuropharmacology Unit, Department of Pharmacology, University of Oxford, Oxford, OX1 3TH, UK. daniel.dautan@iit.it.
Research line Genetic of Cognition, Italian Institute of Technology, Genova, Italy. daniel.dautan@iit.it.

Icnelia Huerta-Ocampo (I)

Center for Molecular and Behavioral Neuroscience, Rutgers University, Newark, NJ, USA.
MRC Anatomical Neuropharmacology Unit, Department of Pharmacology, University of Oxford, Oxford, OX1 3TH, UK.

Nadine K Gut (NK)

Center for Molecular and Behavioral Neuroscience, Rutgers University, Newark, NJ, USA.

Miguel Valencia (M)

University of Navarra, Neuroscience Program, CIMA, 31008, Pamplona, Spain.
IdiSNA, Navarra Institute for Health Research, 31008, Pamplona, Spain.

Krishnakanth Kondabolu (K)

Center for Molecular and Behavioral Neuroscience, Rutgers University, Newark, NJ, USA.

Yuwoong Kim (Y)

Center for Molecular and Behavioral Neuroscience, Rutgers University, Newark, NJ, USA.

Todor V Gerdjikov (TV)

Department of Neuroscience, Physiology and Behavior, University of Leicester, Leicester, LE1 9HN, UK.

Juan Mena-Segovia (J)

Center for Molecular and Behavioral Neuroscience, Rutgers University, Newark, NJ, USA. juan.mena@rutgers.edu.

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