Activity-dependent constraints on catecholamine signaling.

CP: Neuroscience catecholamine dopamine locus coeruleus neurotransmission norepinephrine phasic firing tonic firing ventral tegmental area

Journal

Cell reports
ISSN: 2211-1247
Titre abrégé: Cell Rep
Pays: United States
ID NLM: 101573691

Informations de publication

Date de publication:
14 Dec 2023
Historique:
received: 11 06 2023
revised: 24 10 2023
accepted: 22 11 2023
medline: 15 12 2023
pubmed: 15 12 2023
entrez: 15 12 2023
Statut: aheadofprint

Résumé

Catecholamine signaling is thought to modulate cognition in an inverted-U relationship, but the mechanisms are unclear. We measured norepinephrine and dopamine release, postsynaptic calcium responses, and interactions between tonic and phasic firing modes under various stimuli and conditions. High tonic activity in vivo depleted catecholamine stores, desensitized postsynaptic responses, and decreased phasic transmission. Together, these findings provide a more complete understanding of the inverted-U relationship, offering insights into psychiatric disorders and neurodegenerative diseases with impaired catecholamine signaling.

Identifiants

pubmed: 38100349
pii: S2211-1247(23)01578-4
doi: 10.1016/j.celrep.2023.113566
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

113566

Informations de copyright

Copyright © 2023 The Authors. Published by Elsevier Inc. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of interests The authors declare no competing interests.

Auteurs

Li Li (L)

Department of Anesthesiology & Pain Medicine, University of Washington, Seattle, WA 98195, USA; Center for Neurobiology of Addiction, Pain, and Emotion, University of Washington, Seattle, WA 98195, USA; Seattle Children's Research Institute, Seattle, WA 98101, USA. Electronic address: lili1@uw.edu.

Akshay N Rana (AN)

Department of Anesthesiology & Pain Medicine, University of Washington, Seattle, WA 98195, USA; Center for Neurobiology of Addiction, Pain, and Emotion, University of Washington, Seattle, WA 98195, USA.

Esther M Li (EM)

Department of Anesthesiology & Pain Medicine, University of Washington, Seattle, WA 98195, USA; Center for Neurobiology of Addiction, Pain, and Emotion, University of Washington, Seattle, WA 98195, USA; Department of Psychology, University of Washington, Seattle, WA 98105, USA.

Jiesi Feng (J)

State Key Laboratory of Membrane Biology, School of Life Sciences, Peking University, Beijing 100871, China.

Yulong Li (Y)

State Key Laboratory of Membrane Biology, School of Life Sciences, Peking University, Beijing 100871, China; PKU-IDG/McGovern Institute for Brain Research, Beijing 100871, China; Peking-Tsinghua Center for Life Sciences, New Cornerstone Science Laboratory, Academy for Advanced Interdisciplinary Studies, Peking University, Beijing 100871, China.

Michael R Bruchas (MR)

Department of Anesthesiology & Pain Medicine, University of Washington, Seattle, WA 98195, USA; Center for Neurobiology of Addiction, Pain, and Emotion, University of Washington, Seattle, WA 98195, USA; Department of Bioengineering, University of Washington, Seattle, WA 98105, USA; Department of Pharmacology, University of Washington, Seattle, WA 98195, USA. Electronic address: mbruchas@uw.edu.

Classifications MeSH