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Cells
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Dopamine Signaling: From Synapses to Behavior
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Dopamine Signaling: From Synapses to Behavior

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cells of the Nervous System".

Deadline for manuscript submissions: closed (10 March 2022) | Viewed by 23253

Special Issue Editor

Dr. Jérôme Baufreton

E-Mail Website
Guest Editor
Institut des Maladies Neurodégénératives, Université de Bordeaux, Bordeaux, France
Interests: basal ganglia; cellular excitability; motor control; dopamine-dependent plasticity; Parkinson’s disease; synaptic transmission; dopaminergic neurons ; dopamine receptors

Special Issue Information

Dear Colleagues,

Dopamine (DA) is a catecholamine which is instrumental for learning and motivation. DA is synthesized and released by midbrain dopamine neurons which innervate motor and limbic circuits to regulate ongoing behaviors. DA acts on D1- and D2-like receptor families to dynamically modulate cellular excitability and synaptic plasticity in a circuit-specific manner, and to ultimately control motivated behaviors. Most recent studies have unraveled new mechanisms about DA signaling such as co-release of neurotransmitters by DA terminals and local control of DA release by receptors located on synaptic terminals independently of dopaminergic neuron firing activity. In addition, the use of genetically-encoded biosensors and subcellular approaches tends toward a re-evaluation of the anatomical organization of DA release sites and suggests a more rapid DA coding than originally described. These new findings profoundly alter our current knowledge of DA functions both in healthy and diseased conditions.

The aim of this Special Issue is to present articles that investigate molecular, synaptic, and circuit mechanisms underlying DA signaling in order to better understand how DA sculpts neuronal activity and DA-dependent behaviors.

Dr. Jérôme Baufreton
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • dopamine synthesis and release
  • dopamine receptors signaling
  • basal ganglia
  • limbic circuits
  • dopamine-dependent plasticity
  • motor control
  • learning
  • movement disorders
  • motivation
  • schizophrenia

Published Papers (2 papers)

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Review

19 pages, 1098 KiB  
Review
Dopamine: The Neuromodulator of Long-Term Synaptic Plasticity, Reward and Movement Control
by Luisa Speranza, Umberto di Porzio, Davide Viggiano, Antonio de Donato and Floriana Volpicelli
Cells 2021, 10(4), 735; https://doi.org/10.3390/cells10040735 - 26 Mar 2021
Cited by 87 | Viewed by 16765
Abstract
Dopamine (DA) is a key neurotransmitter involved in multiple physiological functions including motor control, modulation of affective and emotional states, reward mechanisms, reinforcement of behavior, and selected higher cognitive functions. Dysfunction in dopaminergic transmission is recognized as a core alteration in several devastating [...] Read more.
Dopamine (DA) is a key neurotransmitter involved in multiple physiological functions including motor control, modulation of affective and emotional states, reward mechanisms, reinforcement of behavior, and selected higher cognitive functions. Dysfunction in dopaminergic transmission is recognized as a core alteration in several devastating neurological and psychiatric disorders, including Parkinson’s disease (PD), schizophrenia, bipolar disorder, attention deficit hyperactivity disorder (ADHD) and addiction. Here we will discuss the current insights on the role of DA in motor control and reward learning mechanisms and its involvement in the modulation of synaptic dynamics through different pathways. In particular, we will consider the role of DA as neuromodulator of two forms of synaptic plasticity, known as long-term potentiation (LTP) and long-term depression (LTD) in several cortical and subcortical areas. Finally, we will delineate how the effect of DA on dendritic spines places this molecule at the interface between the motor and the cognitive systems. Specifically, we will be focusing on PD, vascular dementia, and schizophrenia. Full article
(This article belongs to the Special Issue Dopamine Signaling: From Synapses to Behavior)
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17 pages, 3909 KiB  
Review
Axonal Modulation of Striatal Dopamine Release by Local γ-Aminobutyric Acid (GABA) Signalling
by Bradley M. Roberts, Emanuel F. Lopes and Stephanie J. Cragg
Cells 2021, 10(3), 709; https://doi.org/10.3390/cells10030709 - 23 Mar 2021
Cited by 18 | Viewed by 5608
Abstract
Striatal dopamine (DA) release is critical for motivated actions and reinforcement learning, and is locally influenced at the level of DA axons by other striatal neurotransmitters. Here, we review a wealth of historical and more recently refined evidence indicating that DA output is [...] Read more.
Striatal dopamine (DA) release is critical for motivated actions and reinforcement learning, and is locally influenced at the level of DA axons by other striatal neurotransmitters. Here, we review a wealth of historical and more recently refined evidence indicating that DA output is inhibited by striatal γ-aminobutyric acid (GABA) acting via GABAA and GABAB receptors. We review evidence supporting the localisation of GABAA and GABAB receptors to DA axons, as well as the identity of the striatal sources of GABA that likely contribute to GABAergic modulation of DA release. We discuss emerging data outlining the mechanisms through which GABAA and GABAB receptors inhibit the amplitude as well as modulate the short-term plasticity of DA release. Furthermore, we highlight recent data showing that DA release is governed by plasma membrane GABA uptake transporters on striatal astrocytes, which determine ambient striatal GABA tone and, by extension, the tonic inhibition of DA release. Finally, we discuss how the regulation of striatal GABA-DA interactions represents an axis for dysfunction in psychomotor disorders associated with dysregulated DA signalling, including Parkinson’s disease, and could be a novel therapeutic target for drugs to modify striatal DA output. Full article
(This article belongs to the Special Issue Dopamine Signaling: From Synapses to Behavior)
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