Research Topic

Dopamine Neuron Diversity in Circuits and Diseases

About this Research Topic

Midbrain dopamine neurons are essential to the normal functioning of the mammalian brain and dysfunction in these circuits is observed in a range of neuropsychiatric disorders as diverse as Parkinson’s, depression, and schizophrenia. Midbrain dopamine neurons are not homogeneous but rather display diverse molecular signatures, physiological characteristics, anatomical connections, and functional roles during behavior. How this diversity impacts downstream circuits in the striatum and elsewhere and how dysfunction in particular dopamine populations generates unique neuropsychiatric symptoms are currently topics of intense investigation.

Although tremendous progress has been made on dissecting specific features of dopamine neuron subtypes, key questions remain. For instance, how do molecularly distinct dopamine sub-populations differ in terms of anatomical connections, signaling properties, and behavioral roles? How are dopamine release dynamics differentially regulated in downstream regions to control specific aspects of behavior, such as learning and motivation? Can the dysfunction of particular dopamine signals or molecularly defined subpopulations be attributed to particular symptoms of disease? These questions are now being addressed in animal models amenable to genetic targeting, using newly developed molecular and optical approaches to monitor and manipulate neural signaling in distinct dopaminergic subpopulations during behavior.


This Research Topic focuses on the function of dopamine circuits with the aim of providing an overview of this wide-ranging topic. A particular emphasis will be on genetically and anatomically distinct dopamine circuits, their unique roles in behaviors, and their involvement in models of diseases. We seek Original Research, Review, Mini-Review, Hypothesis and Theory, Perspective, Clinical Trial, Case Report and Opinion articles that cover, but are not limited to, the following topics:

• Molecular and anatomical heterogeneity of dopamine circuits
• Dopamine dynamics in distinct midbrain or downstream regions during behavior
• Local modulation of dopamine release
• Impact of distinct dopamine release dynamics on target regions
• Dopamine circuit dysfunction in genetic models of neuropsychiatric diseases
• Novel approaches to measure or manipulate dopaminergic signals with improved spatiotemporal resolution and genetic specificity during behavior


Keywords: Substantia nigra, ventral tegmental area, motivation, Parkinson’s disease, striatum


Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.

Midbrain dopamine neurons are essential to the normal functioning of the mammalian brain and dysfunction in these circuits is observed in a range of neuropsychiatric disorders as diverse as Parkinson’s, depression, and schizophrenia. Midbrain dopamine neurons are not homogeneous but rather display diverse molecular signatures, physiological characteristics, anatomical connections, and functional roles during behavior. How this diversity impacts downstream circuits in the striatum and elsewhere and how dysfunction in particular dopamine populations generates unique neuropsychiatric symptoms are currently topics of intense investigation.

Although tremendous progress has been made on dissecting specific features of dopamine neuron subtypes, key questions remain. For instance, how do molecularly distinct dopamine sub-populations differ in terms of anatomical connections, signaling properties, and behavioral roles? How are dopamine release dynamics differentially regulated in downstream regions to control specific aspects of behavior, such as learning and motivation? Can the dysfunction of particular dopamine signals or molecularly defined subpopulations be attributed to particular symptoms of disease? These questions are now being addressed in animal models amenable to genetic targeting, using newly developed molecular and optical approaches to monitor and manipulate neural signaling in distinct dopaminergic subpopulations during behavior.


This Research Topic focuses on the function of dopamine circuits with the aim of providing an overview of this wide-ranging topic. A particular emphasis will be on genetically and anatomically distinct dopamine circuits, their unique roles in behaviors, and their involvement in models of diseases. We seek Original Research, Review, Mini-Review, Hypothesis and Theory, Perspective, Clinical Trial, Case Report and Opinion articles that cover, but are not limited to, the following topics:

• Molecular and anatomical heterogeneity of dopamine circuits
• Dopamine dynamics in distinct midbrain or downstream regions during behavior
• Local modulation of dopamine release
• Impact of distinct dopamine release dynamics on target regions
• Dopamine circuit dysfunction in genetic models of neuropsychiatric diseases
• Novel approaches to measure or manipulate dopaminergic signals with improved spatiotemporal resolution and genetic specificity during behavior


Keywords: Substantia nigra, ventral tegmental area, motivation, Parkinson’s disease, striatum


Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.

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Submission Deadlines

10 January 2021 Manuscript
26 April 2021 Manuscript Extension

Participating Journals

Manuscripts can be submitted to this Research Topic via the following journals:

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Topic Editors

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Submission Deadlines

10 January 2021 Manuscript
26 April 2021 Manuscript Extension

Participating Journals

Manuscripts can be submitted to this Research Topic via the following journals:

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