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Cellular and Molecular Neurobiology

, Volume 39, Issue 1, pp 31–59 | Cite as

Dopamine: Functions, Signaling, and Association with Neurological Diseases

  • Marianne O. Klein
  • Daniella S. Battagello
  • Ariel R. Cardoso
  • David N. Hauser
  • Jackson C. BittencourtEmail author
  • Ricardo G. CorreaEmail author
Review Paper

Abstract

The dopaminergic system plays important roles in neuromodulation, such as motor control, motivation, reward, cognitive function, maternal, and reproductive behaviors. Dopamine is a neurotransmitter, synthesized in both central nervous system and the periphery, that exerts its actions upon binding to G protein-coupled receptors. Dopamine receptors are widely expressed in the body and function in both the peripheral and the central nervous systems. Dopaminergic signaling pathways are crucial to the maintenance of physiological processes and an unbalanced activity may lead to dysfunctions that are related to neurodegenerative diseases. Unveiling the neurobiology and the molecular mechanisms that underlie these illnesses may contribute to the development of new therapies that could promote a better quality of life for patients worldwide. In this review, we summarize the aspects of dopamine as a catecholaminergic neurotransmitter and discuss dopamine signaling pathways elicited through dopamine receptor activation in normal brain function. Furthermore, we describe the potential involvement of these signaling pathways in evoking the onset and progression of some diseases in the nervous system, such as Parkinson’s, Schizophrenia, Huntington’s, Attention Deficit and Hyperactivity Disorder, and Addiction. A brief description of new dopaminergic drugs recently approved and under development treatments for these ailments is also provided.

Keywords

Dopamine pathway Neurotransmitter Central nervous system Neurodegenerative diseases 

Abbreviations

AD

Alzheimer’s disease

ADHD

Attention deficit/hyperactivity disorder

ALDH

Aldehyde dehydrogenase

BDNF

Brain-derived neurotropic factor

CaMKII

Calcium/calmodulin-dependent kinase II

cAMP

Cyclic 3,5 adenine-monophosphate

CDK5

Cyclin-dependent kinase 5

CK1

Casein kinase 1

CK2

Casein kinase 2

COMT

Catechol-O-methyl transferase

CREB

cAMP Response element-binding protein

CSF

Cerebral spinal fluid

DAG

Diacylglycerol

DARPP-32

cAMP-Regulated phosphoprotein 32-kDa

DAT

Dopamine transporter

DJ-1

PARK7 (Parkinson disease protein 7)

DOPAC

3,4-Dihydroxyphenylacetic acid

DOPAL

3,4-Dihydroxyphenylaldehyde

ELKs

Glutamine, leucine, lysine, and serine-rich protein

ERK

Extracellular-signal regulated kinases

FDA

US Food and Drug Administration

GABA

γ-Amino butyric acid

GIRK

G protein inwardly rectifying potassium channel

GPCR

G protein-coupled receptor

GRK

G protein-coupled receptor kinase

GSK3

Glycogen synthase kinase 3

GSTM2

Glutathione transferase

GTP

Guanosine triphosphate

HVA

Homovanillic acid

HD

Huntington’s disease

HTT

Huntingtin gene

IGF

Insulin growth factor

IP3

Inositol trisphosphate

JNK

c-Jun kinase

L-DOPA

Levodopa

LB

Lewy bodies

LRRK2

Leucine-rich repeat kinase 2

MAPK

Mitogen-activated protein kinase

MAPT

Microtubule-associated protein

MAT

Monoamine transporter

MAO

Monoamine oxidase

mTORC2

mTOR complex 2

NAc

Nucleus accumbens

NET

Norepinephrine transporter

NMDA

Glutamate N-methyl-d-aspartate

Parkin

PRKN

PD

Parkinson’s disease

PDPK1

Phosphatidylinositol-dependent kinase 1

PIP2

Phosphatidylinositol-2-phosphate

PIP3

Phosphatidylinositol-3-phosphate

PKA

Protein kinase A

PKC

Protein kinase C

PLC

Phospholipase C

PP1

Protein phosphatase 1

PP2A

Protein phosphatase 2A

PP2B

Protein phosphatase 2B

RGS

Regulators of G protein signaling

RIM

Rab3a-interacting molecule

ROS

Reactive oxygen species

RTK

Receptor tyrosine kinase

SNCA

α-Synuclein

STEP

Striatal-enriched tyrosine phosphatase

SZ

Schizophrenia

TAAR

Trace amine-associated receptors

VMAT2

Vesicular monoamine transporter

VTA

Ventral tegmental area

Notes

Acknowledgements

This review was supported by São Paulo State Foundation for the Support of Research (FAPESP, Brazil; Grant #2016/02224-1 to JCB, Grant #2017/17998-5 to MOK, and Grant #2017/18019-0 to ARC). DSB is a fellowship recipient of the Agency for the Advancement of Higher Education (CAPES, Brazil). JCB is a recipient of grants from the National Council for Scientific and Technological Development (CNPq, Brazil; Grant #426378/2016-4), CAPES, and the Comité Français d’Evaluation de la Coopération Universitaire avec le Brésil (French Committee for the Evaluation of Academic and Scientific Cooperation with Brazil; CAPES-COFECUB Grant #848/15). RGC was partially supported by a Special Visiting Researcher (PVE) grant from the “Science without Borders” Program (CAPES).

Author Contributions

In this review, all authors had full access to the data and take all responsibility for its integrity and accuracy. MOK, DSB, and ARC drafted the manuscript, under supervision of JCB and RGC. MOK and DSB conceptualized and designed the figures. DNH, JCB, and RGC made critical revisions of the manuscript for their relevant intellectual content. JCB and RGC obtained the funding. All authors read and approved the final manuscript.

Compliance with Ethical Standards

Conflict of interest

The authors declare that they have no conflict of interest.

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© Springer Science+Business Media, LLC, part of Springer Nature 2018

Authors and Affiliations

  1. 1.Laboratory of Chemical Neuroanatomy, Department of Anatomy, Institute of Biomedical SciencesUniversity of São Paulo (USP)São PauloBrazil
  2. 2.Center for Translational NeuroscienceSanford Burnham Prebys (SBP) Medical Discovery InstituteLa JollaUSA
  3. 3.Center for Neuroscience and Behavior, Institute of PsychologyUSPSão PauloBrazil

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