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Adenosine Receptors and the Central Nervous System

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Book cover Adenosine Receptors in Health and Disease

Part of the book series: Handbook of Experimental Pharmacology ((HEP,volume 193))

Abstract

The adenosine receptors (ARs) in the nervous system act as a kind of “go-between” to regulate the release of neurotransmitters (this includes all known neurotransmitters) and the action of neuromodulators (e.g., neuropeptides, neurotrophic factors). Receptor–receptor interactions and AR–transporter interplay occur as part of the adenosine’s attempt to control synaptic transmission. A2AARs are more abundant in the striatum and A1ARs in the hippocampus, but both receptors interfere with the efficiency and plasticity-regulated synaptic transmission in most brain areas. The omnipresence of adenosine and A2A and A1 ARs in all nervous system cells (neurons and glia), together with the intensive release of adenosine following insults, makes adenosine a kind of “maestro” of the tripartite synapse in the homeostatic coordination of the brain function. Under physiological conditions, both A2A and A1 ARs play an important role in sleep and arousal, cognition, memory and learning, whereas under pathological conditions (e.g., Parkinson’s disease, Alzheimer’s disease, amyotrophic lateral sclerosis, stroke, epilepsy, drug addiction, pain, schizophrenia, depression), ARs operate a time/circumstance window where in some circumstances A1AR agonists may predominate as early neuroprotectors, and in other circumstances A2AAR antagonists may alter the outcomes of some of the pathological deficiencies. In some circumstances, and depending on the therapeutic window, the use of A2AAR agonists may be initially beneficial; however, at later time points, the use of A2AAR antagonists proved beneficial in several pathologies. Since selective ligands for A1 and A2A ARs are now entering clinical trials, the time has come to determine the role of these receptors in neurological and psychiatric diseases and identify therapies that will alter the outcomes of these diseases, therefore providing a hopeful future for the patients who suffer from these diseases.

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Abbreviations

AC:

Adenylate cyclase

ACh:

Acetylcholine

ADO:

Adenosine

ADP:

Adenosine 5′-diphosphate

AK:

Adenosine kinase

AMP:

Adenosine 5′-monophosphate

AMPA:

α-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid

AOPCP:

α, β-Methylene ADP

Ap5A:

Diadenosine pentaphosphate

AR:

Adenosine receptor

ATP:

Adenosine 5′-triphosphate

BDNF:

Brain-derived neurotrophic factor

BRET:

Bioluminescence resonance energy transfer

CamK:

Calmodulin-dependent kinase

cAMP:

Cyclic adenosine 5′-monophosphate

CB:

Cannabinoid

CGRP:

Calcitonin gene-related peptide

DA:

Dopamine

DARPP:

Dopamine- and cAMP-regulated phosphoprotein

DPCPX:

1,3-Dipropyl-8-cyclopentylxanthine

ENT:

Equilibrative nucleoside transporter

ERK:

Extracellular signal-regulated kinase

GABA:

γ-Aminobutyric acid

GAT:

GABA transporter

GLU:

Glutamate

GDNF:

Glial cell line-derived neurotrophic factor

GPCRs:

G-protein-coupled receptors

HEK cells:

Human embryonic kidney cells

HFS:

High-frequency stimulation

IL-6:

Interleukin 6

IP3:

Inositol triphosphate

i.v.:

Intravenous

KO:

Knockout

LFS:

Low-frequency stimulation

LTD:

Long-term depression

LTP:

Long-term potentiation

MAPK:

Mitogen-activated protein kinase

mGluR:

Metabotropic glutamate receptor (mGlu1–8 refer to mGluR subtypes)

NAc:

Nucleus accumbens

nAChR:

Nicotinic acetylcholine receptor

NBTI:

Nitrobenzylthioinosine

NGF:

Nerve growth factor

NMDA:

N-Methyl-d-aspartate

NT:

Neurotransmitter

NTR:

Neurotransmitter receptor

NPY:

Neuropeptide Y

NR:

NMDA receptor subunit

NT-3:

Neurotrophin 3

NTDase:

Ecto-5′-nucleotidase

NTPDase:

Ectonucleoside triphosphate diphosphohydrolase

PDE:

Phosphodiesterase

PKA:

Protein kinase A

PKC:

Protein kinase C

PLC:

Phospholipase C

PTX:

Pertussis toxin

REM:

Rapid eye movement

Trk receptors:

Tropomyosin-related kinase receptors

VIP:

Vasoactive intestinal peptide

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Acknowledgements

The work in the authors’ laboratory is supported by research grants from Fundação para a Ciência e Tecnologia (FCT), Gulbenkian Foundation and the European Union (COST B30).

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Authors and Affiliations

  1. Institute of Pharmacology and Neurosciences, Institute of Molecular Medicine, University of Lisbon, 1649-028, Lisbon, Portugal

    Ana M. Sebastião

  2. Institute of Pharmacology and Neurosciences, Faculty of Medicine and Unit of Neurosciences, Institute of Molecular Medicine, University of Lisbon, 1649-028, Lisboa, Portugal

    Joaquim A. Ribeiro

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  1. Ana M. Sebastião
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  2. Joaquim A. Ribeiro
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Correspondence to Joaquim A. Ribeiro .

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  1. Endacea, Inc.,, Davis Drive 2, Research Triangle Park, 27709-2076, U.S.A.

    Constance N. Wilson

  2. Health Sciences Center, West Virginia University, Health Sciences S. 2267, Morgantown, 26506-9104, U.S.A.

    S. Jamal Mustafa

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Sebastião, A.M., Ribeiro, J.A. (2009). Adenosine Receptors and the Central Nervous System. In: Wilson, C., Mustafa, S. (eds) Adenosine Receptors in Health and Disease. Handbook of Experimental Pharmacology, vol 193. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-540-89615-9_16

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