Control of Motor Function by Adenosine A2A Receptors in Parkinson's and Huntington's Disease

Annalisa Pinna, Jadwiga Wardas, Maria R. Domenici, Patrizia Popoli, Giovanni Cossu, Micaela Morelli

Research output: Chapter in Book/Report/Conference proceedingChapter

Abstract

Adenosine A2A receptors are mainly expressed in the basal ganglia (BG) circuitry, which is responsible for the integration of sensorimotor information that controls the planning and initiation of voluntary movement. Specifically, adenosine A2A receptors are coexpressed with dopamine D2 receptors in the striatopallidal neurons of the BG, and this colocalization provides the anatomical basis for the existence of a functional antagonistic interaction between these receptors. Adenosine A2A receptors are involved in the pathogenesis of Parkinson's disease (PD) and Huntington's disease (HD), two neurological BG-related disorders with different peculiar motor and nonmotor symptoms. This chapter illustrates the role of A2A receptors as possible nondopaminergic strategies for the treatment of PD and HD. By discussing recent studies in rodents and nonhuman primates the chapter summarizes the pharmacology of adenosine A2A receptor antagonist and their interaction with dopaminergic, glutamatergic, cannabinoid and serotonin receptors, with specific relevance to cardinal motor symptoms of PD, motor fluctuations and dyskinesia induced by l-dopa therapy. In addition, the chapter describes the effects of A2A agonists and antagonists in rodent models of HD.

Original languageEnglish
Title of host publicationAdenosine Receptors in Neurodegenerative Diseases
PublisherElsevier Inc.
Pages187-213
Number of pages27
ISBN (Electronic)9780128037454
ISBN (Print)9780128037249
DOIs
Publication statusPublished - Mar 30 2017

Keywords

  • 6-hydroxydopamine lesion
  • A receptor antagonists
  • Dyskinesia
  • Huntington's disease
  • Motor fluctuation
  • MPTP lesion
  • Nonhuman primate models
  • Parkinson's disease
  • Rodent models

ASJC Scopus subject areas

  • Medicine(all)
  • Neuroscience(all)

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