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Animal models for the study of adenosine receptor function
Author(s) -
Yaar R.,
Jones M.R.,
Chen J.F.,
Ravid Katya
Publication year - 2005
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.20138
Subject(s) - receptor , adenosine receptor , adenosine , adenosine a2b receptor , adenylyl cyclase , knockout mouse , biology , adenosine a3 receptor , genetically modified mouse , microbiology and biotechnology , g protein coupled receptor , purinergic signalling , adenosine a1 receptor , adenosine a2a receptor , transgene , medicine , endocrinology , biochemistry , agonist , gene
Adenosine receptors represent a family of G‐protein coupled receptors that are ubiquitously expressed in a wide variety of tissues. This family contains four receptor subtypes: A1 and A3, which mediate inhibition of adenylyl cyclase; and A2a and A2b, which mediate stimulation of this enzyme. Currently, all receptor subtypes have been genetically deleted in mouse models except for the A2b adenosine receptor, and some have been overexpressed in selective tissues of transgenic mice. Studies involving these transgenic mice indicated that receptor levels are rate limiting, as effects were amplified upon increases in receptor level. The knockout models pointed to clusters of activities related to the physiologies of the cardiovascular and the nervous systems, which are either reduced or enhanced upon specific receptor deletion. Interestingly, the trend of effects on these systems is similar in the A1 and A3 adenosine receptor knockout mice and opposite to the effects observed in the A2a adenosine receptor knockout model. This review summarizes in vitro studies on pathways affected by each adenosine receptor, and primarily focuses on the above in vivo models generated to investigate the physiologic role of adenosine receptors. Furthermore, it illustrates the need for multiple adenosine receptor subtype deficiency studies in mice and the deletion of the A2b subtype. © 2005 Wiley‐Liss, Inc.