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Pre‐synaptic adenosine A 2A receptors control cannabinoid CB 1 receptor‐mediated inhibition of striatal glutamatergic neurotransmission
Author(s) -
Martire Alberto,
Tebano Maria Teresa,
Chiodi Valentina,
Ferreira Samira G.,
Cunha Rodrigo A.,
Köfalvi Attila,
Popoli Patrizia
Publication year - 2011
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.2010.07101.x
Subject(s) - glutamatergic , neurotransmission , neuroscience , glutamate receptor , striatum , adenosine a2a receptor , cannabinoid , cannabinoid receptor , neural facilitation , neurochemical , biology , basal ganglia , chemistry , dopamine , receptor , adenosine receptor , agonist , central nervous system , biochemistry
J. Neurochem. (2011) 116 , 273–280. Abstract An interaction between adenosine A 2A receptors (A 2A Rs) and cannabinoid CB 1 receptors (CB 1 Rs) has been consistently reported to occur in the striatum, although the precise mechanisms are not completely understood. As both receptors control striatal glutamatergic transmission, we now probed the putative interaction between pre‐synaptic CB 1 R and A 2A R in the striatum. In extracellular field potentials recordings in corticostriatal slices from Wistar rats, A 2A R activation by CGS21680 inhibited CB 1 R‐mediated effects (depression of synaptic response and increase in paired‐pulse facilitation). Moreover, in superfused rat striatal nerve terminals, A 2A R activation prevented, while A 2A R inhibition facilitated, the CB 1 R‐mediated inhibition of 4‐aminopyridine‐evoked glutamate release. In summary, the present study provides converging neurochemical and electrophysiological support for the occurrence of a tight control of CB 1 R function by A 2A Rs in glutamatergic terminals of the striatum. In view of the key role of glutamate to trigger the recruitment of striatal circuits, this pre‐synaptic interaction between CB 1 R and A 2A R may be of relevance for the pathogenesis and the treatment of neuropsychiatric disorders affecting the basal ganglia.