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Adenosine A 2a Receptor Modulation of Electrically Evoked Endogenous GABA Release from Slices of Rat Globus Pallidus
Author(s) -
Mayfield R. Dayne,
Suzuki Fumio,
Zahniser Nancy R.
Publication year - 1993
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.1471-4159.1993.tb03526.x
Subject(s) - cgs 21680 , adenosine , agonist , medicine , adenosine receptor , endocrinology , gabaergic , adenosine a1 receptor , globus pallidus , adenosine a2a receptor , adenosine receptor antagonist , adenosinergic , receptor , biology , purinergic signalling , chemistry , neuroscience , inhibitory postsynaptic potential , central nervous system , basal ganglia
Abstract: Adenosine A 2a receptors have been localized to GABAergic striatopallidal neurons, but their functional role is unknown. To address this question, the modulation of endogenous GABA release by adenosine A 2a receptors was examined in slices of rat globus pallidus. The selective adenosine A 2a receptor agonist CGS‐21680 (3.0–10 n M ) significantly increased electrically stimulated release (overflow) of GABA, with 10 n M CGS‐21680 resulting in a 44% increase compared with the control. Both the nonselective adenosine receptor antagonist 8‐phenyltheophylline (10 μ M ) and the selective A 2a receptor antagonist KF‐17837 (100 n M ) abolished the CGS‐21680‐induced increase in GABA overflow. Higher concentrations of CGS‐21680 (0.10–1.0 μ M ) decreased GABA overflow by ˜25%.8‐Phenyltheophylline (10 μ M ) antagonized these effects, whereas KF‐17837 (100 n M ) did not, suggesting actions of CGS‐21680 on other adenosine receptors at these concentrations. These results demonstrate that activation of adenosine A 2a receptors augments electrically stimulated release of GABA from globus pallidus slices and suggest a mechanism by which adenosine may modulate GABAergic output from the striatopallidal efferent system.