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Effects of an adenosine A 2A receptor blockade in the nucleus accumbens on locomotion, feeding, and prepulse inhibition in rats
Author(s) -
Nagel Jens,
Schladebach Henning,
Koch Michael,
Schwienbacher Isabel,
Müller Christa E.,
Hauber Wolfgang
Publication year - 2003
Publication title -
synapse
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.809
H-Index - 106
eISSN - 1098-2396
pISSN - 0887-4476
DOI - 10.1002/syn.10240
Subject(s) - nucleus accumbens , prepulse inhibition , adenosine , adenosine receptor , open field , chemistry , receptor , pharmacology , antagonist , blockade , stimulation , medicine , neuroscience , endocrinology , biology , agonist , schizophrenia (object oriented programming) , psychiatry
The nucleus accumbens (NAc) subserves behaviors governed by natural rewards, i.e., feeding or exploration, and has been implicated in control of prepulse inhibition (PPI), a measure of sensorimotor gating. The present study sought to determine whether a tonic stimulation of adenosine A 2A receptors in the rat NAc is involved in control of spontaneous locomotor activity, feeding behavior, and PPI. To this end, bilateral microinfusions of a prodrug (MSX‐3) (3 μg and 5 μg in 1 μl per side) of the selective A 2A receptor antagonist MSX‐2 or vehicle (1 μl per side) were administered into the NAc. Results show that blockade of intra‐NAc adenosine A 2A receptors by a high (5 μg), but not by a low (3 μg), dose of MSX‐3 increased locomotor activity in an open field, reduced food intake, and delayed intake onset in food‐deprived rats examined in a test cage with standard laboratory chow. Furthermore, PPI was significantly disrupted after intra‐NAc infusion of 5 μg, but not 3 μg, MSX‐3. These findings suggest that locomotor activity as well as intact PPI and feeding behavior rely on tonic activation of intra‐NAc A 2A receptors. The data add further support to the view that adenosine is a tonically active modulator of striatal function through actions on A 2A receptors. Synapse 49:279–286, 2003. © 2003 Wiley‐Liss, Inc.