Helplessness and escape performance: glutamate-adenosine interactions in the frontal cortex.
Adenosine has been implicated as a proximate mediator of escape deficits in the learned helplessness paradigm, suggesting that neuronal overactivation-a typical precursor to adenosine release-precedes the inescapable shock-induced impairment (T. R. Minor, W. C. Chang, & J. L. Winslow, 1994). In the present experiments, glutamate (100 microg) injection into the rat frontal cortex produced a deficit in escape performance. Pretest treatment with the adenosine receptor antagonist caffeine (7 mg/kg ip) reversed the effect of glutamate when infused 1 hr. but not 72 hr, after glutamate injection. Finally, microinjection of 2-amino-5-phosphonovaleric acid (5 ng) into the frontal cortex prior to inescapable shock prevented the escape deficit. These findings are consistent with the involvement of N-methyl-D-aspartate receptor activation in the frontal cortex in the helplessness effect.
Hunter
Aimee M
AM
Department of Psychology, University of California, Los Angeles 90095-1563, USA. amhunter@ucla.edu
Balleine
Bernard W
BW
Minor
Thomas R
TR
D000241:Adenosine / Q000494:pharmacology*; D000818:Animals; D001362:Avoidance Learning; D004347:Drug Interactions; D005625:Frontal Lobe / Q000187:drug effects* / Q000502:physiology*; D018698:Glutamic Acid / Q000494:pharmacology*; D008297:Male; D051381:Rats; D017207:Rats, Sprague-Dawley; D016194:Receptors, N-Methyl-D-Aspartate / Q000187:drug effects / Q000502:physiology*
D016194:Receptors, N-Methyl-D-Aspartate; D018698:Glutamic Acid; D000241:Adenosine