Journal
BEHAVIORAL NEUROSCIENCE
Volume 117, Issue 1, Pages 123-135Publisher
AMER PSYCHOLOGICAL ASSOC
DOI: 10.1037/0735-7044.117.1.123
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- NIMH NIH HHS [MH56446] Funding Source: Medline
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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 jig) 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.
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