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Helplessness and escape performance: glutamate-adenosine interactions in the frontal cortex
Aimee M Hunter1, Bernard W Balleine, Thomas R Minor
1Department of Psychology, University of California, Los Angeles 90095-1563, USA. amhunter@ucla.edu
Behavioral Neuroscience
|March 7, 2003
Summary
Caffeine reversed glutamate-induced escape deficits in rats, suggesting adenosine receptor involvement in learned helplessness. N-methyl-D-aspartate receptor activation in the frontal cortex also contributes to helplessness.
Area of Science:
- Neuroscience
- Behavioral Neuroscience
Background:
- Adenosine is implicated in learned helplessness, potentially stemming from neuronal overactivation.
- Learned helplessness is characterized by impaired escape performance following inescapable shock.
Purpose of the Study:
- To investigate the role of adenosine receptors and N-methyl-D-aspartate (NMDA) receptors in the frontal cortex in learned helplessness.
- To determine if caffeine, an adenosine receptor antagonist, can reverse learned helplessness deficits.
Main Methods:
- Glutamate was injected into the rat frontal cortex to induce escape deficits.
- Caffeine was administered at different time points after glutamate injection.
- 2-amino-5-phosphonovaleric acid (AP5), an NMDA receptor antagonist, was microinjected into the frontal cortex before inescapable shock.
Main Results:
- Glutamate injection into the frontal cortex impaired escape performance.
- Caffeine treatment reversed glutamate-induced deficits when given 1 hour, but not 72 hours, after glutamate.
- Pre-shock administration of AP5 prevented the development of escape deficits.
Conclusions:
- Adenosine receptor activation in the frontal cortex plays a role in learned helplessness.
- NMDA receptor activation in the frontal cortex is involved in the helplessness effect.