Journal
EUROPEAN JOURNAL OF NEUROSCIENCE
Volume 24, Issue 9, Pages 2643-2653Publisher
WILEY
DOI: 10.1111/j.1460-9568.2006.05128.x
Keywords
neurophysiology; orbitofrontal; psychostimulant; rat; reversal
Categories
Funding
- NIDA NIH HHS [R01 DA015718-03, R01 DA015718, R01-DA015718] Funding Source: Medline
- NIDCD NIH HHS [T32-DC00054, T32 DC000054] Funding Source: Medline
- NINDS NIH HHS [T32 NS007375, T32-NS07375] Funding Source: Medline
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Recent evidence has linked exposure to addictive drugs to an inability to employ information about adverse consequences, or outcomes, to control behavior. For instance, addicts and drug-experienced animals fail to adapt their behavior to avoid adverse outcomes in gambling and reversal tasks or after changes in the value of expected rewards. These deficits are similar to those caused by damage to the orbitofrontal cortex, suggesting that addictive drugs may cause long-lasting changes in the representation of outcome associations in a circuit that includes the orbitofrontal cortex. Here we test this hypothesis by recording from orbitofrontal neurons in a discrimination task in rats previously exposed to cocaine (30 mg/kg i.p. for 14 days). We found that orbitofrontal neurons recorded in cocaine-experienced rats failed to signal the adverse outcome at the time a decision was made in the task. The loss of this signal was associated with abnormal changes in response latencies on aversive trials. Furthermore, upon reversal of the cue-outcome associations, orbitofrontal neurons in cocaine-treated rats with enduring reversal impairments failed to reverse their cue-selectivity, while orbitofrontal neurons in cocaine-treated rats with normal performance showed an increase in the plasticity of cue-selective firing after reversal. These results provide direct neurophysiological evidence that exposure to cocaine can cause behaviorally relevant changes in the processing of associative information in a circuit that includes the orbitofrontal cortex.
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