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Cocaine-experienced rats exhibit learning deficits in a task sensitive to orbitofrontal cortex lesions
Geoffrey Schoenbaum1, Michael P Saddoris, Seth J Ramus
1University of Maryland School of Medicine, Department of Anatomy and Neurobiology, 685 West Baltimore Street, HSF-1 Rm 280K, Baltimore, MD 21201, USA. schoenbg@schoenbaumlab.org
The European Journal of Neuroscience
|April 14, 2004
Summary
Cocaine exposure causes lasting changes in rat brain function, impairing behavioral control. These effects on the orbitofrontal cortex are distinct from psychomotor sensitization.
Area of Science:
- Neuroscience
- Behavioral Neuroscience
- Addiction Research
Background:
- Addictive drugs, like cocaine, induce persistent neural alterations in the prefrontal cortex.
- These changes are hypothesized to impact behavioral control regulated by the orbitofrontal cortex.
Purpose of the Study:
- To investigate the long-lasting effects of cocaine exposure on orbitofrontal cortex-dependent functions.
- To determine if cocaine-induced behavioral impairments correlate with psychomotor sensitization.
Main Methods:
- Rats received daily cocaine or vehicle injections for 14 days.
- Following a 2-week withdrawal, rats were trained on an odor discrimination task sensitive to orbitofrontal cortex lesions.
- Behavioral performance, including response latency and serial reversal learning, was assessed.
Main Results:
- Cocaine-treated rats exhibited long-lasting locomotor sensitization to cocaine.
- Impaired discrimination learning and slower serial reversal acquisition were observed in cocaine-exposed rats.
- These behavioral deficits mimicked the effects of orbitofrontal cortex lesions.
Conclusions:
- Cocaine exposure induces long-lasting behavioral impairments linked to orbitofrontal cortex function.
- The neural changes underlying these behavioral effects are distinct from those mediating psychomotor sensitization.