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The effects of noradrenergic lesions to the orbitofrontal cortex on reversal learning

Bates AT, Duys AN, Miller CE, Miller R, Mcgaughy J (2011) The effects of noradrenergic lesions to the orbitofrontal cortex on reversal learning. Neuroscience 2011 Abstracts 296.03. Society for Neuroscience, Washington, DC.

Summary: Poor impulse control is one of the major symptoms of disorders such as attention deficit disorder and is hypothesized to result from dysfunction in the prefrontal cortex. Specifically the ability to inhibit responding to a previously reinforced stimulus as required in tests of reversal rely on the functional integrity of the orbitofrontal cortex. Previous work from our lab and others have shown that norepinephrine in the prelimbic cortex is necessary to perform attentional set shifting. Lesions to this region result in attentional set shifting impairments that can be remediated by the administration of a selective noradrenergic reuptake blocker. Though many studies have shown monoamine levels in the orbitofrontal cortex are critical to reversal learning, few studies have directly addressed the impact of norepinephrine depletion in the orbitofrontal cortex on reversal learning. In the present study, we assess the effects of noradrenergic deafferentation of the orbitofrontal cortex in the intra-dimensional/extra-dimensional set shifting task using adult male, Long-Evans hooded rats. Preliminary data support the hypothesis that norepinephrine in orbitofrontal cortex is critical to successful reversal learning as the lesioned animals required more trials to reach criterion performance on reversals than sham-lesioned rats. Performance on the ID and ED portions of the task were not impacted by lesion. After behavioral testing was completed, brains were processed to elucidate norepinephrine transporters (NET). Fiber density of NET positive fibers was assessed in the regions of the orbitofrontal, prelimbic, and cingulate cortices for all subjects. These findings point to the function of the noradrenergic system within the orbitofrontal cortex on mediating impulse control while leaving attentional set shifting performance intact.

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