Eichenbaum HB, Ross R, Raji A, McGaughy JA (2003) Noradrenergic, but not cholinergic, deafferentation of the infralimbic/prelimbic cortex impairs attentional set-shifting. Neuroscience 2003 Abstracts 940.7. Society for Neuroscience, New Orleans, LA.
Summary: Damage to the prefrontal cortex in humans produces deficits in the ability to shift attention to a previously irrelevant stimulus dimension (extra-dimensional shift; EDS) while sparing reversal and intra-dimensional shifts (a novel discrimination without a change in the relevant dimension; IDS). Data from human subjects has also shown the administration of noradrenergic agonists and antagonists disrupts EDS suggesting a role for coeruleal-cortical norepinephrine (NE). Usher and colleagues have proposed that high, tonic levels of NE may maximize behavioral flexibility to allow an optimal responsiveness to changes in the environment e.g. the predictability of reinforcement (Usher et al., Science 283, 1999). Based on these data, a loss of NE would be predicted to impair attentional set-shifting. In a rodent model of attentional set-shifting developed by Brown and colleagues, excitotoxic lesions of the infralimbic/prelimbic cortex (IL/PL) produced impairments in EDS but not IDS or reversal learning (J. Neurosci. 20, 2000). This study confirmed the importance of IL/PL to EDS, but did not address the role of NE in this type of cognition. In the current study, rats were infused with anti-dopamine beta-hydroxylase-saporin (NE-SAP)in IL/PL (0.01 µ g/ µl; 0.5 µl/hemisphere) to produce noradrenergic deafferentation, 192 IgG saporin (ACH-SAP; 0.01 µ g/ µl; 0.5 µl/hemisphere)to produce cholinergic deafferentation, or vehicle then tested in an attentional set-shifting task. NE-SAP rats were impaired in EDS but not in IDS or reversal learning. In contrast, ACH-SAP rats showed no impairment in any aspect of the task. The effect of DBH-SAP lesions on EDS support the hypothesis that NE, but not ACH, is critical to the adaptation of behavior to changes in reinforcement contingencies. The lack of effect of these lesions on reversal learning suggest the robustness of this effect may vary with the extent of behavioral adaptation required.
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