TY - JOUR
T1 - NMDA lesions in the medial prefrontal cortex impair the ability to inhibit responses during reversal of a simple spatial discrimination
AU - Salazar, Rodrigo F.
AU - White, Wesley
AU - Lacroix, Laurent
AU - Feldon, Joram
AU - White, Ilsun M.
N1 - Funding Information:
This study was supported by the ETH grant (TH-32/99-3) and NIH grant (1 R15 MH067606-01) to Ilsun M. White. We thank Lukas Faessler for assistance with surgery and training and Ashley Justice for running an additional experiment. We also thank Dr. Steve Wise for his insightful comments on the manuscript. Peter Schmid for technical support, and Liz Weber for assistance with histological preparation.
PY - 2004/7/9
Y1 - 2004/7/9
N2 - Although lesion studies suggest that the rat medial prefrontal cortex (mPFc) is involved in the process necessary for reversal of a particular set of contingencies, the nature of lesion-induced deficits is unclear. The involvement of rat mPFc in reversal of a simple spatial discrimination was examined in the present study. Our hypothesis was that lesion-induced deficits may reflect a failure to inhibit a learned instrumental response. Lister Hooded rats were trained on a spatial discrimination task (SD), which required a correct barpress matching the cue location, then they were trained on reversal of SD (SDR), which required a correct barpress opposite to the cue location. Rats with mPFc lesions showed a slower learning rate compared to the controls. However, behavior of the lesioned rats during early and later reversal differed. During the initial SDR, the lesioned rats showed a greater number of barpresses during the intertrial interval and a slightly higher percent correct responses than that of the controls. Our data suggest that damage to mPFc may produce a lack of response inhibition, leading to an increase in nondiscriminated bapresses, thereby yielding a 'facilitation' during early reversal. mPFc lesion did not affect either open field activity or prepulse inhibition (PPI), a frequently used measure of sensorimotor gating. Disruption of reversal learning following damage to mPFc is partly due to a failure to inhibit instrumental responses, rather than to disruption of other processes involved in sensorimotor gating or general activity.
AB - Although lesion studies suggest that the rat medial prefrontal cortex (mPFc) is involved in the process necessary for reversal of a particular set of contingencies, the nature of lesion-induced deficits is unclear. The involvement of rat mPFc in reversal of a simple spatial discrimination was examined in the present study. Our hypothesis was that lesion-induced deficits may reflect a failure to inhibit a learned instrumental response. Lister Hooded rats were trained on a spatial discrimination task (SD), which required a correct barpress matching the cue location, then they were trained on reversal of SD (SDR), which required a correct barpress opposite to the cue location. Rats with mPFc lesions showed a slower learning rate compared to the controls. However, behavior of the lesioned rats during early and later reversal differed. During the initial SDR, the lesioned rats showed a greater number of barpresses during the intertrial interval and a slightly higher percent correct responses than that of the controls. Our data suggest that damage to mPFc may produce a lack of response inhibition, leading to an increase in nondiscriminated bapresses, thereby yielding a 'facilitation' during early reversal. mPFc lesion did not affect either open field activity or prepulse inhibition (PPI), a frequently used measure of sensorimotor gating. Disruption of reversal learning following damage to mPFc is partly due to a failure to inhibit instrumental responses, rather than to disruption of other processes involved in sensorimotor gating or general activity.
KW - Openfield activity
KW - Prepulse inhibition
KW - Response inhibition
KW - Spatial learning
UR - http://www.scopus.com/inward/record.url?scp=2942620818&partnerID=8YFLogxK
U2 - 10.1016/j.bbr.2003.10.034
DO - 10.1016/j.bbr.2003.10.034
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C2 - 15196810
AN - SCOPUS:2942620818
SN - 0166-4328
VL - 152
SP - 413
EP - 424
JO - Behavioural Brain Research
JF - Behavioural Brain Research
IS - 2
ER -