Learning deficits in an odor reward-task induced by parafascicular thalamic lesions are ameliorated by pretraining d-cycloserine in the prelimbic cortex

► Pre-training excitotoxic lesions of parafascicular nucleus disrupted an odor discrimination task. ► d-Cycloserine in the prelimbic cortex reversed memory impairments induced by parafascicular lesions. ► d-Cycloserine acts as an enhancing memory treatment in animal models of cognitive impairment. We investigated whether the N-methyl-d-aspartate (NMDA) receptor partial agonist d-cycloserine (DCS) infused into the prelimbic cortex (PLC) would reverse the learning deficits caused by bilateral excitotoxic lesions of the parafascicular nucleus (PFn) in an odor discrimination task (ODT). Rats with PFn lesions received a bilateral infusion of DCS (10μg/side) into the PLC 20min before ODT acquisition. The task retention was evaluated in a drug-free test carried out 24h later. DCS significantly attenuated the PFn lesion-induced deficits as measured by both latency to nose-poke the rewarded odor and number of errors committed during ODT acquisition and retention. Therefore, DCS may be an enhancing memory treatment in animal models of cognitive impairment, such as PFn-lesioned rats. The PFn contribution to learning and memory may possibly be linked to its role in the modulation of glutamatergic PLC activity.