TY - JOUR
T1 - Learning deficits in an odor reward-task induced by parafascicular thalamic lesions are ameliorated by pretraining d-cycloserine in the prelimbic cortex
AU - Villarejo-Rodríguez, Irene
AU - Boadas-Vaello, Pere
AU - Portero-Tresserra, Marta
AU - Vale-Martínez, Anna
AU - Martí-Nicolovius, Margarita
AU - Guillazo-Blanch, Gemma
PY - 2013/2/1
Y1 - 2013/2/1
N2 - 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 (10 μg/side) into the PLC 20. min before ODT acquisition. The task retention was evaluated in a drug-free test carried out 24. h 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. © 2012 Elsevier B.V.
AB - 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 (10 μg/side) into the PLC 20. min before ODT acquisition. The task retention was evaluated in a drug-free test carried out 24. h 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. © 2012 Elsevier B.V.
KW - Glutamate
KW - Intralaminar nuclei
KW - NMDA receptors
KW - Odor learning
KW - Prefrontal cortex
KW - Thalamus
U2 - https://doi.org/10.1016/j.bbr.2012.10.041
DO - https://doi.org/10.1016/j.bbr.2012.10.041
M3 - Article
VL - 238
SP - 289
EP - 292
JO - Behavioural Brain Research
JF - Behavioural Brain Research
SN - 0166-4328
ER -