Much evidence suggests that cognitive flexibility, which can be operationalized in reversal learning tasks, is mediated by cortico-striatal circuitries, with the orbitofrontal cortex (OFC) playing a prominent role. We investigated the effects on reversal learning of pharmacological overactivation of the lateral and medial orbitofrontal cortex (lOFC, mOFC) using a glutamate transporter 1 (GLT-1) inhibitor, dihydrokainate (DHK), which increases extracellular glutamate by blocking its reuptake. We also tested the impact of antagonism of the serotonin 2A receptor (5-HT2AR), which modulates glutamate action, in the mOFC and lOFC on the same task.

Each .csv file corresponds to one experiment: reversal learning data from mOFC & lOFC, with rats receiving either the glutamate transporter 1 (GLT-1) inhibitor, dihydrokainate (DHK) or the antagonist of the serotonin 2A receptor (M-100,907).