Glucose does not reverse impairments on spontaneous alternation induced by the noncompetitive NMDA antagonist MK-801.

N-Methyl-D-aspartate (NMDA) antagonists have been demonstrated to impair acquisition in a variety of tasks, including maze learning. It was previously reported from this laboratory that glucose can reverse the deficits on spontaneous alternation resulting from administration of the competitive NMDA antagonist NPC 12626 in mice. The present study tested the ability of glucose to reverse deficits induced by the noncompetitive NMDA antagonist MK-801. Although subcutaneous administration of 0.10 mg/kg of MK-801 resulted in a deficit on spontaneous alternation, glucose (100 and 250 mg/kg) did not reverse the impairment. This difference in the ability of glucose to reverse the impairment caused by the two NMDA antagonists may reflect their different modes of actions at the NMDA receptor complex.