Improvement of Optokinetic Reflexes by Optokinetic Training (2)

Role of NMDA Recepators

Abstract

To evaluate the involvement of N-methyl-D-aspartic acid (NMDA) receptors in the optokinetic training (OKT)-induced improvement of optokinetic nystagmus (OKN), we examined the effect on the optokinetic reflex of MK-801 ((±)-5-metyl-10, 11-dihydro-5H-dibenzo [a, d] cyclohepten-5, 10-imine maleate). Experiments were performed on pigmented rabbits in which OKN had been improved by OKT for 12 days. When MK-801 was injected intramuscularly, OKN was blocked; this blockade was completely reversed within 72 hrs. At non-intoxic doses (0.05 and 0.1 mg/kg), this drug caused an in-crease in locomotor activity and a reduction of OKN. On the other hand, neither the postrotatory nystagmus (PRN) nor the electroencephalogram (EEG) of the cerebral neocortex and hippocampus was influenced by non-intoxic doses of MK-801. A similar effect was observed on both atropine-sensitive and atropine-resistant EEGs. These results indicate that MK-801-induced impairment of OKN is probably due to its inhibition of NMDA receptors in the oculomotor pathway, suggesting that the activation of this recep-tor may be involved in the improvement of OKN by OKT.