NMDA receptors mediate expression of one form of functional plasticity induced by olfactory deprivation.

Unilateral olfactory deprivation for the first 3 postnatal weeks results in an enhancement of granule cell mediated, feedback inhibition of mitral cells in the rat olfactory bulb. Granule cells are excited by mitral cells by both non-NMDA and NMDA receptors. The present report describes the effect of the NMDA antagonist MK-801 (0.75 mg/kg) on the expression of deprivation enhanced inhibition. The results demonstrate that (1) enhancement of lateral olfactory tract paired-pulse inhibition of evoked potentials in deprived bulbs was stimulus intensity dependent, with the greatest difference expressed at highest stimulus intensities; (2) MK-801 reduced inhibition in both undeprived and deprived bulbs in a stimulus intensity dependent manner, with the greatest reduction occurring at highest stimulus intensities; (3) MK-801 eliminated the stimulus intensity effect on inhibition in both groups; and (4) following MK-801, deprived bulbs showed the same or less inhibition than undeprived bulbs.