Effect of perinatal monosodium glutamate administration on visual evoked potentials of juvenile and adult rats.
Administration of high doses of monosodium glutamate (MSG) to rats during the first postnatal week results in severe losses of retinal ganglion cells and interneurons in the retina. This study was conducted to determine what effect severe retinal damage would have upon the ontogeny of rat flash evoked potentials (FEPs) and the adult pattern reversal evoked potential (PREP). MSG (4 mg/g) or isotonic saline was administered to rat pups daily from postnatal day (PND) 2 until PND 9. FEPs were recorded following 2 stimulation frequencies from unanesthetized, unrestrained MSG treated and control rats on PND 15, PND 22, and PND 60 or older. PREPs were recorded from unanesthetized, restrained rats older than PND 60 from each treatment group. On PND 15, 9 of 12 control animals exhibited responses to light flashes, while only 4 of 13 MSG treated animals did so. All animals from both treatment groups exhibited FEPs on PND 22 and beyond. All FEP peak latencies were significantly increased in MSG treated animals with the magnitude of the effect being greater during development. Peak N1 amplitude was reduced in MSG treated animals by 50% or more at each age. Frequency x treatment interactions were observed on peak P2 and peak N3 latency, and a frequency x age x treatment interaction was observed on peak N3 amplitude. MSG treatment severely impaired the ability to generate PREPS. Only small responses to the pattern reversal stimulus could be detected and the normal PREP peaks could not be identified with confidence. Perinatal MSG treatment results in profound alterations in FEP ontogeny and the generation of PREPs.