REGIONAL BRAIN ATROPHY AND REDUCTIONS IN GLUTAMATE RELEASE AND UPTAKE AFTER INTRASTRIATAL KAINIC ACID

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Abstract
1 Neurochemical changes and tissue weights were measured following intrastriatal injection of 2.5 μg of kainic acid in 2 μl of 0.9% w/v NaCl solution (saline) in the rat. 2 After kainic acid the striatum and neocortex on the injected side showed a progressive reduction in weight, the neocortex showing the greatest absolute weight loss and the striatum the greatest percentage change. 3 Large (80–90%) reductions in choline acetyltransferase (CAT) and l-glutamate decarboxylase (GAD) activities in the striatum occurred within 2–4 days of the injection and persisted at least 10 weeks. At 10 weeks CAT and GAD activities were unaltered in the neocortex. 4 The absolute content of dopamine in the striatum was not different from control 5 days after the injection of kainic acid but was reduced at 2 and 10 weeks. At 2 weeks the concentration (μg/g wet weight) of dopamine also was reduced but at 10 weeks it was near normal due to atrophy of the striatum. 5 The high affinity glutamate uptake into a crude synaptosomal preparation of the striatum was reduced by 64% 5 days after kainic acid and was still reduced by 67% at 10 weeks. 6 The efflux of glutamate from slices of the striatum in the presence of 52 mm K+ was reduced by approximately 75% 5 days and 15 weeks after kainic acid. 7 In vitro kainic acid (10−4m) neither altered the high affinity uptake of radiolabelled glutamate into a homogenate of the striatum, nor released endogenous glutamate from slices of striatum.