Calcium deposit formation and glial reaction in rat brain after ibotenic acid-induced basal forebrain lesion.

Abstract

The mechanisms underlying amino acid neurotoxicity may involve a rise in the intracellular concentration of calcium. Some neurons appear to die as a consequence of increased intracellular calcium levels induced by excitatory amino acids. One month after injection of ibotenic acid in the rat basal forebrain, the induced formation of calcium deposits and concomitant glial reaction were studied. Alizarine Red-positive calcium deposits were observed after ibotenic acid injection in the ventral part of the globus pallidus, but not in the medial septum. These deposits were present in the globus pallidus, ventral pallidum, substantia innominata, zona incerta, lateral hypothalamic area, entopeduncular nucleus, medial amygdaloid nucleus and several thalamic nuclei. Three types of round shaped deposit were identified morphologically. Differential astroglial and microglial reactions, studied autoradiographically with the monoamine oxidase-B marker [3H]Ro19-6327 and the peripheral benzodiazepine receptor marker [3H]Ro5-4864 respectively, were observed after both lesions. Our data suggest that excitotoxic lesions in the globus pallidus and medial septum lead with time to different neurodegenerative consequences and glial reactions. This differential sensitivity is discussed on the basis of the presence of different glutamate receptor subtypes and calcium-binding proteins.