Pilocarpine-Induced Activation of In Vivo Aspartate and Glutamate Release in Dorsal Hippocampus

An increased release of aspartate and glutamate, observed during ischemia in numerous studies, is believed to be a causal factor in the subsequent ‘excitotoxic’ neuropathology (Benveniste et al., 1984; see Meldrum, 1990). A similar mechanism is expected to be involved in seizure-induced brain injury (see Meldrum, 1991). Increased in vivo release of aspartate and glutamate has been reported to be associated with some forms of experimental seizures (Dodd & Bradford, 1976; Lehmann, 1987) and with ictal events in patients undergoing assessment for temporal lobectomy (Mattson et al., 1991; Do et al., 1991; Ronne-Engstrom et al., 1991). However, there have also been several studies that have failed to show an increased release of aspartate and glutamate in different brain regions following electrical stimulation or administration of convulsant drugs (Korf & Venema, 1985; Lehmann et al., 1985; Millan et al., 1991). A concomitant enhancement of excitatory amino acid (EAA) reuptake under these conditions, shown by Perschak and Cuenod (1990), would contribute to the lack of increased extracellular levels of aspartate and glutamate.