Induction Of Neuronal Damage Research Articles

Alterations in extracellular amino acids and Ca2+ following excitotoxin administration and during status epilepticus.

Neuroexcitatory amino acids are considered to act as transmitters in several pathways of the mammalian brain. Very recently, disturbances in glutamatergic and/or aspartatergic systems have been associated with various pathological states. Thus, there is evidence to suggest that an uncontrolled release of excitatory amino acids and a subsequent post-synaptic overexcitation is involved in the induction of neuronal damage which occurs after ischemia (Benveniste et al., 1984; Simon et al., 1984; Hagberg et al., 1985; Wieloch et al., 1985) and hypoglycemia (Sandberg et al., 1985; Wieloch, 1985). Similar mechanisms are proposed to operate during status epilepticus-induced neuronal necrosis (Griffiths et al., 1982). No direct measurements of extracellular amino acids during status epilepticus have been reported and we have therefore addressed this issue using the brain dialysis method.