AMPLIFICATION OF GLUTAMATE-INDUCED OXIDATIVE STRESS

Glutamate is a ubiquitous neurotransmitter which causes excess neurona l excitotoxicity and neurodegenerative insults such as stroke, trauma and seizures. A salient feature of the activation of glutamate recepto rs is the induction of oxidative burst. Moreover, glutamate stimulates Ca2+ influx and translocates protein kinase C (PKC). PKC mediates cel lular processes mediated via phosphorylations which may be essential f or oxidative burst in many cells. Subsequent oxidative stress may be a causal factor of neurodegenerative diseases. Increased glutamate rele ase and oxidative burst may thus both be essential in the cascade of e vents leading to neuronal damage. Glutamate may also mediate neurotoxi c effects of environmental toxic agents such as lead which amplify glu tamate excitotoxicity. In these interactions, excessive activation of glutamate receptors and oxidative burst may converge into a common pat hway leading to cell death through a cascade involving PKC or other pr oteins important in oxidative burst in neurons.