Other Neurochemical Changes in Neurotoxicity Mediated by Glutamate

17 Other Neurochemical Changes in Neurotoxicity Mediated by Glutamate 

Administration of KA also produces profound alterations in energy metabolites in the striatum within 2 h of injection (Retz and Coyle, 1982). The depletion in ATP levels may result from either an inhibition of ATP synthesis or an increase in ATP consumption in toxicity induced by KA. Collective evidence suggests that the reduction in glucose levels and concomitant increase in lactate after intrastriatal injections of KA result from an increase in energy consumption during toxicity. It has been proposed that in toxicity induced by KA, ATP depletion to a critical level invariably precedes the onset of cell death (Coyle, 1983). 

Acarin L., Paris J., Gonzalez B., and Castellano B. (2002). Glial expression of small heat shock proteins following an excitotoxic lesion in the immature rat brain. Glia 38 1-14. 

Akbar M. T., Wells D. J., Latchman D. S., and De Belleroche J. (2001). Heat shock protein 27 shows a distinctive widespread spatial and temporal pattern of induction in CNS glial and neuronal cells compared to heat shock protein 70 and caspase 3 following kainate administration. Brain Res. Mol. Brain Res. 93 148-163. 

A1 Noori S. and Swann J. W. (2000). A role for sodium and chloride in kainic acid-induced beading of inhibitory intemeuron dendrites. Neuroscience 101 337-348. 

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