Heat Shock Protein Expression in Neurotoxicity Mediated by Glutamate

13 Heat Shock Protein Expression in Neurotoxicity Mediated by Glutamate 

Of the various HSP, heme oxygenase-1, HO-1, by generating the vasoactive molecule carbon monoxide and the potent antioxidant bilirubin, represents a novel protective system potentially active against brain oxidative injury (Rossler et al., 

6 Glutamate Receptors and Other Neurochemical Parameters in Excitotoxicity 

KA treatment causes a marked increase in cholesterol 24-hydroxylase immunoreactivity in glial cells of the affected CA fields (Fig. 6.8). The number of glial cells positive for cholesterol 24-hydroxylase increases significantly from 1 week (1312 195 cells / mm2) to 2 weeks (1815 225 cells / mm2) after kainate injection, when compared to saline-injected rats (0 0 cells / mm2). The cells positive for cholesterol 24-hydroxylase were GFAP positive. No increase in cholesterol 24-hydroxylase immunoreactivity in glial cells was observed in the hippocampus or other parts of the brain that were not affected by the kainate injections. 

Ceramide or N-acylsphingosine is a component of microdomains or lipid rafts. These structures serve as platforms for neural cell signaling and events related to signal transduction. Ceramide is generated either by de novo synthesis or by hydrolysis 

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