Excitotoxicity-Mediated Neurochemical Changes in Neurological Disorders
Reference240 articles.
1. Acarin L., Paris J., González 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.
2. Ahn M. J., Sherwood E. R., Prough D. S., Lin C. Y., and DeWitt D. S. (2004). The effects of traumatic brain injury on cerebral blood flow and brain tissue nitric oxide levels and cytokine expression. J. Neurotrauma 21:1431–1442.
3. 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.
4. Alberdi E., Sánchez-Gómez M. V., Marino A., and Matute C. (2002). Ca2+ influx through AMPA or kainate receptors alone is sufficient to initiate excitotoxicity in cultured oligodendrocytes. Neurobiol. Dis. 9:234–243.
5. Alberdi E., Sánchez-Gómez M. V., Torre I., Domercq M., Pérez-Samartín A., Pérez-Cerdá F., and Matute C. (2006). Activation of kainate receptors sensitizes oligodendrocytes to complement attack. J. Neurosci. 26:3220–3228.