Abstract
Activated glial cells (microglia and astrocytes) are a histopathologic feature of numerous neurodegenerative diseases. Microglial cells have been demonstrated to migrate to and to proliferate and differentiate at sites of inflammation (1). In the cerebral cortex, glia comprise greater than 85% of the total population of brain cells. Of these, astrocytes account for about 85% of the glial cell population, while microglia constitute up to 10 to 15% of brain glial cells. Functional evidence has suggested that glial cells express receptors for opiates, such as morphine (2, 3) and endogenous opioids, such as dynorphin (4). A rapidly growing body of studies suggests that activated glial cells cause neuronal injury via releasing immune mediators, such as cytokines, reactive oxygen or nitrogen intermediates, and toxins (5). Results of these studies have raised an interesting question regarding the potential role of opiates in modulating neuronal injury.
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References
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© 1996 Plenum Press, New York
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Chao, C.C., Hu, S., Peterson, P.K. (1996). Opiates, Glia, and Neurotoxicity. In: Friedman, H., Eisenstein, T.K., Madden, J., Sharp, B.M. (eds) AIDS, Drugs of Abuse, and the Neuroimmune Axis. Advances in Experimental Medicine and Biology, vol 402. Springer, Boston, MA. https://doi.org/10.1007/978-1-4613-0407-4_5
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DOI: https://doi.org/10.1007/978-1-4613-0407-4_5
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