Abstract
Cortical spreading depression (CSD), a transient and propagating suppression of the e1ectrical activity of the brain (Leao, 1944), is supposed to be elicited during small traumatic injury (Gardner-Medwin, 1984; Mutch and Hansen, 1984; Rothner, 1989), during surgery (Gardner-Medwin, 1984), during local vascular· occlusions (Kempinsky, 1954) and within post-infarction penumbra zone (Nedergard and Astrup, 1986; Hakim, 1987). The corresponding short lasting (minutes), but dramatic electrolyte shifts (Nicholson and Kraig, 1981) are accompanied by a transient increase of local cortical blood flow (LCBF) followed by a long lasting hypoperfusion (hours, Lauritzen et al. 1982). Glutamate (glu) and aspartate (asp) have been described as possib1e endogenous mediators of CSD (Van Harreve1d, 1959) indicating the involvement of the NMDA receptor (Marrannes et al. 1988, Scheller et al. 1990) in generation of CSD as a common final feature (Gardner-Medwin, 1984; Faden et al. 1989) for all of the known, different stimuli generating CSD.
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© 1992 Springer Science+Business Media New York
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Scheller, D., Heister, U., Tegtmeier, F. (1992). Generation and Propagation of Cortical Spreading Depression is Mediated by the NMDA Receptor. In: Globus, M.YT., Dietrich, W.D. (eds) The Role of Neurotransmitters in Brain Injury. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-3452-5_16
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DOI: https://doi.org/10.1007/978-1-4615-3452-5_16
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