Summary
The density of ionotropic glutamate receptors on the ischemia-vulnerable CA1 pyramidal cells is one of the highest in the CNS. Postischemic use of the AMPA antagonist NBQX has shown up to 80% protection against cell death. Three groups of rats given NBQX (30 mg/kg × 3) immediately after ischemia and with a survival period of 6 days, 3 weeks, and 8 weeks were compared to untreated groups of ischemic rats. Countings of CA1 pyramidal cells showed an equal, significant protection in all three groups (20%–40% cell loss). Thus, if glutamate antagonist treatment is instituted immediately after ischemia, the obtained protection is permanent. Others [11] have shown that a 6-h delay of treatment results in loss of protection. The very delayed loss in the latter situation could be a variant of the maturation phenomeon described by Ito and colleague (1975) [9].
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© 1997 Springer-Verlag Berlin Heidelberg
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Diemer, N.H., Bruhn, T., Christensen, T., Nielsen, M., Johansen, F.F. (1997). Glutamate-Mediated Mechanisms in Delayed Neuronal Death After Cerebral Ischemia. In: Ito, U., Kirino, T., Kuroiwa, T., Klatzo, I. (eds) Maturation Phenomenon in Cerebral Ischemia II. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-60546-8_7
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DOI: https://doi.org/10.1007/978-3-642-60546-8_7
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