Abstract
The striatum is highly vulnerable to ischemia. It also is innervated richly by both the corticostriatal glutamatergic pathway and nigrostriatal dopaminergic projections, which have been shown to interact with each other [1]. Excitatory amino acids, such as glutamate, may contribute to ischemic cell death by causing an intracellular overload of Ca2+ [2]. It has been suggested that dopamine contributes to ischemic cell death by producing oxygen radicals [3] or by potentiating the excitotoxic effects of glutamate [4].
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© 1995 Springer-Verlag Tokyo
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Shirotani, T., Shima, K., Iwata, M., Kita, H., Chigasaki, H. (1995). Delayed Neuronal Damage Following Focal Ischemic Injury in Stroke-Prone Spontaneously Hypertensive Rats. In: Tsubokawa, T., Marmarou, A., Robertson, C., Teasdale, G. (eds) Neurochemical Monitoring in the Intensive Care Unit. Springer, Tokyo. https://doi.org/10.1007/978-4-431-68522-7_3
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DOI: https://doi.org/10.1007/978-4-431-68522-7_3
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