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Blockade of Late-Onset Reduction of Muscarinic Acetylcholine Receptors by Immunosuppressants in Forebrain Ischemia

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Immunosuppressant Analogs in Neuroprotection

Abstract

Five minutes of transient ischemia induces an almost complete loss of neurons in the CA 1 regions of the gerbil hippocampus within a few days; this phenomenon is known as “delayed neuronal death” (1). However, pyramidal neurons in the CA3 regions usually survive after transient cerebral ischemia. The ischemia-induced pyramidal cell changes in the hippocampal CA 1 regions suggest that synaptic connections between pyramidal cells and their afferent nerve endings may be transiently or persistently destroyed. Although the molecular basis for the permanent neuronal destruction induced by transient ischemia has not been fully determined, there are several plausible hypotheses. Ischemic neuronal damage may be induced by several factors, including the following mechanisms:

  1. 1.

    Hypoxia and energy failure (2)

  2. 2.

    Oxidative stress (3–5)

  3. 3.

    Immune mechanisms (6–10)

  4. 4.

    Apoptosis (5, 11, 12)

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Tanaka, Ki., Asanuma, M., Ogawa, N. (2003). Blockade of Late-Onset Reduction of Muscarinic Acetylcholine Receptors by Immunosuppressants in Forebrain Ischemia. In: Borlongan, C.V., Isacson, O., Sanberg, P.R. (eds) Immunosuppressant Analogs in Neuroprotection. Humana Press, Totowa, NJ. https://doi.org/10.1007/978-1-59259-315-6_11

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