Summary
An important feature of ischemic brain damage is the exceptional vulnerability of specific cell types. In the Mongolian gerbil, silver impregnation revealed that four brain regions are exceptionally vulnerable to 5 min of complete forebrain ischemia: (1) hippocampal areas CA1, CA2–CA3a and CA4; (2) the dorsolateral striatum; (3) the somatosensory neocortex; and (4) the dorsomedial portion of the lateral septal nucleus. The ischemic lesion evolved with time in all four regions, but at different rates. The development of argyrophilia was delayed for the longest time in hippocampal area CAlb (maximal in 3 d) and for the shortest time in hippocampal area CA4 and the striatum (maximal in 24 h or less). The mechanism for delayed neuronal death in area CAlb has been suggested to involve the activation of excitatory afferent pathways. Indeed an ipsilateral entorhinal cortical lesion partially protected CA1b pyramidal cells from ischemic cell death. However, the entorhinal cortical lesion had no protective effect in other hippocampal regions. This result suggests either that synaptic excitation is crucial for only the most delayed form of ischemic cell death or that the medial temporo-ammonic tract, and not the perforant path, is involved in the damage to area CAlb.
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© 1988 Plenum Press, New York
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Crain, B.J., Nadler, J.V. (1988). Selective Neuronal Cell Death after Transient Forebrain Ischemia in the Mongolian Gerbil. In: Somjen, G. (eds) Mechanisms of Cerebral Hypoxia and Stroke. Advances in Behavioral Biology, vol 35. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-5562-5_4
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