Hypothermia protects somatostatinergic neurons in rat dentate hilus from zinc accumulation and cell death after cerebral ischemia (original) (raw)

Abstract

We have previously shown that somatostatin (SS) immunoreactive (-i) neurons, located in the rat dentate hilus, are vulnerable to cerebral ischemia (Johansen et al., 1987). Within 40 h after ischemia, the cells show clear signs of cell death. At the same time, we observed that dying cells, located in the projection field of the mossy fibers (dentate hilus and CA3 mossy fiber layer), accumulate free zinc. We now demonstrate that the hilar cells, accumulating zinc after ischemia, are SS-i cells. Since it is known that hypothermia can ameliorate ischemic brain damage, we furthermore studied whether hypothermia (29°C) protects the vulnerable SS-i neurons in hilus from zinc accumulation and ischemic cell death. We found that hypothermia both prevented ischemia-induced neuronal zinc accumulation and cell death. We speculate that hilar SS-i cells are highly vulnerable to ischemia, and develop rapid ischemic cell death, because they accumulate zinc shortly after ischemia.

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  1. Flemming F. Johansen
    Present address: , 11 Frederik V’s vej, DK-2100, Copenhagen Ø, Denmark

Authors and Affiliations

  1. PharmaBiotec Research Center: Institute of Neuropathology, University of Copenhagen, Denmark
    Flemming F. Johansen, Michael Berg & Nils Henrik Diemer
  2. PharmaBiotec Research Center: Institute of Neurobiology, University of Aarhus, Denmark
    Niels Tønder & Jens Zimmer

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  1. Flemming F. Johansen
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  2. Niels Tønder
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  3. Michael Berg
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  4. Jens Zimmer
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  5. Nils Henrik Diemer
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Johansen, F.F., Tønder, N., Berg, M. et al. Hypothermia protects somatostatinergic neurons in rat dentate hilus from zinc accumulation and cell death after cerebral ischemia.Molecular and Chemical Neuropathology 18, 161–172 (1993). https://doi.org/10.1007/BF03160030

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