Literature DB >> 10081604

Hypothermia prevents biphasic glutamate release and corresponding neuronal degeneration after transient spinal cord ischemia in the rat.

T Ishikawa1, M Marsala.   

Abstract

1. Spinal cord ischemia evoked a biphasic increase in CSF-Glu during 20 min of ischemia (40%) and at 2 hr after reperfusion (70%) in the nontreated group that was attenuated by all treated groups. But MK-801 (15 micrograms i.t.) did not affect the increased Glu at 2 hr (80%). 2. The argyrophilia observed in laminae II-V at 8 hr after reperfusion was attenuated by hypothermia (33 degrees C) and combination with MK-801, but the attenuation was less with MK-801. 3. Mild hypothermia attenuated the biphasic increase in CSF-Glu and corresponding development of neuronal damage after spinal cord ischemia. 4. Mild hypothermia with NMDA antagonism did not yield any further effects, suggesting that hypothermia itself plays a pivotal role in the protection.

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Year:  1999        PMID: 10081604     DOI: 10.1023/a:1006973026514

Source DB:  PubMed          Journal:  Cell Mol Neurobiol        ISSN: 0272-4340            Impact factor:   5.046


  24 in total

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Review 3.  Glutamate and the pathophysiology of hypoxic--ischemic brain damage.

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9.  Postischemic moderate hypothermia inhibits CA1 hippocampal ischemic neuronal injury.

Authors:  R Busto; W D Dietrich; M Y Globus; M D Ginsberg
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10.  Profound systemic hypothermia inhibits the release of neurotransmitter amino acids in spinal cord ischemia.

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Review 7.  Therapeutic Hypothermia in Spinal Cord Injury: The Status of Its Use and Open Questions.

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