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

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.

• Authors: T Ishikawa, M Marsala
• Journal: Cellular and molecular neurobiology (Cell Mol Neurobiol) Vol. 19 Issue 2 Pg. 199-208 (Apr 1999) ISSN: 0272-4340 [Print] United States
• PMID: 10081604 (Publication Type: Journal Article)

Chemical References

• Excitatory Amino Acid Antagonists
• Receptors, N-Methyl-D-Aspartate
• Glutamic Acid
• Dizocilpine Maleate

Topics

• Animals
• Combined Modality Therapy
• Denervation
• Dizocilpine Maleate (pharmacology)
• Excitatory Amino Acid Antagonists (pharmacology)
• Glutamic Acid (cerebrospinal fluid, metabolism)
• Hypothermia, Induced
• Injections, Spinal
• Male
• Microdialysis
• Nerve Degeneration (drug therapy, physiopathology, prevention & control)
• Rats
• Rats, Sprague-Dawley
• Receptors, N-Methyl-D-Aspartate (physiology)
• Reperfusion Injury (drug therapy, physiopathology)
• Spinal Cord (blood supply, chemistry, physiopathology)