The effect of clonidine on cell survival,glutamate, and aspartate release in normo- and hyperglycemic rats after near complete forebrain ischemia |
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Authors: | Email author" target="_blank">W?Scott?JellishEmail author John?Murdoch Gisela?Kindel Xin?Zhang Fletcher?A?White |
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Institution: | (1) Department of Anesthesiology, Loyola University Medical Center, 2160 South First Ave., Maywood, IL, 60153, USA;(2) Department of Cell Biology, Neurobiology and Anatomy, Loyola University Medical Center, 2160 South First Ave., Maywood, IL, 60153, USA |
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Abstract: | The present study was undertaken to investigate the effects of the α2 adrenergic agonist, clonidine, on the near complete
cerebral ischemia (NCFI) evoked release of glutamate and aspartate from normo- and hyperglycemic rodent brain tissue using
microdialysis tissue techniques. Hemodynamic variables, blood lactate, and glucose levels were monitored throughout the 40 min
NCFI occlusion period. After 48 h, rats were killed and the extent of neuronal injury was determined in the cortex, striatum,
and hippocampus. Hemodynamic variables recorded during ischemia improved with clonidine treatment in both normo- and hyperglycemic
groups. Glutamate and aspartate levels were greatly increased over control values during normo- and hyperglycemic NCFI treatment.
Clonidine pretreatment suppressed the release of both glutamate and aspartate during NCFI in normo- and hyperglycemic rodents
when compared with NCFI-treated normo- and hyperglycemic rats without the drug. Significant neuroprotection of cells in the
cortex, striatum, and hippocampus was also observed in drug-treated animals 48 h postischemia. The combined effects of diminished
glutamate release after NCFI and reduced neuronal injury in both normo- and hyperglycemic states suggests that clonidine treatment
during NCFI is neuroprotective. The neuroprotective effect of clonidine during ischemia may be ascribed to both a sensitization
of central sympathetic activity and a reduced release of glutamate thereby reducing NMDA receptor activation and neuronal
damage. |
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Keywords: | α 2 agonists Near complete forebrain ischemia Glutamate Hyperglycemia |
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