Regional Energy Balance in Rat Brain After Transient Forebrain Ischemia

Regional Energy Balance in Rat Brain After Transient Forebrain Ischemia Abstract: Phosphocreatine, ATP, and glucose were severely depleted, and the lactate levels were increased in the paramedian neocortex, dorsal‐lateral striatum, and CA1 zone of hippocampus of rats exposed to 30 min of forebrain ischemia. Upon recirculation of the brain, phosphocreatine, ATP, and lactate concentrations recovered to control values in the paramedian neocortex and CA1 zone of hippocampus and to near‐control values in the striatum. The phosphocreatine and ATP concentrations then fell and the lactate levels rose in the striatum after 6–24 h, and in the CA1 zone of hippocampus after 24–72 h. The initial recovery and subsequent delayed changes in the phosphocreatine, ATP, and lactate concentrations in the striatum and hippocampus coincided with the onset and progression of morphological injury in these brain regions. The results suggest that cells in these regions regain normal or near‐normal mitochondrial function and are viable, in terms of energy production, for many hours before unknown mechanisms cause irreversible neuronal injury. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Journal of Neurochemistry Wiley

Regional Energy Balance in Rat Brain After Transient Forebrain Ischemia

Journal of Neurochemistry, Volume 40 (5) – May 1, 1983

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Publisher
Wiley
Copyright
1983 International Society for Neurochemistry
ISSN
0022-3042
eISSN
1471-4159
D.O.I.
10.1111/j.1471-4159.1983.tb13599.x
Publisher site
See Article on Publisher Site

Abstract

Abstract: Phosphocreatine, ATP, and glucose were severely depleted, and the lactate levels were increased in the paramedian neocortex, dorsal‐lateral striatum, and CA1 zone of hippocampus of rats exposed to 30 min of forebrain ischemia. Upon recirculation of the brain, phosphocreatine, ATP, and lactate concentrations recovered to control values in the paramedian neocortex and CA1 zone of hippocampus and to near‐control values in the striatum. The phosphocreatine and ATP concentrations then fell and the lactate levels rose in the striatum after 6–24 h, and in the CA1 zone of hippocampus after 24–72 h. The initial recovery and subsequent delayed changes in the phosphocreatine, ATP, and lactate concentrations in the striatum and hippocampus coincided with the onset and progression of morphological injury in these brain regions. The results suggest that cells in these regions regain normal or near‐normal mitochondrial function and are viable, in terms of energy production, for many hours before unknown mechanisms cause irreversible neuronal injury.

Journal

Journal of NeurochemistryWiley

Published: May 1, 1983

References

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