Alleviation of Brain Injury-Induced Cerebral Metabolic Depression by Amphetamine: A Cytochrome Oxidase Histochemistry Study
Measurements of oxidative metabolic capacity following the ablation of rat sensorimotor cortex and ,he administration of amphetamine were examined to determine their effects on the metabolic dysfunction that follows brain injury. Twenty-four hours after surgery, rats sustaining either sham operation...
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| Main Authors: | , , , |
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| Format: | Article |
| Language: | English |
| Published: |
Wiley
2000-01-01
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| Series: | Neural Plasticity |
| Online Access: | http://dx.doi.org/10.1155/NP.2000.109 |
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| Summary: | Measurements of oxidative metabolic
capacity following the ablation of rat sensorimotor
cortex and ,he administration of amphetamine
were examined to determine their
effects on the metabolic dysfunction that
follows brain injury. Twenty-four hours after
surgery, rats sustaining either sham operations
or unilateral cortical ablation were administered
a single injection of D-amphetamine (2 mg/kg;
i.p.) or saline and then sacrificed 24 h later.
Brain tissue was processed for cytochrome
oxidase histochemistry, and 12 bilateral cerebral
areas were measured, using optical density as
an index of the relative amounts of the
enzyme. Compared with that of the control
groups, cytochrome oxidase in the injured
animals was significantly reduced throughout
the cerebral cortex and in 5 of II subcortical
structures. This injury-induced depression of
oxidative capacity was most pronounced in
regions of the hemisphere ipsilateral to the
ablation. Animals given D-amphetamine had less depression of oxidative capacity, which
was most pronounced bilaterally in the cerebral
cortex, red nucleus, and superior colliculus;
and in the nucleus accumbens, caudateputamen,
and globus pallidus ipsilaterai to the
ablation. The ability of D-amphetamine to
alleviate depressed cerebral oxidative metabolism
following cortical injury may be one mechanism
by which drugs increasing noradrenaline
release accelerate functional recovery in both
animals and humans. |
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| ISSN: | 2090-5904 1687-5443 |