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Alterations of putative neurotransmitters and enzymes during ischemia in gerbil cerebral cortex

Journal of Neural Transmission. Supplementum
|January 1, 1978
PubMed

Insights

Short-term bilateral carotid artery occlusion in gerbils caused reversible changes in neurotransmitter levels and enzyme activities. These findings suggest a non-controlled release of neurotransmitters during ischemic events.

Area of Science:

  • Neuroscience
  • Biochemistry
  • Ischemia Research

Background:

  • Cerebral ischemia can lead to reversible neurological deficits.
  • Understanding the biochemical changes during transient ischemia is crucial for developing therapeutic strategies.

Purpose of the Study:

  • To investigate the biochemical alterations in the brain following short-term, reversible bilateral carotid artery occlusion in Mongolian gerbils.
  • To elucidate the changes in neurotransmitter levels and enzyme activities during and after ischemic periods.

Main Methods:

  • Bilateral common carotid arteries of Mongolian gerbils were occluded for periods up to 15 minutes.
  • Levels of cyclic AMP, GABA, norepinephrine, dopamine, serotonin, and glutamate were measured.
  • Activities of adenylate cyclase, glutamate decarboxylase, monoamine oxidase, GABA-transaminase, Na+-K+-ATPase, total protein kinase, and acetylcholinesterase were assessed.

Main Results:

  • Initial increases in cyclic AMP and GABA levels, with enhanced adenylate cyclase and glutamate decarboxylase activities.
  • Decreased norepinephrine levels and reduced activities of monoamine oxidase, GABA-transaminase, and Na+-K+-ATPase.
  • Subsequent reductions in dopamine, serotonin, and glutamate concentrations, alongside decreased protein kinase and acetylcholinesterase activities with longer ischemia durations.

Conclusions:

  • The observed biochemical changes are consistent with a non-controlled release of neurotransmitters during transient cerebral ischemia.
  • These findings provide insights into the complex neurochemical cascade triggered by short-term ischemic events.

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