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Neurochemical approaches to the amelioration of brain injury

  • Hanna M. Pappius
Part of the Journal of Neural Transmission book series (NEURAL SUPPL, volume 29)

Summary

The studies reported here represent a continuing search for mechanisms which may play a role in neurological disturbances resulting from brain injury. In particular, they are part of an effort to elucidate the involvement of both the serotonergic and noradrenergic neurotransmitter systems in the widespread decrease in cortical glucose utilization, interpreted as reflecting a functional depression, associated with a focal cortical lesion in the rat. Quinolinic acid, an endogenous metabolite of L-tryptophan, a neurotoxin and an N-methyl-D-asparate (NMDA) receptor agonist was found to accumulate in cortical areas of a traumatized rat hemisphere in parallel with a previously demonstrated increase of 5-hydroxyindoleacetic acid. Ketanserin (20mg/kg/day), a 5-HT2 receptor blocker ameliorated the depression of glucose utilization in traumatized brain while MK-801 (3mg/kg, before and after lesion), an NMDA receptor blocker, had no effect. Alpha1-adrenergic receptors, quantitated in vivo with [125I]-HEAT (iodo-2-[β-(4-hydroxyphenyl)-ethyl-aminomethyl]tetralone), were found to be elevated in cortical areas of the lesioned hemisphere, but not in other structures.

Keywords

Biogenic Amine Quinolinic Acid Cereb Blood Flow Injured Brain Functional Disturbance 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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Copyright information

© Springer-Verlag 1990

Authors and Affiliations

  • Hanna M. Pappius
    • 1
    • 2
  1. 1.The Goad Unit of the Donner Laboratory of Experimental Neurochemistry, Montreal Neurological InstituteMcGill UniversityMontrealCanada
  2. 2.Montreal Neurological InstituteMontrealCanada

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