Literature DB >> 1884213

Excitatory amino acids rise to toxic levels upon impact injury to the rat spinal cord.

D Liu1, W Thangnipon, D J McAdoo.   

Abstract

The release of glutamate, aspartate, glutamine and asparagine upon impact injury to the rat spinal cord was characterized by sample collection from the site of injury by microdialysis. Injury caused dramatic and long-lasting increases in the concentrations of the excitatory amino acids. Determination of the relationship between unperturbed extracellular levels and the levels of amino acids in the collected fluids indicates that the concentrations of these amino acids were probably high enough to kill neurons for longer than one hour following impact injury to the spinal cord. Increases in the concentrations of the metabolically related non-neurotransmitters asparagine and glutamine were considerably smaller. The latter observations suggest that much of the increase in levels of the excitatory amino acids resulted from neuronal activity rather than from simple damage.

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Year:  1991        PMID: 1884213     DOI: 10.1016/0006-8993(91)90984-4

Source DB:  PubMed          Journal:  Brain Res        ISSN: 0006-8993            Impact factor:   3.252


  53 in total

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8.  Remote activation of microglia and pro-inflammatory cytokines predict the onset and severity of below-level neuropathic pain after spinal cord injury in rats.

Authors:  Megan Ryan Detloff; Lesley C Fisher; Violetta McGaughy; Erin E Longbrake; Phillip G Popovich; D Michele Basso
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9.  Reduction in expression of the astrocyte glutamate transporter, GLT1, worsens functional and histological outcomes following traumatic spinal cord injury.

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