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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(More)
In the majority of patients, spinal cord injury (SCI) results in abnormal pain syndromes in which non-noxious stimuli become noxious (allodynia). To reduce allodynia, it would be desirable to implant a permanent biological pump such as adrenal medullary chromaffin cells (AM), which secrete catecholamines and opioid peptides, both antinociceptive substances,(More)
Spinal cord injury (SCI) often results in abnormal pain syndromes in patients. We present a recently developed SCI mammalian model of chronic central pain in which the spinal cord is contused at T8 using the NYU impactor device (10-g rod, 2.0-mm diameter, 12.5-mm drop height), an injury which is characterized behaviorally as moderate. Recovery of locomotor(More)
Release of amino acids, particularly the neurotoxin glutamate, in and around the site of an experimental spinal cord injury was characterized over time by microdialysis. Increases in amino acid concentrations caused by injury decline steeply and then slowly over distance from the impact area, becoming undetectable beyond about 5 mm from the injury(More)
Spinal cord injury (SCI) results in abnormal locomotor and pain syndromes in humans. T13 spinal hemisection in the rat results in development of permanent mechanical allodynia and thermal hyperalgesia partially due to interruption of descending inhibitory modulators such as serotonin (5-HT). We hypothesize that lumbar transplantation of nonmitotic cells(More)
"Free Zn2+" (rapidly exchangeable Zn2+) is stored along with glutamate in the presynaptic terminals of specific specialized (gluzinergic) cerebrocortical neurons. This synaptically releasable Zn2+ has been recognized as a potent modulator of glutamatergic transmission and as a key toxin in excitotoxic neuronal injury. Surprisingly (despite abundant work on(More)
We investigated in vivo in rats whether sufficient glutamate is released following spinal cord injury (SCI) to kill oligodendrocytes. Microdialysis sampling was used to establish the level of glutamate released (550 +/- 80 microM) in the white matter during SCI. This glutamate concentration was administered into the spinal cords of other rats and the(More)
Spinal cord injury (SCI)-induced neurodegeneration leads to irreversible and devastating motor and sensory dysfunction. Post-traumatic outcomes are determined by events occurring during the first 24 hours after SCI. An increase in extracellular glutamate concentration to neurotoxic levels is one of the earliest events after SCI. We used Affymetrix DNA(More)
Microdialysis was used to administer paraquat into the spinal cord of the anesthetized rat to determine the effects of the in vivo generation of the superoxide anion (O2.-) on neurons. Exposure to paraquat caused blockage of axonal conduction, destruction of the cell bodies of neurons, and a general release of amino acids. Thus, paraquat is quite harmful to(More)