TY - JOUR
T1 - Increased levels of the excitotoxin quinolinic acid in spinal cord following contusion injury
AU - Blight, Andrew R.
AU - Saito, Kuniaki
AU - Heyes, Melvyn P.
N1 - Funding Information:
This study was carried out in part at the Center lk~r Paralysis Research of Purdue University and was partly supported by Grant NS-21122 from NIH, NINDS. We appreciate the technical assistance of Mr. J,S. Crowley and L. Cornio.
PY - 1993/12/31
Y1 - 1993/12/31
N2 - Products of inflammatory phagocytes are potential contributors to secondary pathology following spinal cord trauma. In the present study we quantified the levels of the neurotoxin and product of activated macrophages, quinolinic acid (QUIN), in the lower thoracic spinal cord of adult guinea pigs 5 days after brief compression injury. At the injured site (T13), elevations in tissue QUIN levels (> 10-fold) accompanied proportional increases in the activity of indoleamine-2,3 dioxygenase (> 2-fold) and the concentrations of l-kynurenine (> 2.5-fold). In contrast, no significant changes occured in two uninjured regions examined compared to controls, namely cervical spinal cord (C2) and the somatosensory cortex. Further studies of QUIN as a potential contributor to spinal cord injury are warranted.
AB - Products of inflammatory phagocytes are potential contributors to secondary pathology following spinal cord trauma. In the present study we quantified the levels of the neurotoxin and product of activated macrophages, quinolinic acid (QUIN), in the lower thoracic spinal cord of adult guinea pigs 5 days after brief compression injury. At the injured site (T13), elevations in tissue QUIN levels (> 10-fold) accompanied proportional increases in the activity of indoleamine-2,3 dioxygenase (> 2-fold) and the concentrations of l-kynurenine (> 2.5-fold). In contrast, no significant changes occured in two uninjured regions examined compared to controls, namely cervical spinal cord (C2) and the somatosensory cortex. Further studies of QUIN as a potential contributor to spinal cord injury are warranted.
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U2 - 10.1016/0006-8993(93)91167-Q
DO - 10.1016/0006-8993(93)91167-Q
M3 - Article
C2 - 8149236
AN - SCOPUS:0027764234
VL - 632
SP - 314
EP - 316
JO - Molecular Brain Research
JF - Molecular Brain Research
SN - 0006-8993
IS - 1-2
ER -