Administration of glutamate into the spinal cord at extracellular concentrations reached post-injury causes functional impairments

• Published in: Neuroscience letters 2005-08, Vol.384 (3), p.271-276
• Main Authors: Xu, Guo-Ying, Hughes, Michael G., Zhang, Liping, Cain, Lisa, McAdoo, David J.
• Format: Article
• Language: English
• Subjects: Activity box; Animals; Biological and medical sciences; Dose-Response Relationship, Drug; Excitotoxicity; Extracellular Fluid - metabolism; Functional impairment; Fundamental and applied biological sciences. Psychology; Gait Disorders, Neurologic - chemically induced; Gait Disorders, Neurologic - diagnosis; Gait Disorders, Neurologic - metabolism; Gait Disorders, Neurologic - pathology; Glutamate; Glutamic Acid - metabolism; Glutamic Acid - toxicity; Male; Microdialysis; Neurons - drug effects; Neurons - pathology; Oligodendrocyte; Rats; Rats, Sprague-Dawley; Spinal Cord - drug effects; Spinal Cord - pathology; Spinal Cord Injuries - chemically induced; Spinal Cord Injuries - diagnosis; Spinal Cord Injuries - metabolism; Spinal Cord Injuries - pathology; Spinal cord injury; Vertebrates: nervous system and sense organs
• ISSN: 0304-3940; 1872-7972
• DOI: 10.1016/j.neulet.2005.04.100

In vivo experiments addressing the role of released glutamate in damage caused by neurotrauma seldom administer glutamate itself because it usually produces relatively little damage when administered into central nervous system (CNS) tissue in vivo. However, because of recent observations that glutamate administered into the spinal cord at the levels attained following spinal cord injury (SCI) kills neurons and oligodendrocytes, we tested the effects of administering glutamate at those concentrations on locomotor function. The Basso–Beattie–Bresnahan (BBB) test and activity box measures demonstrated that those glutamate concentrations produce lasting functional impairments. Several parameters provided by the activity box provided sensitive measures of the degree of post-SCI impairment, demonstrating their substantial potential for evaluating outcomes of SCI. Results obtained also enhance evidence that glutamate toxicity contributes to secondary damage following SCI and suggest that damage to white matter is an important contributor to such damage.