• Christopher P Smith, George T Somogyi, Erin T Bird, Michael B Chancellor, and Timothy B Boone.
• Department of Urology, Baylor College of Medicine and the Veterans Affairs Spinal Cord Injury Unit, Houston TX, USA. smithcp@msx.upmc.edu
• Brain Res. Brain Res. Protoc. 2002 Feb 1; 9 (1): 57-64.

AbstractWe describe an animal model to study neurotransmitter changes in parallel with urodynamic testing following Spinal Cord Injury (SCI). Urodynamic access was achieved using a subcutaneously placed 7 French dual lumen portacatheter. Spinal cord injury was induced by weight drop technique onto exposed dura at T8. The L6-S1 detrusor nuclei were localized stereotactically and microdialysis probe placement was confirmed through histologic methods. Chronic urodynamics revealed detrusor hyperreflexia (DH) 14 days following SCI. In vivo microdialysis of spinal cord amino acids was performed using CMA 11 (240 uM) probes in halothane-anesthetized rats at baseline and intervals of 20-30 min following spinal cord injury. Significant increases in the excitatory amino acid glutamate, and the inhibitory amino acids, glycine and taurine, were seen following spinal cord injury. Amino acid levels peaked at approximately 40 min following contusion injury with glycine demonstrating the highest levels of all amino acids measured. This neurogenic rat model provides a useful means of examining the effects of spinal cord injury on bladder function. By utilizing spinal cord microdialysis, one could intervene at the level of the detrusor nuclei to modulate bladder function.

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