The influence of glycine and related compounds on spinal cord injury-induced spasticity.

Abstract

Spasticity is a frequent and complex sequel to spinal cord injury. The neurochemical basis for the origin of spasticity is largely unknown. Glycine is among the most abundant neurotransmitters in the spinal cord. However, the role of glycine and related compounds in spasticity have received little attention. An ischemic spinal cord injury was created in rabbits, by an intraaortic balloon occlusion technique, which produced lower limb spasticity. A catheter was inserted into the cisterna magna and the spinal cord was bathed with 100 microM solutions of glycine, strychnine, D-serine, beta-alanine, MK-801, or artificial CSF for 4 hours at a rate of 10 microliters/min. H-reflexes were monitored before and during infusion by stimulating the posterior tibial nerve and recording from the plantar surface of the foot. Glycine, D-serine, and MK-801 depressed the H wave, strychnine produced a heightened H wave, and beta-alanine caused no significant changes. These results indicate that glycine and related compounds may influence spasticity.