Gabapentin suppresses spasticity in the spinal cord–injured rat

Abstract Spasticity poses a major detrimental impact on the quality of life in a significant number of people with spinal cord injury (SCI). Recent observations in our laboratory suggest that spinal transection at the sacral S2 level induces a significant increase in glutamatergic input to sacrocaud...

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Bibliographic Details
Published in:Neuroscience 2007-11, Vol.149 (4), p.813-821
Main Authors: Kitzman, P.H, Uhl, T.L, Dwyer, M.K
Format: Article
Language:English
Subjects:
Amines - pharmacology
Analysis of Variance
Animals
Anticonvulsants - therapeutic use
Anticonvulsants. Antiepileptics. Antiparkinson agents
Behavior, Animal - drug effects
Biological and medical sciences
Cross-Over Studies
Cyclohexanecarboxylic Acids - pharmacology
Disease Models, Animal
Electromyography - methods
Female
Fundamental and applied biological sciences. Psychology
gamma-Aminobutyric Acid - pharmacology
Medical sciences
muscle hyperreflexia
Muscle Spasticity - etiology
Neurology
Neuropharmacology
Pharmacology. Drug treatments
presynaptic glutamate inhibition
Rats
Rats, Sprague-Dawley
Reflex, Abnormal - drug effects
Spinal Cord Injuries - complications
Time Factors
Vertebrates: nervous system and sense organs
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Summary:Abstract Spasticity poses a major detrimental impact on the quality of life in a significant number of people with spinal cord injury (SCI). Recent observations in our laboratory suggest that spinal transection at the sacral S2 level induces a significant increase in glutamatergic input to sacrocaudal motoneurons during the time spasticity is present in the tail muscles. The present study examined the efficacy of gabapentin, an agent that has been shown to reduce glutamate release, in managing spasticity within the tail musculature. Method In this blinded, crossover study adult Sprague-Dawley rats with S2 spinal transections were tested behaviorally for the progression of spasticity in the tail musculature using our established system. When the animals demonstrated a significant level of spastic behavior (e.g. increased response to quick stretch, noxious and non-noxious cutaneous stimuli), they received either saline or the antiepileptic agent gabapentin (GBP; 50 mg/kg i.p.) and were assessed behaviorally and electrophysiologically at 1, 3, 6, 12 and 24 h post-injection. Results Both spastic behavior and electromyography (EMG) activity were significantly decreased at 1 and 3 h post-GBP injection when compared with the activity level following administration of saline. Spastic behavior and EMG activity gradually increased over time and returned to baseline activity by 24 h post-injection. Conclusion Gabapentin diminishes both the behavioral and electrophysiological manifestation of SCI-induced spasticity, in the tail musculature, in a time dependent manner.
ISSN:0306-4522
1873-7544
DOI:10.1016/j.neuroscience.2007.07.020