Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0026838 (spasticity)
 6,471 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Spasticity of the midline (axial) musculature may hinder (1) performing transfers, (2) efficient extremity and head movements, and (3) efficient respiration. Currently, gaps exist in our knowledge of the pathophysiology involved in spasticity development within the axial musculature. The goals of this study were (1) to study the effects of S(2) transection on the number and distribution of glutamatergic inputs, arising from primary afferents, and glycinergic inputs to sacrocaudal motoneurons; and (2) to correlate changes in these synaptic inputs with the development of spasticity within the tail musculature, which are the caudal counterparts to the trunk axial musculature. Animals with S(2) spinal transection were tested behaviorally using our established system. At 1, 2, 4, and 12 weeks post-injury, sacrocaudal motoneurons were retrogradely labeled with cholera toxin beta-subunit (CTB), and temporal changes in vesicular glutamate transporter 1 (VGLUT1) and glycine transporter 2 (GlyT2) inputs to CTB-labeled motoneurons were visualized using antibodies specific for each synaptic type and confocal microscopy. These time points correspond to each of 4 stages of spasticity development. There was no significant change in either VGLUT1 or GlyT2 labeling of sacrocaudal motoneurons at any of the time points examined. Spinal cord injury-induced spasticity, in the tail musculature, does not appear to involve either an increase in monosynaptic glutamatergic inputs from myelinated afferents or a decrease in glycinergic inputs to sacrocaudal motoneurons.
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PMID:VGLUT1 and GLYT2 labeling of sacrocaudal motoneurons in the spinal cord injured spastic rat. 1713 99

Spasticity obstructs motor function recovery post-stroke, and has been reported to occur in spinal cord injury and electrophysiological studies. The purpose of the present study was to assess spinal cord circuit spasticity in post-stroke mice. At 3, 7, 21, and 42 d after photothrombotic ischemic cortical injury in C57BL/6J mice, we observed decreased rate-dependent depression (RDD) of the Hoffmann reflex (H reflex) in the affected forelimb of mice compared with the limbs of sham mice and the non-affected forelimb. This finding suggests a hyper-excitable stretch reflex in the affected forelimb. We then performed immunohistochemical and western blot analyses to examine the expression of the potassium-chloride cotransporter 2 (KCC2) and phosphorylation of the KCC2 serine residue, 940 (S940), since this is the main chloride extruder that affects neuronal excitability. We also performed immunohistochemical analyses on the number of vesicular glutamate transporter 1 (vGluT1)-positive boutons to count the number of Ia afferent fibers that connect to motoneurons. Western bolts revealed that, compared with sham mice, experimental mice had significantly reduced KCC2 expression at 7 d post-stroke, and dephosphorylated S940 at 3 and 7 d post-stroke in motoneuron plasma membranes. We also observed a lower density of KCC2-positive areas in the plasma membrane of motoneurons at 3 and 7 d post-stroke. However, western blot and immunohistochemical analyses revealed that there were no differences between groups 21 and 42 d post-stroke, respectively. In addition, at 7 and 42 d post-stroke, experimental mice exhibited a significant increase in vGluT1 boutons compared with sham mice. Our findings suggest that both the down-regulation of KCC2 and increases in Ia afferent fibers are involved in post-stroke spasticity.
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PMID:Down-regulation of KCC2 expression and phosphorylation in motoneurons, and increases the number of in primary afferent projections to motoneurons in mice with post-stroke spasticity. 2554 54