DECREASED CHOLINE-ACETYLTRANSFERASE ACTIVITY IN THE MURINE SPINAL-CORD MOTONEURONS UNDER CHRONIC MECHANICAL COMPRESSION

The tiptoe-walking Yoshimura (twy) mouse is a model of chronic spinal cord compression caused by ossification of intraspinal ligaments. Chol ine acetyltransferase (CAT), which is known to be a specific marker of cholinergic neurons, best reflects spinal motoneuron function. Change s in CAT immunoreactivity following chronic spinal cord compression in twy mice were investigated quantitatively in order to elucidate spina l motoneuron functional changes according to the degree and direction of compression. Thirty 24-week-old twy mice were used in this study. T hey were divided into three groups according to the direction of spina l cord compression (anterior, posterior, and lateral) and the CAT immu noreactivities in whole sections of their upper cervical spinal cords were investigated quantitatively using a fluorescence microphotometry system. The lateral compression group showed histological spinal moton euron atrophy and loss on the compressed, but not the non-compressed, side. Spinal motoneuron atrophy and loss were observed when the severi ty of spinal canal stenosis due to the ossified lesion, expressed as t he occupation rate, was 30% or more, but the spinal motoneurons appear ed normal when it was below 30%. The CAT immunofluorescence intensity of the anterior-horn showed a linear negative correlation with the deg ree of canal stenosis. When the occupation rate was below 20%, the CAT immunofluorescence intensities in the anterior horns of the compressi on and control groups did not differ significantly. The CAT immunofluo rescence intensity of twy mice with occupation rates of 20% or more we re significantly lower than that of those with occupation rates below 20%. Furthermore, the CAT immunofluorescence intensity was significant ly lower on the compressed than the non-compressed side of the lateral compression group. Thus, our findings indicate that an occupation rat e of about 20% may be the critical level for functional changes in the spinal motoneurons.