Spinal cord transection causes dramatic, sustained decrease of vesicular acetylcholine transporter VAChT in terminals contacting motoneurons, as reported by Kitzman (2006, Exp Neurol 197). Cholinergic projection is known to regulate excitability of motoneurons during locomotion. The question arises if locomotor exercise of spinal, paraplegic animals might restore the role of this projection. Three groups of adult rats were tested: intact control (n=6), spinal (n=7) and spinal trained subjected to 5 weeks of treadmill locomotor training (n=8). Animals were spinalized at low thoracic segments. Gastrocnemius/soleus and anterior tibial motoneurons were prelabeled with fl uorescent dyes (FG, DY), injected to the muscles. VAChT immunoreactivity (IR) was detected using polyclonal Sigma antibody. We have found that the spinal cord transection caused a decrease of VAChT IR in boutons synapsing on cell bodies and proximal dendrites of motoneurons in L3 and L4 segments compared with that of intact rats. Surprisingly, training caused its further decay. Mean number of VAChT IR boutons did not differ consistently between groups. However, in the extensor motoneuron pools of trained animals the number of bigger VAChT IR boutons was clearly higher than in spinal non-trained and intact animals. The latter effect is in line with functional improvement of spinal trained animals, which is the most prominent in the support phase of locomotion. Supported by MSE P-N/029/2006 and N N401 0480 33 grants.
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