Changes in dynamin and actin mRNA expression in the dorsal column-medial lemniscal system following dorsal column lesion.

Transection of the third cervical hindlimb dorsal column nerve fibers in the spinal cord leads to a partial deafferentation atrophy of the neurons of the ascending dorsal column-medial lemniscal neural network (DC-ML) up to the cortex. We now examine the alteration of the steady-state level mRNA coding for the synaptic vesicle protein, dynamin I and the cytoskeletal protein beta-actin as early indicators of direct and trans-synaptic changes in the relay nuclei of the DC-ML. Rats were sacrificed at 6, 24, 72, and 240 hr after C3 hindlimb dorsal column or sham lesion. By 24 hr, there are changes in the steady-state levels of mRNA coding for both dynamin I and beta-actin in regions of the brain containing the first (nucleus gracilis of medulla) and third synaptic relays (cortex). Beta-actin mRNA is increased at both 6 and 24 hr in the nucleus gracilis. The changes in dynamin I mRNA in the nucleus gracilis are early and biphasic, elevated at 6 hr but decreased compared to sham by 24 hr. In both regions, the initial fluctuations of dynamin I and beta-actin mRNA levels are transient. By 72 hr, the levels are no different from those of sham-lesioned animals. In the somatomotor cortex, there is an additional increase in beta-actin mRNA levels at 240 hr. The increased steady-state levels of dynamin and actin mRNA following a hindlimb dorsal column lesion suggest that increased synaptic vesicle recycling and actin cytoskeleton rearrangement are some of the early responses to deafferentation made by the neurons of the DC-ML synaptic relays.