Increased sensory neuron apoptotic death 2 weeks after peripheral axotomy in C57BL/6J mice compared to A/J mice.

摘要

Peripheral nerve transection results in a disconnection of the neuron from its target. As a result, a series of metabolic changes occur in the cell body that may cause neuronal death, mainly by apoptotic mechanisms. Although neurons from neonatal animals are the most susceptible, peripheral, lesion-induced, neuronal loss also occurs in adults, and is particularly evident in mouse sensory neurons. However, differences in genetic background cause particular isogenic strains of mice to react unevenly to peripheral nerve lesion. In this work, we investigated the occurrence of apoptosis as well as the ultrastructural changes in the dorsal root ganglion sensory neurons and satellite cells of C57BL/6J and A/J mice 2 weeks after ipsilateral sciatic nerve transection at the mid-thigh level. C57BL/6J mice displayed a stronger sensory neuron chromatolytic reaction that resulted in an increased loss of neurons when compared with isogenic A/J mice (p<0.01). Additionally, most of the degenerating neurons displayed the classic features of apoptosis. These findings reinforced previous data obtained by the terminal-deoxynucleotidyl transferase nick-end labeling (TUNEL) technique.