Autophagy in long propriospinal neurons is activated after spinal cord injury in adult rats.

Spinal cord injury (SCI) is a common disease worldwide that causes permanent neuronal dysfunction without an effective treatment. Long propriospinal neurons (LPSNs) that are spared from injury play a key role in spontaneous recovery after SCI. Traumatic injury of the central nervous system can activate autophagy, which could be a target in the development of a new therapeutic strategy to prevent neuronal loss. Our research focused on whether autophagy is involved in the loss of LPSNs after introducing spinal cord injury in adult rats. Different sacrifice time points were chosen to characterize autophagy and apoptosis. Autophagy and a blocked autophagy flux reached their peaks at 3 d after injury, while apoptosis reached its peak at 7 d after injury when the number of LPSNs significantly decreased. Both autophagy and apoptosis contributed to the loss of LPSNs, and apoptosis was the main cause of cell death. However, autophagy may prevent programmed LPSN cell death (apoptosis), which could promote cell survival.