Effects of melatonin on neural reconstruction after acute spinal cord injury through regulation of endoplasmic reticulum stress response and autophagy

Abstract

It has been reported that autophagy and endoplasmic reticulum (ER) stress response cause improved hindlimb motor function and reduced damage of axons in spinal cord injured animals, respectively. However, the effects of melatonin on neural reconstruction and motor recovery through regulation of ER stress response and autophagy have not been well described. Therefore, the purpose of this study is to elucidate the effects of melatonin treatment on neural reconstruction and motor recovery through regulation of ER stress response and autophagy.To verify the effect of melatonin injection on post‐SCI alterations regarding neural cells, autophagy, and ER stress response, we analyzed markers at protein level, and morphological changes. At day 3 after SCI, melatonin did not cause behavioral improvement (p<.05). At molecular levels, melatonin suppressed the loss of astrocytes after SCI (p<.05). Beclin‐1 expression was decreased by melatonin treatment (p<.05). In other words, autophagy activation in SCI+MT was lower than that of SCI group, indicating melatonin‐mediated suppression of autophagic cell death. In addition, GRP78 expression was preserved in SCI+MT group with no difference compared to non‐injured groups. Namely, ER stress response was advanced by melatonin. In histological analysis, it was proved that dendritic branches were preserved by melatonin treatment.In conclusion, exogenous treatment of melatonin may result in neural reconstruction after SCI through regulating autophagy and ER stress response at the injured spinal segments.Support or Funding InformationNRF‐2017R1A2A2A01067169, KGM4611821, 2016 Creative Research Program of Inje University, Republic of KoreaThis abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.