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Effects of endogenous melatonin regulated by conditional controlled photoperiodicity on neural reorganization through ER stress response and autophagy pathway after spinal cord injury
Author(s) -
Jin Yunho,
Hong Yonggeun
Publication year - 2016
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.30.1_supplement.lb641
Subject(s) - endogeny , melatonin , neuroprotection , autophagy , unfolded protein response , spinal cord injury , downregulation and upregulation , endoplasmic reticulum , spinal cord , endocrinology , medicine , neuroscience , circadian rhythm , biology , microbiology and biotechnology , apoptosis , biochemistry , gene
Spinal cord injury (SCI) causes serious neurological deficits. The purpose of this study was to elucidate the effect of endogenous melatonin on neural reorganization and locomotor recovery through regulation of autophagy and endoplasmic reticulum (ER) stress response after SCI. To diversify the concentration of endogenous melatonin, subjected animals were divided into 5 groups; group1 (12‐hr light/12‐hr dark, L/D), group2 (6‐hr light/18‐hr dark, 6L/18D), group3 (24‐hr dark, DD), group4 (18‐hr light/6‐hr dark, 18L/6D), group5 (24‐hr light, LL). At 7 days after injury, locomotor test based on BBB (Basso, Beattie, Bresnahan) scale was conducted to identify functional recovery and the animals were sacrificed for further molecular and histological analyses. The rats under LL condition showed great recovery of motor function after SCI. Moreover, the expression of neuronal marker and autophagy marker was also upregulated in DD group. However, the protective role of ER stress response seems to be ambiguous. In conclusion, autophagy rather than ER stress response in SCI might play a critical role in neuroprotection, which is thought to be intensified by endogenous melatonin induced by conditional controlled photoperiodicity. Support or Funding Information Funding : NRF‐2012R1A1A2005089, NRF‐2013R1A2A2A01067169