Abstract
We investigated the effects of environmental lighting conditions regulating endogenous melatonin production on neural repair, following experimental spinal cord injury (SCI). Rats were divided into three groups randomly: the SCI + L/D (12/12‐h light/dark), SCI + LL (24‐h constant light), and SCI + DD (24‐h constant dark) groups. Controlled light/dark cycle was pre‐applied 2 weeks before induction of spinal cord injury. There was a significant increase in motor recovery as well as body weight from postoperative day (POD) 7 under constant darkness. However, spontaneous elevation of endogenous melatonin in cerebrospinal fluid was seen at POD 3 in all of the SCI rats, which was enhanced in SCI + DD group. Augmented melatonin concentration under constant dark condition resulted in facilitation of neuronal differentiation as well as inhibition of primary cell death. In the rostrocaudal region, elevated endogenous melatonin concentration promoted neural remodeling in acute phase including oligodendrogenesis, excitatory synaptic formation, and axonal outgrowth. The changes were mediated via NAS‐TrkB‐AKT/ERK signal transduction co‐regulated by the circadian clock mechanism, leading to rapid motor recovery. In contrast, exposure to constant light exacerbated the inflammatory responses and neuroglial loss. These results suggest that light/dark control in the acute phase might be a considerable environmental factor for a favorable prognosis after SCI.Support or Funding InformationNational Research Foundation (NRF‐2013R1A2A2A01067169, NRF‐2015R1C1A2A01055691, NRF‐2017R1D1A1B03029565), Korea.
Highlights
Spinal cord injury (SCI) is a type of traumatic disorder of the central nervous system (CNS) that causes severe physical disability accompanied by neurological problems [1]
SCI means that the signal from the brain cannot be conveyed via upper to lower motor neurons, leading to muscle paralysis below the injury level [4]
Since SCI may accompany these pathologic states leading to physical disability and mortality, effective care to minimize neural damage for favorable prognosis should be required
Summary
Spinal cord injury (SCI) is a type of traumatic disorder of the central nervous system (CNS) that causes severe physical disability accompanied by neurological problems [1]. Mechanical trauma primarily kills either neurons or glial cells in the injury epicenter, and insidious secondary damage follows in the penumbra. The latter is mediated by intracellular injurious signaling molecules that form a deleterious network, which can persist for several years [2]. SCI means that the signal from the brain cannot be conveyed via upper to lower motor neurons, leading to muscle paralysis below the injury level [4]. Since SCI may accompany these pathologic states leading to physical disability and mortality, effective care to minimize neural damage for favorable prognosis should be required
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