Acta neurologica Scandinavica · 2005
The effects of environmental light--dark changes on experimental mild traumatic brain injury.
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Ucar T, Ozkaya G, Demir N, Gurer I, Akyuz M, Onal M Z
Аннотация
OBJECTIVES: The aim of this study was to investigate the effects of environmental light-dark changes on the outcome of mild traumatic brain injury (MTBI) using an experimental rodent model. The functions of endogenous and exogenous melatonin on the outcome of injury were also investigated
METHODS: Mild traumatic brain injury was experimentally induced in 56 male Sprague-Dawley rats using a weight-drop device. Animals were divided into four groups of 14 each as follows: (i) sham-operated (trauma only, normal day-night cycle), (ii) treated with melatonin (trauma+melatonin, normal day-night cycle), (iii) darkness-induced (trauma+48 h constant dark), and (iv) treated with melatonin and darkness-induced (trauma+48 h constant dark+melatonin). Melatonin (50 mg/kg) was administered, intraperitoneally, immediately after trauma. EEG recordings were taken at three time periods (pretrauma, immediately after trauma, and 48 h after trauma). Motor functions were tested pretrauma, 24 and 48 h post-trauma. Serum melatonin levels were determined pretrauma and 48 h post-trauma. Tissue samples from right frontal area were taken 48 h after trauma for light and electron microscopic examinations.
CONCLUSION: Following MTBI light deprivation alone and light deprivation in combination with exogenously administered melatonin indicated significant neuroprotective effects. Although there may be other important pathways, darkness-induced elevation in endogenous melatonin secretion appears to play an important role in this neuroprotective outcome.
METHODS: Mild traumatic brain injury was experimentally induced in 56 male Sprague-Dawley rats using a weight-drop device. Animals were divided into four groups of 14 each as follows: (i) sham-operated (trauma only, normal day-night cycle), (ii) treated with melatonin (trauma+melatonin, normal day-night cycle), (iii) darkness-induced (trauma+48 h constant dark), and (iv) treated with melatonin and darkness-induced (trauma+48 h constant dark+melatonin). Melatonin (50 mg/kg) was administered, intraperitoneally, immediately after trauma. EEG recordings were taken at three time periods (pretrauma, immediately after trauma, and 48 h after trauma). Motor functions were tested pretrauma, 24 and 48 h post-trauma. Serum melatonin levels were determined pretrauma and 48 h post-trauma. Tissue samples from right frontal area were taken 48 h after trauma for light and electron microscopic examinations.
CONCLUSION: Following MTBI light deprivation alone and light deprivation in combination with exogenously administered melatonin indicated significant neuroprotective effects. Although there may be other important pathways, darkness-induced elevation in endogenous melatonin secretion appears to play an important role in this neuroprotective outcome.