Nelson Krysta R, Stevens Shanlee M, McLoon Linda K
Department of Ophthalmology and Visual Neurosciences, University of Minnesota, Minneapolis, Minnesota, United States.
Invest Ophthalmol Vis Sci. 2016 Oct 1;57(13):5834-5842. doi: 10.1167/iovs.16-19679.
We tested the hypothesis that short-term treatment with brain derived neurotrophic factor (BDNF) would alter the contractile characteristics of rabbit extraocular muscle (EOM).
One week after injections of BDNF in adult rabbit superior rectus muscles, twitch properties were determined in treated and control muscles in vitro. Muscles were also examined for changes in mean cross-sectional areas, neuromuscular junction size, and percent of myofibers expressing specific myosin heavy chain isoforms, and sarcoendoplasmic reticulum calcium ATPases (SERCA) 1 and 2.
Brain derived neurotrophic factor-treated muscles had prolonged relaxation times compared with control muscles. Time to 50% relaxation, time to 100% relaxation, and maximum rate of relaxation were increased by 24%, 27%, and 25%, respectively. No significant differences were seen in time to peak force, twitch force, or maximum rate of contraction. Brain derived neurotrophic factor treatment significantly increased mean cross-sectional areas of slow twitch and tonic myofibers, with increased areas ranging from 54% to 146%. Brain derived neurotrophic factor also resulted in an increased percentage of slow twitch myofibers in the orbital layers, ranging from 54% to 77%, and slow-tonic myofibers, ranging from 44% to 62%. No significant changes were seen SERCA1 or 2 expression or in neuromuscular junction size.
Short-term treatment with BDNF significantly prolonged the duration and rate of relaxation time and increased expression of both slow-twitch and slow-tonic myosin-expressing myofibers without changes in neuromuscular junctions or SERCA expression. The changes induced by BDNF treatment might have potential therapeutic value in dampening/reducing uncontrolled eye oscillations in nystagmus.
我们检验了如下假设，即脑源性神经营养因子（BDNF）的短期治疗会改变兔眼外肌（EOM）的收缩特性。
在成年兔上直肌注射BDNF一周后，在体外测定治疗组和对照组肌肉的抽搐特性。还检查了肌肉的平均横截面积、神经肌肉接头大小、表达特定肌球蛋白重链亚型的肌纤维百分比以及肌浆网钙ATP酶（SERCA）1和2的变化。
与对照肌肉相比，经脑源性神经营养因子治疗的肌肉松弛时间延长。50%松弛时间、100%松弛时间和最大松弛速率分别增加了24%、27%和25%。在峰值力时间、抽搐力或最大收缩速率方面未观察到显著差异。脑源性神经营养因子治疗显著增加了慢抽搐和紧张性肌纤维的平均横截面积，增加幅度在54%至146%之间。脑源性神经营养因子还导致眼眶层中慢抽搐肌纤维的百分比增加，范围在54%至77%之间，慢紧张性肌纤维的百分比增加，范围在44%至62%之间。SERCA1或2的表达以及神经肌肉接头大小未见显著变化。
BDNF的短期治疗显著延长了松弛时间的持续时间和速率，并增加了表达慢抽搐和慢紧张性肌球蛋白的肌纤维的表达，而神经肌肉接头或SERCA表达没有变化。BDNF治疗引起的这些变化可能在抑制/减少眼球震颤中不受控制的眼球振荡方面具有潜在的治疗价值。
