Brain injury results in lower levels of melatonin receptors subtypes MT1 and MT2.
Brain injury results in lower levels of melatonin receptors subtypes MT1 and MT2.
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DOI：
10.1016/j.neulet.2017.03.053
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发表时间：
2017-05-22
影响因子：
2.5
通讯作者：
Dixon CE
中科院分区：
文献类型：
--
作者：
Osier ND;Pham L;Pugh BJ;Puccio A;Ren D;Conley YP;Alexander S;Dixon CE
创伤性脑损伤（TBI）是一种毁灭性的、代价高昂的获得性疾病，通过多种机制影响所有年龄、种族和地域的个体。创伤性脑损伤对褪黑激素受体的影响尚不清楚。本研究的目的是探讨实验性脑外伤后两种褪黑激素受体亚型（MT1和MT2）是否发生内源性变化。选取成年雄性大鼠25只，每组6 ~ 7只。大鼠被随机分配接受控制皮质冲击模型的TBI或假手术，并在术后6或24小时处死。脑收获，解剖，快速冷冻，直到制备出全细胞裂解液，上清液被引用并用于免疫印迹。一抗用于探测褪黑激素受体（MT1和MT2）， β肌动蛋白用于负载控制。使用ImageJ和Image Lab软件对数据进行量化，采用t检验比较均值。褪黑激素受体水平以脑区域和时间点依赖的方式降低。24小时时额叶皮质MT1和MT2减少，6小时和24小时时海马体MT1和MT2减少。损伤后MT1和MT2较少，这可能会改变对MEL治疗的反应。需要对脑外伤后MT1和MT2的特征进行研究，包括探索时间过程和区域模式，在不同样本中进行复制，以及使用其他变量，特别是与睡眠相关的结果。大鼠脑外伤导致MT1和MT2水平降低；有必要对这些发现进行重复研究，并对较低受体水平的后果进行评估。
Traumatic brain injury (TBI) is a devastating and costly acquired condition that affects individuals of all ages, races, and geographies via a number of mechanisms. The effects of TBI on melatonin receptors remains unknown. The purpose of this study is to explore whether endogenous changes in two melatonin receptor subtypes (MT1 and MT2) occur after experimental TBI. A total of 25 adult male Sprague Dawley rats were used with 6 or 7 rats per group. Rats were randomly assigned to receive either TBI modeled using controlled cortical impact or sham surgery and to be sacrificed at either 6- or 24- hours post-operatively. Brains were harvested, dissected, and flash frozen until whole cell lysates were prepared, and the supernatant fluid aliquoted and used for western blotting. Primary antibodies were used to probe for melatonin receptors (MT1 and MT2), and beta actin for a loading control. ImageJ and Image Lab software were used to quantify the data which was analyzed using t-tests to compare means. Melatonin receptors levels were reduced in a brain region- and time point-dependent manner. Both MT1 and MT2 were reduced in the frontal cortex at 24 hours and in the hippocampus at both 6 hours and 24 hours. MT1 and MT2 are less abundant after injury, which may alter response to MEL therapy. Studies characterizing MT1 and MT2 after TBI are needed, including exploration of the time course and regional patterns, replication in diverse samples, and use of additional variables, especially sleep-related outcomes. TBI in rats resulted in lower levels of MT1 and MT2; replication of these findings is necessary as is evaluation of the consequences of lower receptor levels.
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