Department of Anatomical Sciences, School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran.
Department of Biology and Anatomical Sciences, Shahid Sadoughi University of Medical Sciences, Yazd, Iran.
Neurosci Lett. 2023 Mar 28;801:137136. doi: 10.1016/j.neulet.2023.137136. Epub 2023 Feb 18.
All living cells, including neurons, generate ultra-weak photon emission (UPE) during biological activity, and in particular, in the brain, it has been shown that UPE is correlated with neuronal activity and associated metabolic processes. Various intracellular factors, as well as external factors, can reduce or increase the intensity of UPE. In this study, we have used Methamphetamine (METH) as one potentially effective external factor, which is a substance that has the property of stimulating the central nervous system. METH can impair mitochondrial function by causing toxicity via various pathways, including an increase in the number of mitochondria, hyperthermia, the increased metabolic activity of the brain, and the production of glutamate and excess calcium. In addition to mitochondrial dysfunction, METH alters cellular homeostasis, leading to cell damage and the production of excess ROS. The aim of this study is to measure and compare the UPE intensity and reactive oxygen species (ROS) levels of the prefrontal, motor, and visual cortex before and after METH administration. Twenty male rats were randomly assigned to two groups, the control, and METH groups. In the control group, 2 h after injection of normal saline and without any intervention, and in the experimental group 2 h after IP injection of 20 mg/kg METH, sections were prepared from three areas: prefrontal, motor, and V1-V2 cortex, which were used to evaluate the emission of UPE using a photomultiplier tube (PMT) device and to evaluate the amount of ROS. The results showed that the amount of ROS and UPE in the experimental group in all three areas significantly increased compared to the control group. So, METH increases UPE and ROS in the prefrontal, motor, and visual regions, and there is a direct relationship between UPE intensity and ROS production. Therefore, UPE may be used as a dynamic reading tool to monitor oxidative metabolism in physiological processes related to ROS and METH research. Also, the results of this experiment may create a new avenue to test the hypothesis that the excess in UPE generation may lead to the phenomenon of phosphene and visual hallucinations.
所有活细胞，包括神经元，在生物活动过程中都会产生超微弱光子发射（UPE），特别是在大脑中，已经表明 UPE 与神经元活动和相关代谢过程相关。各种细胞内因素以及外部因素都可以减少或增加 UPE 的强度。在这项研究中，我们使用了甲基苯丙胺（METH）作为一种潜在的有效外部因素，它是一种具有刺激中枢神经系统性质的物质。METH 可以通过多种途径引起毒性，从而损害线粒体功能，包括增加线粒体数量、体温升高、大脑代谢活性增加、谷氨酸和过量钙的产生。除了线粒体功能障碍外，METH 还会改变细胞内稳态，导致细胞损伤和过量 ROS 的产生。本研究旨在测量和比较 METH 给药前后前额叶、运动和视觉皮层的 UPE 强度和活性氧（ROS）水平。20 只雄性大鼠随机分为两组，对照组和 METH 组。在对照组中，在注射生理盐水后 2 小时，并且在没有任何干预的情况下，在实验组中，在 IP 注射 20mg/kg METH 后 2 小时，从三个区域制备切片：前额叶、运动和 V1-V2 皮层，用于使用光电倍增管（PMT）设备评估 UPE 的发射，并评估 ROS 的量。结果表明，实验组在所有三个区域的 ROS 和 UPE 量与对照组相比均显著增加。因此，METH 增加了前额叶、运动和视觉区域的 UPE 和 ROS，并且 UPE 强度与 ROS 产生之间存在直接关系。因此，UPE 可以用作监测与 ROS 和 METH 研究相关的生理过程中氧化代谢的动态读数工具。此外，该实验的结果可能为测试过量 UPE 产生可能导致闪光幻视和视觉幻觉现象的假设开辟新途径。
