Journal of Translational Neurosciences

Description

After an acute ischemic stroke, even in patients who have undergone thrombolytic therapy or embolectomy, it is very difficult to recover the damage to neural function. Clinical case studies and animal models have demonstrated that current technologies like Magnetic Resonance Imaging (MRI) cannot accurately predict or evaluate the progression of functional neural injury resulting from cerebral ischemia-reperfusion. In order to reliably guide the development of pharmacological and neurotechnological means for better stroke treatment, it is necessary to develop methods for identifying and evaluating functional injury following stroke. In normal or pathological conditions, almost all life, including microorganisms, plants, animals, and humans, can spontaneously radiate a very weak photon beam. Biological ultra-weak photon emissions, also known as UPE, are the result of a coherent electromagnetic field inside the cells.

Biophoton Activity and Transmission in the Neural Circuit of Animal Brain

Biophotons were initially thought to be the basis for cell-to-cell communication in plants, bacteria, and some animal cells, despite early experimental evidence indicating that biophoton generation is primarily related to mitochondrial respiration, lipid oxidation, and other metabolic activities. Biophotonic activities also known as emissions have also been found to travel along neural fibers. Recent research has demonstrated that neural biophotons are involved in higher brain functions and may play a significant role in neural information transmission and processing. An Ultraweak Biophoton Imaging System (UBIS), a novel biophoton imaging technique, has been used in our previous research to demonstrate that 50 mM glutamate can induce biophoton activity and transmission in the neural circuit of animal brain slices in vitro. Beginning, upkeep, washing, and reapplication. These characteristics were linked to the initiation, maintenance, and reapplication effects of glutamate on its receptor or the washing effect of presynaptic vesicle release, according to additional research. As a result, these results offer a novel method for analyzing the functional changes that occur in neural circuits as a result of transient focal cerebral ischemia-reperfusion. We report delayed functional neural circuit injury in rats caused by cerebral ischemia-reperfusion in the current study. Male Wistar rats ranging in age from eight to twelve weeks and weighing between 250 and 320 grams were purchased from the Hubei Provincial Laboratory Animal Public Service Center in Wuhan, China. They were kept in a room at the Experimental Animal Center of South-Central University for Nationalities with a 12-hour light/dark cycle and were provided with food and water on an as-needed basis.

Marker of Tissue Dehydrogenase and Mitochondrial Dysfunction

After transient Middle Cerebral Artery Occlusion (MCAO), the recovery time was increased from 6 hours to 1 week. This resulted in a significant decrease in the infarct area, as shown by TTC staining, as well as an improvement in behavioral scores using the Zea Longa test. Both of these changes became very apparent after one week of recovery. These findings demonstrate the viability of conventional animal models of transient focal cerebral ischemia-reperfusion and are in line with a significant number of studies that have already been published. TTC staining, as a marker of tissue dehydrogenase and mitochondrial dysfunction, cannot reliably reflect functional neural circuit injury, even though it is more intuitive and reliable for evaluating the acute infarct area caused by ischemia in animal models. However, TTC staining is also more intuitive and reliable. As a result, it has long been thought that this method has underestimated the area of the infarct. In conclusion, a biophoton imaging method was used to identify the delayed functional neural circuit injury caused by cerebral ischemia-reperfusion. This provided not only a novel functional evaluation method for animal models of cerebral ischemia-reperfusion, but also new concepts for gaining a better understanding of the functional changes caused by cerebral ischemia-reperfusion. Additionally, it may be a useful method for the evaluation of new drugs for the treatment of stroke.