Neurotox Res. 2022 Sep 3. doi: 10.1007/s12640-022-00565-9. Online ahead of print.
Photobiomodulation therapy has become the focus of medical research in many areas such as Alzheimer’s disease (AD), because of its modulatory effect on cellular processes through light energy absorption via photoreceptors/chromophores located in the mitochondria. However, there are still many questions around the underlying mechanisms. This study was carried out to unravel whether the function-structure of ATP-sensitive mitoBKCa channels, as crucial components for maintenance of mitochondrial homeostasis, can be altered subsequent to light therapy in AD. Induction of AÎ² neurotoxicity in male Wistar rats was done by intracerebroventricular injection of AÎ²1-42. After a week, light-treated rats were exposed to 40-Hz white light LEDs, 15 min for 7 days. Electrophysiological properties of mitoBKCa channel were investigated using a channel incorporated into the bilayer lipid membrane, and mitoBKCa-Î²2 subunit expression was determined using western blot analysis in AÎ²-induced toxicity and light-treated rats. Our results describe that conductance and open probability (Po) of mitoBKCa channel decreased significantly and was accompanied by a Po curve rightward shift in mitochondrial preparation in AÎ²-induced toxicity rats. We also showed a significant reduction in expression of mitoBKCa-Î²2 subunit, which is partly responsible for a leftward shift in BKCa Po curve in low calcium status. Interestingly, we provided evidence of a significant improvement in channel conductance and Po after light therapy. We also found that light therapy improved mitoBKCa-Î²2 subunit expression, increasing it close to saline group. The current study explains a light therapy improvement in brain mitoBKCa channel function in the AÎ²-induced neurotoxicity rat model, an effect that can be linked to increased expression of Î²2 subunit.
PMID:36057039 | DOI:10.1007/s12640-022-00565-9