A VALUE AND CONTRIBUTORS TO INCREASED ENERGY POTENTIAL IN A CELL MEMBRANE ESPECIALLY BY LOW INTENSITY FOCUSED ULTRASOUND (LIFU): A REVIEW

Low-Intensity Focused Ultrasound (LIFU) can modulate region-specific brain activity in vivo in a reversible and non-invasive manner, suggesting that it could be used to treat neurological disorders such as epilepsy and Parkinson's disease. Although in vivo studies demonstrate that LIFU has bioeffects on neuronal activity, they only hint at possible mechanisms and do not fully explain how this technology accomplishes these effects. According to one theory, LIFU may cause local membrane depolarization by mechanically disrupting the neuronal cell membrane or activating channels or other membrane proteins. Proteins that detect membrane mechanical perturbations, such as those regulated by membrane tension, are prime candidates for activation in response to LIFU, resulting in the observed neurological responses. We examine how LIFU affects the activation of the purified and reconstituted in liposomes bacterial mechanosensitive channel MscL. Additionally, two bacterial voltage-gated channels, KvAP and NaK2K F92A were investigated. Surprisingly, the findings indicate that ultrasound modulation and membrane perturbation do not result in channels but rather in pores at the membrane protein-lipid interface. However, apparent reductions in pore formation have been observed in vesicles containing high MscL mechanosensitive channel concentrations, implying that this membrane-tension-sensitive protein may increase membrane elasticity, presumably through channel expansion of the plane of the membrane independent of channel gating