한빛사논문
- 조회486
Sangjin Yoo1, David R. Mittelstein2, Robert C. Hurt3, Jerome Lacroix1,4 & Mikhail G. Shapiro1,*
1Division of Chemistry and Chemical Engineering, California Institute of Technology, Pasadena, CA 91125, USA. 2Division of Engineering and Applied Science, California Institute of Technology, Pasadena, CA 91125, USA. 3Division of Biology and Biological Engineering, California Institute of Technology, Pasadena, CA 91125, USA. 4Graduate College of Biomedical Sciences, Western University of Health Sciences, Pomona, CA 91766, USA.
*Corresponding author.
Abstract
Ultrasonic neuromodulation has the unique potential to provide non-invasive control of neural activity in deep brain regions with high spatial precision and without chemical or genetic modification. However, the biomolecular and cellular mechanisms by which focused ultrasound excites mammalian neurons have remained unclear, posing significant challenges for the use of this technology in research and potential clinical applications. Here, we show that focused ultrasound excites primary murine cortical neurons in culture through a primarily mechanical mechanism mediated by specific calcium-selective mechanosensitive ion channels. The activation of these channels results in a gradual build-up of calcium, which is amplified by calcium- and voltage-gated channels, generating a burst firing response. Cavitation, temperature changes, large-scale deformation, and synaptic transmission are not required for this excitation to occur. Pharmacological and genetic inhibition of specific ion channels leads to reduced responses to ultrasound, while over-expressing these channels results in stronger ultrasonic stimulation. These findings provide a mechanistic explanation for the effect of ultrasound on neurons to facilitate the further development of ultrasonic neuromodulation and sonogenetics as tools for neuroscience research.
논문정보
- Research article
- 2022년 01월 (BRIC 등록일 2022-03-04)
- 국외 연구진
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