| Literature DB >> 31588000 |
Soo-Jin Oh1, Jung Moo Lee2, Hyun-Bum Kim3, Jungpyo Lee4, Sungmin Han5, Jin Young Bae6, Gyu-Sang Hong7, Wuhyun Koh8, Jea Kwon2, Eun-Sang Hwang3, Dong Ho Woo7, Inchan Youn5, Il-Joo Cho9, Yong Chul Bae6, Sungon Lee10, Jae Wan Shim11, Ji-Ho Park12, C Justin Lee13.
Abstract
Low-intensity, low-frequency ultrasound (LILFU) is the next-generation, non-invasive brain stimulation technology for treating various neurological and psychiatric disorders. However, the underlying cellular and molecular mechanism of LILFU-induced neuromodulation has remained unknown. Here, we report that LILFU-induced neuromodulation is initiated by opening of TRPA1 channels in astrocytes. The Ca2+ entry through TRPA1 causes a release of gliotransmitters including glutamate through Best1 channels in astrocytes. The released glutamate activates NMDA receptors in neighboring neurons to elicit action potential firing. Our results reveal an unprecedented mechanism of LILFU-induced neuromodulation, involving TRPA1 as a unique sensor for LILFU and glutamate-releasing Best1 as a mediator of glia-neuron interaction. These discoveries should prove to be useful for optimization of human brain stimulation and ultrasonogenetic manipulations of TRPA1.Entities:
Keywords: Best1; NMDAR; TRPA1; astrocyte; glutamate; neuromodulation; ultrasound
Year: 2019 PMID： 31588000 DOI： 10.1016/j.cub.2019.08.021
Source DB: PubMed Journal: Curr Biol ISSN： 0960-9822 Impact factor: 10.834