ASIC1a is required for neuronal activation via low-intensity ultrasound stimulation in mouse brain
Autor: | Cheng-Han Lee, Ya-Chih Chien, Chih-Cheng Chen, Ya-Cherng Chu, Shao-Shien Lin, Chen-Ming Hao, Yueh-Chun Huang, Dar-Ming Lai, Hsiao-Hsin Tai, Sherry Hsu, Jaw-Lin Wang, Jormay Lim, Wen-Shiang Chen, Wei-Hao Liao |
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Jazyk: | angličtina |
Rok vydání: | 2021 |
Předmět: |
Doublecortin Domain Proteins
Time Factors Mouse Stimulation Mechanotransduction Cellular Biology (General) Mechanotransduction Phosphorylation Cytoskeleton Extracellular Signal-Regulated MAP Kinases Mice Knockout Neurons Chemistry ultrasound General Neuroscience Neurogenesis Ultrasound calcium signal Brain General Medicine medicine.anatomical_structure Ultrasonic Waves Medicine micropipette mechanoreceptor Microtubule-Associated Proteins Research Article Doublecortin Protein QH301-705.5 Science CHO Cells General Biochemistry Genetics and Molecular Biology Calcium imaging Cricetulus ASIC1a medicine Pressure Animals Calcium Signaling General Immunology and Microbiology business.industry Neuropeptides In vitro neuron Acid Sensing Ion Channels Mice Inbred C57BL Neuron business Neuroscience |
Zdroj: | eLife eLife, Vol 10 (2021) |
ISSN: | 2050-084X |
Popis: | Accumulating evidence has shown transcranial low-intensity ultrasound can be potentially a non-invasive neural modulation tool to treat brain diseases. However, the underlying mechanism remains elusive and the majority of studies on animal models applying rather high-intensity ultrasound that cannot be safely used in humans. Here, we showed low-intensity ultrasound was able to activate neurons in the mouse brain and repeated ultrasound stimulation resulted in adult neurogenesis in specific brain regions. In vitro calcium imaging studies showed that a specific ultrasound stimulation mode, which combined with both ultrasound-induced pressure and acoustic streaming mechanotransduction, is required to activate cultured cortical neurons. ASIC1a and cytoskeletal proteins were involved in the low-intensity ultrasound-mediated mechanotransduction and cultured neuron activation, which was inhibited by ASIC1a blockade and cytoskeleton-modified agents. In contrast, the inhibition of mechanical-sensitive channels involved in bilayer-model mechanotransduction like Piezo or TRP proteins did not repress the ultrasound-mediated neuronal activation as efficiently. The ASIC1a-mediated ultrasound effects in mouse brain such as immediate response of ERK phosphorylation and DCX marked neurogenesis were statistically significantly compromised by ASIC1a gene deletion. Collated data suggest that ASIC1a is the molecular determinant involved in the mechano-signaling of low-intensity ultrasound that modulates neural activation in mouse brain. |
Databáze: | OpenAIRE |
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