ArticleNature communications2026
TRPC4/TRPC5 are critical for neuronal modulation by transcranial focused ultrasound in retrosplenial cortex in male mice.
Article in Nature communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Transcranial focused ultrasound (tFUS) enables non-invasive neuromodulation, yet its underlying molecular mechanisms remain largely elusive. Here, we show that transient receptor potential canonical 4 (TRPC4) and transient receptor potential canonical 5 (TRPC5) channels are critical mediators of tFUS-induced neuronal modulation in the mouse brain. Applying tFUS to the retrosplenial cortex (RSC) in male mice desensitizes mechanical and thermal sensitivity while robustly elicits early growth response 1 (Egr1) expression. Inhibiting these tFUS-induced Egr1 ensembles blocks the somatic sensory effects. Transcriptomic analysis identifies Trpc4 enrichment in tFUS-activated Egr1-positive cells. Both pharmacological inhibition and genetic knockdown of TRPC4 abolish tFUS-mediated sensory modulation. Targeted knockdown further demonstrates that the highly homologous TRPC5 plays a comparable role. In situ proximity ligation assay, co-immunoprecipitation, and live-cell calcium imaging confirm that TRPC4 and TRPC5 form a protein complex in the RSC that facilitates the tFUS response. These findings establish TRPC4/TRPC5 as essential molecular components for tFUS neuromodulation.
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