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MicroRNA-206 (miR-206) has been genetically and transcriptionally linked to schizophrenia and other neuropsychiatric disorders, but its functions in the nervous system are largely unknown. Here we show that miR-206 expression in the brain is restricted to postnatal cerebellar Purkinje cells (PCs). miR-206 was dispensable for PC cell fate specification, dendritic morphogenesis, and cerebellar-regulated motor coordination. Transcriptional profiling with single-nucleus and spatial resolution, integrated with Ago2-associated miRNA-target repression mapping (HITS-CLIP) and ribosome-associated RNA profiling (TRAP-seq), showed that miR-206 regulates translational programs in PCs controlling neuronal excitability. Accordingly, miR-206 deficiency increased the tonic firing of PCs, whereas elevating miR-206 expression shifted PCs from tonic to high-frequency burst firing. Constitutive or PC-specific deletion of miR-206 impaired prepulse inhibition (PPI) of the acoustic startle response, a conserved form of sensorimotor gating disrupted in schizophrenia and related disorders. Restoration of miR-206 expression in PCs rescued PPI deficits in miR-206-deficient mice, while elevating miR-206 expression in PCs impaired PPI in wild-type animals. Together, these findings reveal that a schizophrenia-linked microRNA tunes Purkinje neuron firing dynamics to control sensorimotor gating.<\/jats:p>","DOI":"10.64898\/2026.06.29.734826","type":"posted-content","created":{"date-parts":[[2026,6,30]],"date-time":"2026-06-30T13:45:25Z","timestamp":1782827125000},"source":"Crossref","is-referenced-by-count":0,"title":["Cerebellar microRNA-206 tunes Purkinje neuron firing dynamics to control sensorimotor gating"],"prefix":"10.64898","author":[{"given":"Mary P.","family":"Heyer","sequence":"first","affiliation":[{"name":"Nash Family Department of Neuroscience, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Masago","family":"Ishikawa","sequence":"additional","affiliation":[{"name":"Nash Family Department of Neuroscience, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA"},{"name":"Nathan S. 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