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Previous studies from this and other laboratories have shown that enhancing BDNF expression and\/or TrkB activation in Mecp2-deficient mouse models of RTT can ameliorate or reverse abnormal neurological phenotypes that mimic human RTT symptoms. The present study reports on the preclinical efficacy of a novel, small-molecule, non-peptide TrkB partial agonist, PTX-BD4-3, in heterozygous female Mecp2 mutant mice, a well-established RTT model that recapitulates the genetic mosaicism of the human disease. PTX-BD4-3 exhibited specificity for TrkB in cell-based assays of neurotrophin receptor activation and neuronal cell survival and in in vitro receptor binding assays. PTX-BD4-3 also activated TrkB following systemic administration to wild-type and Mecp2 mutant mice and was rapidly cleared from the brain and plasma with a half-life of \u223c2\u2005h. Chronic intermittent treatment of Mecp2 mutants with a low dose of PTX-BD4-3 (5\u2005mg\/kg, intraperitoneally, once every 3\u2005days for 8\u2005weeks) reversed deficits in two core RTT symptom domains \u2013 respiration and motor control \u2013 and symptom rescue was maintained for at least 24\u2005h after the last dose. Together, these data indicate that significant clinically relevant benefit can be achieved in a mouse model of RTT with a chronic intermittent, low-dose treatment paradigm targeting the neurotrophin receptor TrkB.<\/jats:p>","DOI":"10.1242\/dmm.044685","type":"journal-article","created":{"date-parts":[[2020,11,27]],"date-time":"2020-11-27T15:45:10Z","timestamp":1606491910000},"source":"Crossref","is-referenced-by-count":20,"title":["Restoration of motor learning in a mouse model of Rett syndrome following long-term treatment with a novel small-molecule activator of TrkB"],"prefix":"10.1242","volume":"13","author":[{"given":"Ian","family":"Adams","sequence":"first","affiliation":[{"name":"Case Western Reserve University School of Medicine 1 Department of Neurosciences , , 10900 Euclid Avenue, Cleveland, OH 44106-4975 , USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tao","family":"Yang","sequence":"additional","affiliation":[{"name":"Stanford University School of Medicine 2 Department of Neurology and Neurological Sciences , , Stanford, CA 94305 , USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Frank M.","family":"Longo","sequence":"additional","affiliation":[{"name":"Stanford University School of Medicine 2 Department of Neurology and Neurological Sciences , , Stanford, CA 94305 , USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-3601-4389","authenticated-orcid":false,"given":"David M.","family":"Katz","sequence":"additional","affiliation":[{"name":"Case Western Reserve University School of Medicine 1 Department of Neurosciences , , 10900 Euclid Avenue, Cleveland, OH 44106-4975 , USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"237","published-online":{"date-parts":[[2020,11,27]]},"reference":[{"key":"2024061302323096700_DMM044685C1","doi-asserted-by":"publisher","first-page":"G328","DOI":"10.1152\/ajpgi.00203.2013","article-title":"Brain-derived neurotrophic factor enhances cholinergic contraction of longitudinal muscle of rabbit intestine via activation of phospholipase C","volume":"306","author":"Al-Qudah","year":"2014","journal-title":"Am. 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