{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,8]],"date-time":"2026-10-08T20:02:44Z","timestamp":1791489764776,"version":"4.3.4"},"reference-count":53,"publisher":"The Company of Biologists","issue":"7","license":[{"start":{"date-parts":[[2020,9,3]],"date-time":"2020-09-03T00:00:00Z","timestamp":1599091200000},"content-version":"vor","delay-in-days":1160,"URL":"http:\/\/creativecommons.org\/licenses\/by\/3.0"}],"funder":[{"DOI":"10.13039\/100001819","name":"International Rett Syndrome","doi-asserted-by":"publisher","award":["IRSF-2824"],"award-info":[{"award-number":["IRSF-2824"]}],"id":[{"id":"10.13039\/100001819","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["NS-065027"],"award-info":[{"award-number":["NS-065027"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["HD-074418"],"award-info":[{"award-number":["HD-074418"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100016499","name":"Rett Syndrome Research Trust","doi-asserted-by":"crossref","id":[{"id":"10.13039\/100016499","id-type":"DOI","asserted-by":"crossref"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2017,7,1]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n               <jats:p>Rett syndrome (RTT) is a neurodevelopmental disorder caused by mutations in methyl-CpG-binding protein-2 (MECP2), a transcriptional regulator of many genes, including brain-derived neurotrophic factor (BDNF). BDNF levels are reduced in RTT autopsy brains and in multiple brain areas of Mecp2-deficient mice. Furthermore, experimental interventions that increase BDNF levels improve RTT-like phenotypes in Mecp2 mutant mice. Here, we characterized the actions of a small-molecule ligand of the BDNF receptor TrkB in hippocampal function in Mecp2 mutant mice. Systemic treatment of female Mecp2 heterozygous (HET) mice with LM22A-4 for 4 weeks improved hippocampal-dependent object location memory and restored hippocampal long-term potentiation (LTP). Mechanistically, LM22A-4 acts to dampen hyperactive hippocampal network activity, reduce the frequency and amplitude of miniature excitatory postsynaptic currents (mEPSCs), and reduce the frequency of spontaneous tetrodotoxin-resistant Ca2+ signals in Mecp2 mutant hippocampal neurons, making them comparable to those features observed in wild-type neurons. Together, these observations indicate that LM22A-4 is a promising therapeutic candidate for the treatment of hippocampal dysfunction in RTT.<\/jats:p>","DOI":"10.1242\/dmm.029959","type":"journal-article","created":{"date-parts":[[2017,7,5]],"date-time":"2017-07-05T13:20:23Z","timestamp":1499260823000},"page":"837-845","source":"Crossref","is-referenced-by-count":60,"title":["A small-molecule TrkB ligand restores hippocampal synaptic plasticity and object location memory in Rett syndrome mice"],"prefix":"10.1242","volume":"10","author":[{"given":"Wei","family":"Li","sequence":"first","affiliation":[{"name":"Department of Neurobiology, Civitan International Research Center, University of Alabama at Birmingham, Birmingham, AL 35294, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alba","family":"Bellot-Saez","sequence":"additional","affiliation":[{"name":"Department of Neurobiology, Civitan International Research Center, University of Alabama at Birmingham, Birmingham, AL 35294, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mary L.","family":"Phillips","sequence":"additional","affiliation":[{"name":"Department of Neurobiology, Civitan International Research Center, University of Alabama at Birmingham, Birmingham, AL 35294, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tao","family":"Yang","sequence":"additional","affiliation":[{"name":"Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA 94305, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Frank M.","family":"Longo","sequence":"additional","affiliation":[{"name":"Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA 94305, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-6085-5527","authenticated-orcid":false,"given":"Lucas","family":"Pozzo-Miller","sequence":"additional","affiliation":[{"name":"Department of Neurobiology, Civitan International Research Center, University of Alabama at Birmingham, Birmingham, AL 35294, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"237","reference":[{"key":"2021042500173193900_DMM029959C1","doi-asserted-by":"publisher","first-page":"214","DOI":"10.4161\/epi.2.4.5212","article-title":"MeCP2 deficiency in the brain decreases BDNF levels by REST\/CoREST-mediated repression and increases TRKB production","volume":"2","author":"Abuhatzira","year":"2007","journal-title":"Epigenetics"},{"key":"2021042500173193900_DMM029959C2","doi-asserted-by":"publisher","first-page":"5179","DOI":"10.1523\/jneurosci.5499-06.2007","article-title":"TRPC3 channels are necessary for brain-derived neurotrophic factor to activate a nonselective cationic current and to induce dendritic spine formation","volume":"27","author":"Amaral","year":"2007","journal-title":"J. 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