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These disorders are frequently associated with cognitive deficits in attention or learning and memory, suggesting that persistent activation of dopamine signaling may change neural plasticity to induce cognitive or emotional malfunction.<\/jats:p>\n              <\/jats:sec><jats:sec>\n                <jats:title>Methods<\/jats:title>\n                <jats:p>Dopamine transporter knockdown (DAT-KD) mice were used to mimic a hyper-dopamine state. Novel object recognition (NOR) task was performed to assess the recognition memory. To test the role of dopamine D<jats:sub>3<\/jats:sub> receptor (D<jats:sub>3<\/jats:sub>R) on NOR, DAT-KD mice were treated with either a D<jats:sub>3<\/jats:sub>R antagonist, FAUC365 or by deletion of D<jats:sub>3<\/jats:sub>R. Total or phospho-GSK3 and \u2013ERK1\/2 signals in various brain regions were measured by Western blot analyses. To examine the impact of GSK3 signal on NOR, wild-type mice were systemically treated with GSK3 inhibitor SB216763 or, micro-injected with lentiviral shRNA of GSK3\u03b2 or GSK3\u03b1 in the medial prefrontal cortex (mPFC).<\/jats:p>\n              <\/jats:sec><jats:sec>\n                <jats:title>Results<\/jats:title>\n                <jats:p>We confirmed our previous findings that DAT-KD mice displayed a deficit in NOR memory, which could be prevented by deletion of D<jats:sub>3<\/jats:sub>R or exposure to FAUC365. In WT mice, p-GSK3\u03b1 and p-GSK3\u03b2 were significantly decreased in the mPFC after exposure to novel objects; however, the DAT-KD mice exhibited no such change in mPFC p-GSK3\u03b1\/\u03b2 levels. DAT-KD mice treated with FAUC365 or with D<jats:sub>3<\/jats:sub>R deletion exhibited restored novelty-induced GSK3 dephosphorylation in the mPFC. Moreover, inhibition of GSK3 in WT mice diminished NOR performance and impaired recognition memory. Lentiviral shRNA knockdown of GSK3\u03b2, but not GSK3\u03b1, in the mPFC of WT mice also impaired NOR.<\/jats:p>\n              <\/jats:sec><jats:sec>\n                <jats:title>Conclusion<\/jats:title>\n                <jats:p>These findings suggest that D<jats:sub>3<\/jats:sub>R acts via GSK3\u03b2 signaling in the mPFC to play a functional role in NOR memory. In addition, treatment with D<jats:sub>3<\/jats:sub>R antagonists may be a reasonable approach for ameliorating cognitive impairments or episodic memory deficits in bipolar disorder patients.<\/jats:p>\n              <\/jats:sec>","DOI":"10.1186\/s12929-019-0613-y","type":"journal-article","created":{"date-parts":[[2020,1,3]],"date-time":"2020-01-03T18:03:26Z","timestamp":1578074606000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":17,"title":["Dopamine D3 receptor and GSK3\u03b2 signaling mediate deficits in novel object recognition memory within dopamine transporter knockdown mice"],"prefix":"10.1186","volume":"27","author":[{"given":"Pi-Kai","family":"Chang","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jung","family":"Chu","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ya-Ting","family":"Tsai","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yan-Heng","family":"Lai","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-2996-5781","authenticated-orcid":false,"given":"Jin-Chung","family":"Chen","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"297","published-online":{"date-parts":[[2020,1,3]]},"reference":[{"key":"613_CR1","doi-asserted-by":"publisher","first-page":"3111","DOI":"10.2147\/NDT.S76700","volume":"11","author":"AF Carvalho","year":"2015","unstructured":"Carvalho AF, Bortolato B, Miskowiak K, Vieta E, K\u00f6hler C. 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