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000138769 0247_ $$2doi$$a10.1016/j.nbd.2015.09.001
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000138769 0247_ $$2ISSN$$a0969-9961
000138769 0247_ $$2ISSN$$a1095-953X
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000138769 037__ $$aDZNE-2020-05091
000138769 041__ $$aEnglish
000138769 082__ $$a570
000138769 1001_ $$0P:(DE-2719)9000008$$aAnglada-Huguet, Marta$$b0$$eFirst author
000138769 245__ $$aProstaglandin E2 EP2 activation reduces memory decline in R6/1 mouse model of Huntington's disease by the induction of BDNF-dependent synaptic plasticity.
000138769 260__ $$aOrlando, Fla.$$bAcademic Press$$c2016
000138769 264_1 $$2Crossref$$3print$$bElsevier BV$$c2016-11-01
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000138769 520__ $$aHuntington's disease (HD) patients and mouse models show learning and memory impairment even before the onset of motor symptoms. Deficits in hippocampal synaptic plasticity have been involved in the HD memory impairment. Several studies show that prostaglandin E2 (PGE2) EP2 receptor stimulates synaptic plasticity and memory formation. However, this role was not explored in neurodegenerative diseases. Here, we investigated the capacity of PGE2 EP2 receptor to promote synaptic plasticity and memory improvements in a model of HD, the R6/1 mice, by administration of the agonist misoprostol. We found that misoprostol increases dendritic branching in cultured hippocampal neurons in a brain-derived neurotrophic factor (BDNF)-dependent manner. Then, we implanted an osmotic mini-pump system to chronically administrate misoprostol to R6/1 mice from 14 to 18weeks of age. We observed that misoprostol treatment ameliorates the R6/1 long-term memory deficits as analyzed by the T-maze spontaneous alternation task and the novel object recognition test. Importantly, administration of misoprostol promoted the expression of hippocampal BDNF. Moreover, the treatment with misoprostol in R6/1 mice blocked the reduction in the number of PSD-95 and VGluT-1 positive particles observed in hippocampus of vehicle-R6/1 mice. In addition, we observed an increase of cAMP levels in the dentate ` of WT and R6/1 mice treated with misoprostol. Accordingly, we showed a reduction in the number of mutant huntingtin nuclear inclusions in the dentate gyrus of R6/1 mice. Altogether, these results suggest a putative therapeutic effect of PGE2 EP2 receptor in reducing cognitive deficits in HD.
000138769 536__ $$0G:(DE-HGF)POF3-342$$a342 - Disease Mechanisms and Model Systems (POF3-342)$$cPOF3-342$$fPOF III$$x0
000138769 542__ $$2Crossref$$i2016-11-01$$uhttps://www.elsevier.com/tdm/userlicense/1.0/
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000138769 650_7 $$2NLM Chemicals$$aBrain-Derived Neurotrophic Factor
000138769 650_7 $$2NLM Chemicals$$aReceptors, Prostaglandin E, EP2 Subtype
000138769 650_7 $$0K7Q1JQR04M$$2NLM Chemicals$$aDinoprostone
000138769 650_2 $$2MeSH$$aAnimals
000138769 650_2 $$2MeSH$$aBrain-Derived Neurotrophic Factor: metabolism
000138769 650_2 $$2MeSH$$aCognition Disorders: metabolism
000138769 650_2 $$2MeSH$$aDinoprostone: metabolism
000138769 650_2 $$2MeSH$$aDisease Models, Animal
000138769 650_2 $$2MeSH$$aHippocampus: metabolism
000138769 650_2 $$2MeSH$$aHuntington Disease: metabolism
000138769 650_2 $$2MeSH$$aHuntington Disease: physiopathology
000138769 650_2 $$2MeSH$$aMemory: physiology
000138769 650_2 $$2MeSH$$aMemory Disorders: drug therapy
000138769 650_2 $$2MeSH$$aMemory Disorders: physiopathology
000138769 650_2 $$2MeSH$$aMice, Transgenic
000138769 650_2 $$2MeSH$$aNeuronal Plasticity: physiology
000138769 650_2 $$2MeSH$$aReceptors, Prostaglandin E, EP2 Subtype: metabolism
000138769 7001_ $$0P:(DE-HGF)0$$aVidal-Sancho, Laura$$b1
000138769 7001_ $$0P:(DE-HGF)0$$aGiralt, Albert$$b2
000138769 7001_ $$0P:(DE-HGF)0$$aGarcía-Díaz Barriga, Gerardo$$b3
000138769 7001_ $$0P:(DE-HGF)0$$aXifró, Xavier$$b4
000138769 7001_ $$0P:(DE-HGF)0$$aAlberch, Jordi$$b5$$eCorresponding author
000138769 77318 $$2Crossref$$3journal-article$$a10.1016/j.nbd.2015.09.001$$b : Elsevier BV, 2016-11-01$$p22-34$$tNeurobiology of Disease$$v95$$x0969-9961$$y2016
000138769 773__ $$0PERI:(DE-600)1471408-5$$a10.1016/j.nbd.2015.09.001$$gVol. 95, p. 22 - 34$$p22-34$$q95<22 - 34$$tNeurobiology of disease$$v95$$x0969-9961$$y2016
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000138769 9101_ $$0I:(DE-588)1065079516$$6P:(DE-2719)9000008$$aDeutsches Zentrum für Neurodegenerative Erkrankungen$$b0$$kDZNE
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000138769 9141_ $$y2016
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