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@ARTICLE{AngladaHuguet:138769,
      author       = {Anglada-Huguet, Marta and Vidal-Sancho, Laura and Giralt,
                      Albert and García-Díaz Barriga, Gerardo and Xifró, Xavier
                      and Alberch, Jordi},
      title        = {{P}rostaglandin {E}2 {EP}2 activation reduces memory
                      decline in {R}6/1 mouse model of {H}untington's disease by
                      the induction of {BDNF}-dependent synaptic plasticity.},
      journal      = {Neurobiology of disease},
      volume       = {95},
      issn         = {0969-9961},
      address      = {Orlando, Fla.},
      publisher    = {Academic Press},
      reportid     = {DZNE-2020-05091},
      pages        = {22-34},
      year         = {2016},
      abstract     = {Huntington'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.},
      keywords     = {Animals / Brain-Derived Neurotrophic Factor: metabolism /
                      Cognition Disorders: metabolism / Dinoprostone: metabolism /
                      Disease Models, Animal / Hippocampus: metabolism /
                      Huntington Disease: metabolism / Huntington Disease:
                      physiopathology / Memory: physiology / Memory Disorders:
                      drug therapy / Memory Disorders: physiopathology / Mice,
                      Transgenic / Neuronal Plasticity: physiology / Receptors,
                      Prostaglandin E, EP2 Subtype: metabolism / Brain-Derived
                      Neurotrophic Factor (NLM Chemicals) / Receptors,
                      Prostaglandin E, EP2 Subtype (NLM Chemicals) / Dinoprostone
                      (NLM Chemicals)},
      cin          = {AG Mandelkow 1},
      ddc          = {570},
      cid          = {I:(DE-2719)1013014},
      pnm          = {342 - Disease Mechanisms and Model Systems (POF3-342)},
      pid          = {G:(DE-HGF)POF3-342},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:26369879},
      doi          = {10.1016/j.nbd.2015.09.001},
      url          = {https://pub.dzne.de/record/138769},
}