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dc.contributor.authorPerez-Urrutia N.
dc.contributor.authorMendoza C.
dc.contributor.authorAlvarez-Ricartes N.
dc.contributor.authorOliveros-Matus P.
dc.contributor.authorEcheverria F.
dc.contributor.authorGrizzell J.A.
dc.contributor.authorBarreto G.E.
dc.contributor.authorIarkov A.
dc.contributor.authorEcheverria V.
dc.date.accessioned2020-09-02T22:25:47Z
dc.date.available2020-09-02T22:25:47Z
dc.date.issued2017
dc.identifier10.1016/j.expneurol.2017.06.016
dc.identifier.citation295, , 211-221
dc.identifier.issn00144886
dc.identifier.urihttps://hdl.handle.net/20.500.12728/5783
dc.descriptionPosttraumatic stress disorder (PTSD), chronic psychological stress, and major depressive disorder have been found to be associated with a significant decrease in glial fibrillary acidic protein (GFAP) immunoreactivity in the hippocampus of rodents. Cotinine is an alkaloid that prevents memory impairment, depressive-like behavior and synaptic loss when co-administered during restraint stress, a model of PTSD and stress-induced depression, in mice. Here, we investigated the effects of post-treatment with intranasal cotinine on depressive- and anxiety-like behaviors, visual recognition memory as well as the number and morphology of GFAP + immunoreactive cells, in the hippocampus and frontal cortex of mice subjected to prolonged restraint stress. The results revealed that in addition to the mood and cognitive impairments, restraint stress induced a significant decrease in the number and arborization of GFAP + cells in the brain of mice. Intranasal cotinine prevented these stress-derived symptoms and the morphological abnormalities GFAP + cells in both of these brain regions which are critical to resilience to stress. The significance of these findings for the therapy of PTSD and depression is discussed. © 2017 Elsevier Inc.
dc.language.isoen
dc.publisherAcademic Press Inc.
dc.subjectAstrocytes
dc.subjectCotinine
dc.subjectDepression
dc.subjectMemory
dc.subjectStress
dc.subjectcotinine
dc.subjectglial fibrillary acidic protein
dc.subjectcotinine
dc.subjectglial fibrillary acidic protein
dc.subjectglial fibrillary astrocytic protein, mouse
dc.subjectanimal cell
dc.subjectanimal experiment
dc.subjectanimal model
dc.subjectanimal tissue
dc.subjectArticle
dc.subjectbrain region
dc.subjectcell loss
dc.subjectcognitive defect
dc.subjectcontrolled study
dc.subjectdepression
dc.subjectfrontal cortex
dc.subjecthippocampus
dc.subjectimmobilization stress
dc.subjectimmunocompetent cell
dc.subjectmale
dc.subjectmemory
dc.subjectmood change
dc.subjectmorphology
dc.subjectmouse
dc.subjectnonhuman
dc.subjectposttraumatic stress disorder
dc.subjectpriority journal
dc.subjectvisual memory
dc.subjectanimal
dc.subjectastrocyte
dc.subjectbrain chemistry
dc.subjectC57BL mouse
dc.subjectcomplication
dc.subjectdepression
dc.subjectdrug effects
dc.subjectexercise
dc.subjectintranasal drug administration
dc.subjectMemory Disorders
dc.subjectmental stress
dc.subjectmetabolism
dc.subjectmotor activity
dc.subjectpathology
dc.subjectpsychology
dc.subjectrecognition
dc.subjectswimming
dc.subjectAdministration, Intranasal
dc.subjectAnimals
dc.subjectAstrocytes
dc.subjectBrain Chemistry
dc.subjectCotinine
dc.subjectDepression
dc.subjectGlial Fibrillary Acidic Protein
dc.subjectMale
dc.subjectMemory Disorders
dc.subjectMice
dc.subjectMice, Inbred C57BL
dc.subjectMotor Activity
dc.subjectRecognition (Psychology)
dc.subjectRestraint, Physical
dc.subjectStress, Psychological
dc.subjectSwimming
dc.titleIntranasal cotinine improves memory, and reduces depressive-like behavior, and GFAP + cells loss induced by restraint stress in mice
dc.typeArticle


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