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231225s2021 xx |||||o 00| ||eng c |
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|a 10.1155/2021/6635084
|2 doi
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|a pubmed25n1084.xml
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|a (DE-627)NLM325327637
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|a (NLM)33981335
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|a DE-627
|b ger
|c DE-627
|e rakwb
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|a eng
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|a Abdoulaye, Idriss Ali
|e verfasserin
|4 aut
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|a Ketamine Induces Lasting Antidepressant Effects by Modulating the NMDAR/CaMKII-Mediated Synaptic Plasticity of the Hippocampal Dentate Gyrus in Depressive Stroke Model
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|c 2021
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|a Text
|b txt
|2 rdacontent
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|a ƒaComputermedien
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|2 rdamedia
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|a ƒa Online-Ressource
|b cr
|2 rdacarrier
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|a Date Completed 06.12.2021
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|a Date Revised 16.07.2022
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|a published: Electronic-eCollection
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|a Citation Status MEDLINE
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|a Copyright © 2021 Idriss Ali Abdoulaye et al.
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|a Background: Ketamine has been shown to possess lasting antidepressant properties. However, studies of the mechanisms involved in its effects on poststroke depression are nonexistent
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|a Methods: To investigate these mechanisms, Sprague-Dawley rats were treated with a single local dose of ketamine after middle cerebral artery occlusion and chronic unpredicted mild stress. The effects on the hippocampal dentate gyrus were analyzed through assessment of the N-methyl-D-aspartate receptor/calcium/calmodulin-dependent protein kinase II (NMDAR/CaMKII) pathway, synaptic plasticity, and behavioral tests
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|a Results: Ketamine administration rapidly exerted significant and lasting improvements of depressive symptoms. The biochemical analysis showed rapid, selective upregulation and downregulation of the NMDAR2-β and NMDAR2-α subtypes as well as their downstream signaling proteins β-CaMKII and α-phosphorylation in the dentate gyrus, respectively. Furthermore, the colocalization analysis indicated a significant and selectively increased conjunction of β-CaMKII and postsynaptic density protein 95 (PSD95) coupled with a notable decrease in NMDAR2-β association with PSD95 after ketamine treatment. These changes translated into significant and extended synaptic plasticity in the dentate gyrus
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|a Conclusions: These findings not only suggest that ketamine represents a viable candidate for the treatment of poststroke depression but also that ketamine's lasting antidepressant effects might be achieved through modulation of NMDAR/CaMKII-induced synaptic plasticity in key brain regions
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|a Journal Article
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|a Research Support, Non-U.S. Gov't
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|a Antidepressive Agents
|2 NLM
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|a Disks Large Homolog 4 Protein
|2 NLM
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|a Dlg4 protein, rat
|2 NLM
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|a Receptors, N-Methyl-D-Aspartate
|2 NLM
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|a Ketamine
|2 NLM
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|a 690G0D6V8H
|2 NLM
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|a Calcium-Calmodulin-Dependent Protein Kinase Type 2
|2 NLM
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|a EC 2.7.11.17
|2 NLM
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|a Wu, Shan-Shan
|e verfasserin
|4 aut
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|a Chibaatar, Enkhmurun
|e verfasserin
|4 aut
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|a Yu, Da-Fan
|e verfasserin
|4 aut
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|a Le, Kai
|e verfasserin
|4 aut
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|a Cao, Xue-Jin
|e verfasserin
|4 aut
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|a Guo, Yi-Jing
|e verfasserin
|4 aut
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|i Enthalten in
|t Neural plasticity
|d 1998
|g 2021(2021) vom: 30., Seite 6635084
|w (DE-627)NLM098558390
|x 1687-5443
|7 nnas
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|g volume:2021
|g year:2021
|g day:30
|g pages:6635084
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|u http://dx.doi.org/10.1155/2021/6635084
|3 Volltext
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|d 2021
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|b 30
|h 6635084
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