Subhypnotic doses of propofol impair spatial memory retrieval in rats
Abundant evidence indicates that propofol profoundly affects memory processes, although its specific effects on memory retrieval have not been clarified. A recent study has indicated that hippocampal glycogen synthase kinase-3β(GSK-3β) activity affects memory. Constitutively active GSK-3β is require...
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Published in | Neural regeneration research Vol. 11; no. 12; pp. 1956 - 1961 |
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Main Authors | , , , , , |
Format | Journal Article |
Language | English |
Published |
India
Wolters Kluwer India Pvt. Ltd
01.12.2016
Medknow Publications and Media Pvt. Ltd Medknow Publications & Media Pvt. Ltd First Affiliated Hospital of Anhui Medical University, Hefei, Anhui Province, China Medknow Publications & Media Pvt Ltd Wolters Kluwer Medknow Publications |
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Online Access | Get full text |
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Summary: | Abundant evidence indicates that propofol profoundly affects memory processes, although its specific effects on memory retrieval have not been clarified. A recent study has indicated that hippocampal glycogen synthase kinase-3β(GSK-3β) activity affects memory. Constitutively active GSK-3β is required for memory retrieval, and propofol has been shown to inhibit GSK-3β. Thus, the present study examined whether propofol affects memory retrieval, and, if so, whether that effect is mediated through altered GSK-3β activity. Adult Sprague-Dawley rats were trained on a Morris water maze task(eight acquisition trials in one session) and subjected under the influence of a subhypnotic dose of propofol to a 24-hour probe trial memory retrieval test. The results showed that rats receiving pretest propofol(25 mg/kg) spent significantly less time in the target quadrant but showed no change in locomotor activity compared with those in the control group. Memory retrieval was accompanied by reduced phosphorylation of the serine-9 residue of GSK-3β in the hippocampus, whereas phosphorylation of the tyrosine-216 residue was unaffected. However, propofol blocked this retrieval-associated serine-9 phosphorylation. These findings suggest that subhypnotic propofol administration impairs memory retrieval and that the amnestic effects of propofol may be mediated by attenuated GSK-3β signaling in the hippocampus. |
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Bibliography: | nerve regeneration glycogen synthase kinase-3β propofol memory retrieval Morris water maze neural regeneration Abundant evidence indicates that propofol profoundly affects memory processes, although its specific effects on memory retrieval have not been clarified. A recent study has indicated that hippocampal glycogen synthase kinase-3β(GSK-3β) activity affects memory. Constitutively active GSK-3β is required for memory retrieval, and propofol has been shown to inhibit GSK-3β. Thus, the present study examined whether propofol affects memory retrieval, and, if so, whether that effect is mediated through altered GSK-3β activity. Adult Sprague-Dawley rats were trained on a Morris water maze task(eight acquisition trials in one session) and subjected under the influence of a subhypnotic dose of propofol to a 24-hour probe trial memory retrieval test. The results showed that rats receiving pretest propofol(25 mg/kg) spent significantly less time in the target quadrant but showed no change in locomotor activity compared with those in the control group. Memory retrieval was accompanied by reduced phosphorylation of the serine-9 residue of GSK-3β in the hippocampus, whereas phosphorylation of the tyrosine-216 residue was unaffected. However, propofol blocked this retrieval-associated serine-9 phosphorylation. These findings suggest that subhypnotic propofol administration impairs memory retrieval and that the amnestic effects of propofol may be mediated by attenuated GSK-3β signaling in the hippocampus. 11-5422/R ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 Author contributions: HL and XSL conceived and designed the study. HL performed the experiments. TW, WD and ZJ wrote the paper. YHL and XSL reviewed and edited the paper. All authors approved the final version of the paper. |
ISSN: | 1673-5374 1876-7958 |
DOI: | 10.4103/1673-5374.197137 |