Evidence map›Paper›PMID 28033307›Full record

ArticleMedical science monitor : international medical journal of experimental and clinical research2016

Effect of Sodium Valproate on Cognitive Function and Hippocampus of Rats After Convulsive Status Epilepticus.

Peng Wu, Siqi Hong, Min Zhong, Yi Guo, Hengsheng Chen, Li Jiang

Open access · hybridAbstract read
In one paragraph

Article in Medical science monitor : international medical journal of experimental and clinical research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.2field-weighted citation impact, top 23% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

10 citing papers in PubMed, 20 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 3 institutions in 1 country.

Peng WuDepartment of Neurology, Children's Hospital of Chongqing Medical University, Chongqing, China (mainland).
Siqi HongDepartment of Neurology, Children's Hospital of Chongqing Medical University, Chongqing, China (mainland).
Min ZhongDepartment of Neurology, Children's Hospital of Chongqing Medical University, Chongqing, China (mainland).
Yi GuoDepartment of Neurology, Children's Hospital of Chongqing Medical University, Chongqing, China (mainland).
Hengsheng ChenChongqing International Science and Technology Cooperation Center for Child Development and Disorders, Chongqing, China (mainland).
Li JiangDepartment of Neurology, Children's Hospital of Chongqing Medical University, Chongqing, China (mainland).
Children's Hospital of Chongqing Medical University · CNChongqing Medical University · CNChina International Science and Technology Cooperation · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND The aim of this study was to explore the effect and possible mechanism of sodium valproate (VPA) on the cognitive function and the hippocampus of rats after convulsive status epilepticus (CES). MATERIAL AND METHODS A rat model of CES was established and the Morris water maze was used to observe changes in the cognitive function of the rats after the administration of VPA. Acute hippocampal slices were made to detect field excitatory postsynaptic potential. Western blot analysis was used to test for the expression of CaMKII and p-CaMKII. RESULTS (1) CSE caused no spatial reference memory (SFM) or spatial working memory (SWM) damage to 15-day-old (P15) rats, but caused significant SRM and SWM damage to 35-day-old (P35) rats. VPA damaged the SRM and SWM of P15 rats in both the CSE and control groups. However, VPA improved the memory damage caused by CSE in P35 rats. (2) VPA treatment in vivo increased the induced success rate and the sustainable time of long-term potentiation (LTP) in P35 rats, and also inhibited the expression of CaMKII and p-CaMKII in both P15 and P35 rats. CONCLUSIONS VPA significantly improved spatial cognitive dysfunction in a CSE model of P35 rats, and damaged the spatial memory of normal P15 and P35 rats. Improvements after administration of VPA were closely related to the increase of induced success rate and the prolongation of the sustainable time of LTP. VPA treatment in vivo, which inhibited expression and phosphorylation of CaMKII, showed no obvious inhibition on LTP, which may be related to the elution effect of VPA.

Indexed as

AnimalsCalcium-Calmodulin-Dependent Protein Kinase Type 2CognitionExcitatory Postsynaptic PotentialsHippocampusLearningLong-Term PotentiationMemory, Short-TermPhosphorylationRats, WistarSeizuresSpatial MemoryValproic AcidCalcium-Calmodulin-Dependent Protein Kinase Type 2Valproic Acid

Identifiers

PMID28033307
PMCPMC5218388
OpenAlexW2563110534

What OpenQuestion holds

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Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.