Evidence map›Paper›PMID 26100875›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2015

Enhanced memory consolidation in mice lacking the circadian modulators Sharp1 and -2 caused by elevated Igf2 signaling in the cortex.

Ali Shahmoradi, Konstantin Radyushkin, Moritz J Rossner

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

17 citing papers in PubMed, 27 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

3 authors at 2 institutions in 1 country.

Ali ShahmoradiDepartment of Neurogenetics, Max Planck Institute of Experimental Medicine, 37075 Göttingen, Germany;
Konstantin RadyushkinDepartment of Neurogenetics, Max Planck Institute of Experimental Medicine, 37075 Göttingen, Germany;
Moritz J RossnerDepartment of Neurogenetics, Max Planck Institute of Experimental Medicine, 37075 Göttingen, Germany; Department of Psychiatry, Ludwig Maximilian University, 80336 Munich, Germany moritz.rossner@med.uni-muenchen.de.
Max Planck Institute of Experimental Medicine · DELudwig-Maximilians-Universität München · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The bHLH transcription factors SHARP1 and SHARP2 are partially redundant modulators of the circadian system. SHARP1/DEC2 has been shown to control sleep length in humans and sleep architecture is also altered in double mutant mice (S1/2(-/-)). Because of the importance of sleep for memory consolidation, we investigated the role of SHARP1 and SHARP2 in cognitive processing. S1/2(-/-) mice show enhanced cortex (Cx)-dependent remote fear memory formation as well as improved reversal learning, but do not display alterations in hippocampus (Hi)-dependent recent fear memory formation. SHARP1 and SHARP2 single null mutants do not display any cognitive phenotype supporting functional redundancy of both factors. Molecular and biochemical analyses revealed elevated insulin-related growth factor 2 (IGF2) signaling and increased phosphorylation of MAPK and S6 in the Cx but not the Hi of S1/2(-/-) mice. No changes were detected in single mutants. Moreover, adeno-associated virus type 2-mediated IGF2 overexpression in the anterior cingulate cortex enhanced remote fear memory formation and the analysis of forebrain-specific double null mutants of the Insulin and IGF1 receptors revealed their essential function for memory formation. Impaired fear memory formation in aged S1/2(-/-) mice indicates that elevated IGF2 signaling in the long term, however, has a negative impact on cognitive processing. In summary, we conclude that the bHLH transcription factors SHARP1 and SHARP2 are involved in cognitive processing by controlling Igf2 expression and associated signaling cascades. Our analyses provide evidence that the control of sleep and memory consolidation may share common molecular mechanisms.

Indexed as

Memory, Long-TermSignal TransductionAnimalsBasic Helix-Loop-Helix ProteinsBlotting, WesternCerebral CortexGene ExpressionHomeodomain ProteinsInsulin-Like Growth Factor Binding Protein 5Insulin-Like Growth Factor IIMice, Inbred C57BLMice, KnockoutMitogen-Activated Protein KinasesPhosphorylationReceptor, IGF Type 1Receptor, InsulinBasic Helix-Loop-Helix ProteinsBhlhb3 protein, mouseBhlhe40 protein, mouseHomeodomain ProteinsInsulin-Like Growth Factor Binding Protein 5Insulin-Like Growth Factor IIMitogen-Activated Protein KinasesReceptor, IGF Type 1Receptor, InsulinTranscription Factorsagingcortexinsulin-like signalingMAPK signalingmemory consolidation

Identifiers

PMID26100875
PMCPMC4500222
OpenAlexW1538529288

What OpenQuestion holds

Textmetadata
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.