Evidence map›Paper›PMID 21752339›Full record

ArticleNeuropharmacology

NMDA receptor subunit composition determines the polarity of leptin-induced synaptic plasticity.

Peter R Moult, Jenni Harvey

Open access · greenAbstract read
In one paragraph

Article in Neuropharmacology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
1.9field-weighted citation impact, top 16% 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

36 citing papers in PubMed, 68 citations in OpenAlex.

  1. Review
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  3. Brain-Bone Axis in Physiological and Pathological Conditions.International journal of molecular sciences · 2025
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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

2 authors at 2 institutions in 1 country.

Peter R MoultCentre for Neuroscience, Division of Medical Sciences, Ninewells Hospital and Medical School, University of Dundee, Dundee, UK.
Jenni Harvey
Ninewells Hospital · GBUniversity of Dundee · GB

Funding

Wellcome Trust 075821
6 · The paper itself

Abstract

Leptin is a hormone that crosses the blood-brain barrier and regulates numerous CNS functions. The hippocampus in particular is an important site for leptin action. Indeed, leptin markedly influences excitatory synaptic transmission and synaptic plasticity in this brain region. Recent studies indicate that leptin modulation of hippocampal excitatory synaptic transmission is age-dependent however the cellular basis for this is unclear. Here we show that early in development leptin evokes a transient (P11-18) or persistent (P5-8) depression of synaptic transmission, whereas leptin evokes a long lasting increase (LTP) in synaptic strength in adulthood. The synaptic depressions induced by leptin required activation of NMDA receptor GluN2B subunits and the ERK signalling cascade. Conversely, leptin-induced LTP in adult was mediated by GluN2A subunits and involved PI 3-kinase dependent signalling. In addition, low-frequency stimulus (LFS)-evoked LTD occluded the persistent effects of leptin at P5-8 and vice versa. Similarly, synaptically-induced LTP occluded the persistent increase in synaptic transmission induced by leptin, indicating that similar expression mechanisms underlie leptin-induced LTD and LFS-induced LTD at P5-8, and leptin-induced LTP and HFS-induced LTP in adult. These findings have important implications for the role of leptin in hippocampal synaptic function during early neuronal development and in aging.

Indexed as

Age FactorsAnimalsBlood-Brain BarrierCell PolarityElectric StimulationExcitatory Postsynaptic PotentialsGABA AntagonistsHippocampusLeptinLong-Term PotentiationLong-Term Synaptic DepressionMaleNeuronal PlasticityPatch-Clamp TechniquesPhosphatidylinositol 3-KinasesPicrotoxinGABA AntagonistsLeptinPhosphatidylinositol 3-KinasesPicrotoxinReceptors, N-Methyl-D-Aspartate

Identifiers

PMID21752339
PMCPMC3300059
OpenAlexW1972469557

What OpenQuestion holds

Textmetadata
LicenceTDM
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.