Evidence map›Paper›PMID 24712995›Full record

ArticleThe European journal of neuroscience2014

BDNF contributes to both rapid and homeostatic alterations in AMPA receptor surface expression in nucleus accumbens medium spiny neurons.

Jeremy M Reimers, Jessica A Loweth, Marina E Wolf

Open access · greenAbstract read
In one paragraph

Article in The European journal of neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

42 citing papers in PubMed, 68 citations in OpenAlex.

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  15. BDNF Therapeutic Mechanisms in Neuropsychiatric Disorders.International journal of molecular sciences · 2022
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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 1 institution in 1 country.

Jeremy M ReimersDepartment of Neuroscience, Rosalind Franklin University of Medicine and Science, 3333 Green Bay Road, North Chicago, IL, 60064-3095, USA.
Jessica A Loweth
Marina E Wolf
Rosalind Franklin University of Medicine and Science · US

Funding

Dopamine and Glutamate Receptor InteractionsR37DA015835 · NIDA · ROSALIND FRANKLIN UNIV OF MEDICINE &SCI · PI WOLF, MARINA ELIZABETH · 2003 to 2012
$2.8M
Synaptic mechanisms maintaining persistent cocaine craving.R01DA015835 · NIDA · ROSALIND FRANKLIN UNIV OF MEDICINE & SCI · PI WOLF, MARINA ELIZABETH · 2014 to 2018
$1.8M
Psychostimulants and PlasticityK05DA029099 · NIDA · ROSALIND FRANKLIN UNIV OF MEDICINE & SCI · PI WOLF, MARINA ELIZABETH · 2010 to 2014
$622k
Cocaine-induced AMPAR plasticity: modulation by metabotropic glutamate receptors?F32DA030844 · NIDA · ROSALIND FRANKLIN UNIV OF MEDICINE & SCI · PI LOWETH, JESSICA ANNE · 2011 to 2013
$155k
NIDA NIH HHS DA015835NIDA NIH HHS DA029099NIDA NIH HHS DA030844NIDA NIH HHS F32 DA030844NIDA NIH HHS K05 DA029099NIDA NIH HHS R01 DA015835NIDA NIH HHS R37 DA015835
6 · The paper itself

Abstract

Brain-derived neurotrophic factor (BDNF) plays a critical role in plasticity at glutamate synapses and in the effects of repeated cocaine exposure. We recently showed that intracranial injection of BDNF into the rat nucleus accumbens (NAc), a key region for cocaine addiction, rapidly increases α-amino-3-hyroxy-5-methyl-4-isoxazole-propionic acid receptor (AMPAR) surface expression. To further characterize BDNF's role in both rapid AMPAR trafficking and slower, homeostatic changes in AMPAR surface expression, we investigated the effects of acute (30 min) and long-term (24 h) treatment with BDNF on AMPAR distribution in NAc medium spiny neurons from postnatal rats co-cultured with mouse prefrontal cortex neurons to restore excitatory inputs. Immunocytochemical studies showed that acute BDNF treatment increased cell surface GluA1 and GluA2 levels, as well as their co-localization, on NAc neurons. This effect of BDNF, confirmed using a protein crosslinking assay, was dependent on ERK but not AKT signaling. In contrast, long-term BDNF treatment decreased AMPAR surface expression on NAc neurons. Based on this latter result, we tested the hypothesis that BDNF plays a role in AMPAR 'scaling down' in response to a prolonged increase in neuronal activity produced by bicuculline (24 h). Supporting this hypothesis, decreasing BDNF signaling with the extracellular BDNF scavenger TrkB-Fc prevented the scaling down of GluA1 and GluA2 surface levels in NAc neurons normally produced by bicuculline. In conclusion, BDNF exerts bidirectional effects on NAc AMPAR surface expression, depending on duration of exposure. Furthermore, BDNF's involvement in synaptic scaling in the NAc differs from its previously described role in the visual cortex.

Indexed as

AnimalsBicucullineBrain-Derived Neurotrophic FactorCells, CulturedExcitatory Postsynaptic PotentialsHomeostasisMiceNeuronsNucleus AccumbensProtein TransportRatsRats, Sprague-DawleyReceptors, AMPASynaptic MembranesBicucullineBrain-Derived Neurotrophic FactorReceptors, AMPAco-culturemouseratreceptor traffickingsynaptic scaling

Identifiers

PMID24712995
PMCPMC4410784
OpenAlexW2060936720

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.