Evidence map›Paper›PMID 27552586›Full record

ArticleTranslational psychiatry2016

Loss of promoter IV-driven BDNF expression impacts oscillatory activity during sleep, sensory information processing and fear regulation.

J L Hill, N F Hardy, D V Jimenez, K R Maynard, A S Kardian, C J Pollock, R J Schloesser, K Martinowich

Open access · goldAbstract read
In one paragraph

Article in Translational psychiatry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

31 citing papers in PubMed, 55 citations in OpenAlex.

  1. Article
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  4. Stimulus-Dependent Expression ofThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2025
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  8. Regulation of Satiety byBiomolecules · 2023
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  9. Diverse Functions of MultipleBiomolecules · 2023
    Review
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  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review
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

8 authors at 4 institutions in 1 country.

J L HillLieber Institute for Brain Development, Johns Hopkins Medical Campus, Baltimore, MD, USA.
N F HardyLieber Institute for Brain Development, Johns Hopkins Medical Campus, Baltimore, MD, USA.
D V JimenezLieber Institute for Brain Development, Johns Hopkins Medical Campus, Baltimore, MD, USA.
K R MaynardLieber Institute for Brain Development, Johns Hopkins Medical Campus, Baltimore, MD, USA.
A S KardianLieber Institute for Brain Development, Johns Hopkins Medical Campus, Baltimore, MD, USA.
C J PollockLieber Institute for Brain Development, Johns Hopkins Medical Campus, Baltimore, MD, USA.
R J SchloesserSheppard Pratt-Lieber Research Institute, Inc., Baltimore, MD, USA.
K MartinowichLieber Institute for Brain Development, Johns Hopkins Medical Campus, Baltimore, MD, USA.
Johns Hopkins Medicine · USJohns Hopkins University · USLieber Institute for Brain Development · USSheppard and Enoch Pratt Hospital · US

Funding

INTERDISCIPLINARY TRAINING PROGRAM IN NEUROSCIENCEST32MH015330 · NIMH · JOHNS HOPKINS UNIVERSITY · PI MARGOLIS, RUSSELL L · 1985 to 2024
$6.2M
Regulation of neural activity in fear circuits by promoter IV derived BDNFR01MH105592 · NIMH · LIEBER INSTITUTE, INC. · PI MARTINOWICH, KERI · 2015 to 2024
$5.6M
NIMH NIH HHS R01 MH105592NIMH NIH HHS T32 MH015330
6 · The paper itself

Abstract

Posttraumatic stress disorder is characterized by hyperarousal, sensory processing impairments, sleep disturbances and altered fear regulation; phenotypes associated with changes in brain oscillatory activity. Molecules associated with activity-dependent plasticity, including brain-derived neurotrophic factor (BDNF), may regulate neural oscillations by controlling synaptic activity. BDNF synthesis includes production of multiple Bdnf transcripts, which contain distinct 5' noncoding exons. We assessed arousal, sensory processing, fear regulation and sleep in animals where BDNF expression from activity-dependent promoter IV is disrupted (Bdnf-e4 mice). Bdnf-e4 mice display sensory hyper-reactivity and impaired electrophysiological correlates of sensory information processing as measured by event-related potentials (ERP). Utilizing electroencephalogram, we identified a decrease in slow-wave activity during non-rapid eye movement sleep, suggesting impaired sleep homeostasis. Fear extinction is controlled by hippocampal-prefrontal cortical BDNF signaling, and neurophysiological communication patterns between the hippocampus (HPC) and medial prefrontal cortex (mPFC) correlate with behavioral performance during extinction. Impaired fear extinction in Bdnf-e4 mice is accompanied by increased HPC activation and decreased HPC-mPFC theta phase synchrony during early extinction, as well as increased mPFC activation during extinction recall. These results suggest that activity-dependent BDNF signaling is critical for regulating oscillatory activity, which may contribute to altered behavior.

Indexed as

AnimalsArousalBrain-Derived Neurotrophic FactorBrain WavesElectroencephalographyEvoked PotentialsExtinction, PsychologicalFearHippocampusMicePrefrontal CortexPrepulse InhibitionPromoter Regions, GeneticReflex, StartleSleepStress Disorders, Post-TraumaticBrain-Derived Neurotrophic Factor

Identifiers

PMID27552586
PMCPMC5022093
OpenAlexW2514937621

What OpenQuestion holds

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LicenceCC BY
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.