Evidence map›Paper›PMID 27613435›Full record

ArticleCerebral cortex (New York, N.Y. : 1991)2016

From Shortage to Surge: A Developmental Switch in Hippocampal-Prefrontal Coupling in a Gene-Environment Model of Neuropsychiatric Disorders.

Henrike Hartung, Nicole Cichon, Vito De Feo, Stephanie Riemann, Sandra Schildt, Christoph Lindemann, Christoph Mulert, Joseph A Gogos, Ileana L Hanganu-Opatz

Abstract read
In one paragraph

Article in Cerebral cortex (New York, N.Y. : 1991), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
–field-weighted citation impact
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

27 citing papers in PubMed.

  1. Developmental Olfactory Dysfunction and Abnormal Odor Memory in Immune-ChallengedThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2025
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  13. THE DEVELOPING BRAIN REVEALED DURING SLEEP.Current opinion in physiology · 2020
    Article
  14. Article
  15. Article
  16. Article
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  18. Article
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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

9 authors.

Henrike HartungDevelopmental Neurophysiology, Institute of Neuroanatomy, University Medical Center Hamburg-Eppendorf, 20251 Hamburg, Germany.
Nicole CichonDevelopmental Neurophysiology, Institute of Neuroanatomy, University Medical Center Hamburg-Eppendorf, 20251 Hamburg, Germany.
Vito De FeoDevelopmental Neurophysiology, Institute of Neuroanatomy, University Medical Center Hamburg-Eppendorf, 20251 Hamburg, Germany.
Stephanie RiemannDevelopmental Neurophysiology, Institute of Neuroanatomy, University Medical Center Hamburg-Eppendorf, 20251 Hamburg, Germany.
Sandra SchildtDevelopmental Neurophysiology, Institute of Neuroanatomy, University Medical Center Hamburg-Eppendorf, 20251 Hamburg, Germany.
Christoph LindemannDevelopmental Neurophysiology, Institute of Neuroanatomy, University Medical Center Hamburg-Eppendorf, 20251 Hamburg, Germany.
Christoph MulertDepartment of Psychiatry and Psychotherapy, University Medical Center Hamburg-Eppendorf, 20246 Hamburg, Germany.
Joseph A GogosDepartment of Neuroscience, Columbia University, New York, NY 10032, USA.
Ileana L Hanganu-OpatzDevelopmental Neurophysiology, Institute of Neuroanatomy, University Medical Center Hamburg-Eppendorf, 20251 Hamburg, Germany.

Funding

Elucidating the Effect of Disc 1 on Neurodevelopment and Synaptic TransmissionR01MH080234 · NIMH · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI GOGOS, JOSEPH A · 2007 to 2016
$3.3M
NIMH NIH HHS R01 MH080234
6 · The paper itself

Abstract

Cognitive deficits represent a major burden of neuropsychiatric disorders and result in part from abnormal communication within hippocampal-prefrontal circuits. While it has been hypothesized that this network dysfunction arises during development, long before the first clinical symptoms, experimental evidence is still missing. Here, we show that pre-juvenile mice mimicking genetic and environmental risk factors of disease (dual-hit GE mice) have poorer recognition memory that correlates with augmented coupling by synchrony and stronger directed interactions between prefrontal cortex and hippocampus. The network dysfunction emerges already during neonatal development, yet it initially consists in a diminished hippocampal theta drive and consequently, a weaker and disorganized entrainment of local prefrontal circuits in discontinuous oscillatory activity in dual-hit GE mice when compared with controls. Thus, impaired maturation of functional communication within hippocampal-prefrontal networks switching from hypo- to hyper-coupling may represent a mechanism underlying the pathophysiology of cognitive deficits in neuropsychiatric disorders.

Indexed as

Cognition DisordersDevelopmental DisabilitiesGene-Environment InteractionAnimalsAnimals, NewbornDisease Models, AnimalEvoked PotentialsFemaleHippocampusInterferon InducersMiceMice, Inbred C57BLMice, TransgenicMutationNerve Tissue ProteinsNeural PathwaysDisc1 protein, mouseInterferon InducersNerve Tissue ProteinsPoly I-Cdevelopmentnetwork oscillationsprefrontal cortexschizophreniasynchrony

Identifiers

PMID27613435
PMCPMC5066837

What OpenQuestion holds

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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.