Evidence map›Paper›PMID 20927045›Full record

ArticleNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology2011

Disrupted activity in the hippocampal-accumbens circuit of type III neuregulin 1 mutant mice.

Malcolm W Nason, Avishek Adhikari, Marjan Bozinoski, Joshua A Gordon, Lorna W Role

Open access · bronzeAbstract read
In one paragraph

Article in Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.1field-weighted citation impact, top 27% 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

22 citing papers in PubMed, 28 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. Sensory encoding in Neuregulin 1 mutants.Brain structure & function · 2016
    Article
  11. Review
  12. Review
  13. Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Review
  20. The importance of the NRG-1/ErbB4 pathway for synaptic plasticity and behaviors associated with psychiatric disorders.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012
    Article
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

5 authors at 3 institutions in 1 country.

Malcolm W NasonDepartment of Neurobiology and Behavior and Center for Nervous System Disorders, SUNY Stony Brook University, Stony Brook, NY 11794-5230, USA.
Avishek Adhikari
Marjan Bozinoski
Joshua A Gordon
Lorna W Role
Stony Brook University · USColumbia University · USNew York State Psychiatric Institute

Funding

Neural mechanisms of increased anxiety in serotonin 1A receptor-deficient miceR01MH081968 · NIMH · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI LEONARDO, EDUARDO DAVID · 2008 to 2017
$3.7M
NIMH NIH HHS K08 MH098623NIMH NIH HHS R01 MH081968
6 · The paper itself

Abstract

Neuregulin 1 (Nrg1), a schizophrenia susceptibility gene, is involved in fundamental aspects of neurodevelopment. Mice lacking any one of the several isoforms of Nrg1 have a variety of schizophrenia-related phenotypes, including deficits in working memory and sensorimotor gating, loss of spines in pyramidal neurons in the ventral subiculum, loss of dendrites in cortical pyramidal cells, loss of parvalbumin-positive interneurons in the prefrontal cortex, and altered plasticity in corticolimbic synapses. Mice heterozygous for a disruption in exon 7 of the Nrg1 gene lack Type III (cysteine-rich-domain-containing) isoforms and have sensorimotor gating deficits that may involve changes in the activity of a circuit involving projections from the ventral hippocampus (vHPC) to medium spiny neurons in the nucleus accumbens (nACC). To explore the neural basis of these deficits, we examined electrophysiological activity in the nACC and vHPC of these mice. Under urethane anesthesia, bursts of spontaneous activity propagated from the vHPC to the nACC in both wild-type and mutant mice. However, these bursts were weaker in mutant nACC, with reduced local field potential amplitude and spiking activity. Single units in mutant nACC fired less frequently within the bursts, and more frequently outside of the bursts. Moreover, within-burst nACC spiking was less modulated by vHPC activity, as determined by phase-locking to the low-frequency oscillatory components of the bursts. These data suggest that the efficacy of vHPC input to the nACC is reduced in the Type III Nrg1 heterozygotes, supporting a role for Nrg1 in the functional profile of hippocampal-accumbens synapses.

Indexed as

Action PotentialsAnimalsCysteineGenetic Predisposition to DiseaseHippocampusMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicNeural PathwaysNeuregulin-1NeuronsNucleus AccumbensProtein IsoformsProtein Structure, TertiaryCysteineNeuregulin-1Nrg1 protein, mouseProtein Isoforms

Identifiers

PMID20927045
PMCPMC3005939
OpenAlexW2073073326

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.