Evidence map›Paper›PMID 30723982›Full record

ArticleHippocampus2019

Disrupted-in-schizophrenia 1 overexpression disrupts hippocampal coding and oscillatory synchronization.

Karola Kaefer, Hugo Malagon-Vina, Desiree D Dickerson, Joseph O'Neill, Svenja V Trossbach, Carsten Korth, Jozsef Csicsvari

Abstract read
In one paragraph

Article in Hippocampus, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing 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

19 citing papers in PubMed.

  1. Article
  2. Review
  3. The Structure of Hippocampal CA1 Interactions Optimizes Spatial Coding across Experience.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Review
  11. eLife · 2022
    Article
  12. Article
  13. Review
  14. Review
  15. Review
  16. Article
  17. Article
  18. Article
  19. 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

7 authors.

Karola KaeferInstitute of Science and Technology Austria (IST Austria), Am Campus 1, Klosterneuburg, Austria.
Hugo Malagon-VinaInstitute of Science and Technology Austria (IST Austria), Am Campus 1, Klosterneuburg, Austria.
Desiree D DickersonInstitute of Science and Technology Austria (IST Austria), Am Campus 1, Klosterneuburg, Austria.
Joseph O'NeillSchool of Psychology, Cardiff University, 70 Park Place, Cardiff, United Kingdom.
Svenja V TrossbachDepartment Neuropathology, Medical Faculty, Heinrich Heine University Düsseldorf, Moorenstrasse 5, Düsseldorf, Germany.
Carsten KorthDepartment Neuropathology, Medical Faculty, Heinrich Heine University Düsseldorf, Moorenstrasse 5, Düsseldorf, Germany.
Jozsef CsicsvariInstitute of Science and Technology Austria (IST Austria), Am Campus 1, Klosterneuburg, Austria.ORCID 0000-0002-5193-4036

Funding

EU-FP7 MC-ITN IN- SENS 607616
6 · The paper itself

Abstract

Aberrant proteostasis of protein aggregation may lead to behavior disorders including chronic mental illnesses (CMI). Furthermore, the neuronal activity alterations that underlie CMI are not well understood. We recorded the local field potential and single-unit activity of the hippocampal CA1 region in vivo in rats transgenically overexpressing the Disrupted-in-Schizophrenia 1 (DISC1) gene (tgDISC1), modeling sporadic CMI. These tgDISC1 rats have previously been shown to exhibit DISC1 protein aggregation, disturbances in the dopaminergic system and attention-related deficits. Recordings were performed during exploration of familiar and novel open field environments and during sleep, allowing investigation of neuronal abnormalities in unconstrained behavior. Compared to controls, tgDISC1 place cells exhibited smaller place fields and decreased speed-modulation of their firing rates, demonstrating altered spatial coding and deficits in encoding location-independent sensory inputs. Oscillation analyses showed that tgDISC1 pyramidal neurons had higher theta phase locking strength during novelty, limiting their phase coding ability. However, their mean theta phases were more variable at the population level, reducing oscillatory network synchronization. Finally, tgDISC1 pyramidal neurons showed a lack of novelty-induced shift in their preferred theta and gamma firing phases, indicating deficits in coding of novel environments with oscillatory firing. By combining single cell and neuronal population analyses, we link DISC1 protein pathology with abnormal hippocampal neural coding and network synchrony, and thereby gain a more comprehensive understanding of CMI mechanisms.

Indexed as

Cortical SynchronizationAnimalsBehavior, AnimalCA1 Region, HippocampalElectrodes, ImplantedElectrophysiological PhenomenaExploratory BehaviorGamma RhythmHippocampusMaleNerve Tissue ProteinsPyramidal CellsRatsRats, Sprague-DawleyRestSchizophreniaDisc1 protein, ratNerve Tissue ProteinsDISC1electrophysiologyhippocampusoscillationsplace cellsprotein pathology

Identifiers

PMID30723982
PMCPMC6767395

What Socratic holds

Textmetadata
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 Socratic graph.