Evidence map›Paper›PMID 32737188›Full record

ArticleeNeuro

Traumatic Brain Injury Preserves Firing Rates But Disrupts Laminar Oscillatory Coupling and Neuronal Entrainment in Hippocampal CA1.

Paul F Koch, Carlo Cottone, Christopher D Adam, Alexandra V Ulyanova, Robin J Russo, Maura T Weber, John D Arena, Victoria E Johnson, John A Wolf

Open access · goldAbstract read
In one paragraph

Article in eNeuro. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.0field-weighted citation impact, top 26% 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

12 citing papers in PubMed, 19 citations in OpenAlex.

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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 at 2 institutions in 1 country.

Paul F KochCenter for Brain Injury and Repair, Department of Neurosurgery, University of Pennsylvania, Philadelphia, Pennsylvania 19104.ORCID 0000-0002-2494-2671
Carlo CottoneCenter for Brain Injury and Repair, Department of Neurosurgery, University of Pennsylvania, Philadelphia, Pennsylvania 19104.
Christopher D AdamCenter for Brain Injury and Repair, Department of Neurosurgery, University of Pennsylvania, Philadelphia, Pennsylvania 19104.
Alexandra V UlyanovaCenter for Brain Injury and Repair, Department of Neurosurgery, University of Pennsylvania, Philadelphia, Pennsylvania 19104.ORCID 0000-0002-1319-5279
Robin J RussoCenter for Brain Injury and Repair, Department of Neurosurgery, University of Pennsylvania, Philadelphia, Pennsylvania 19104.
Maura T WeberCenter for Brain Injury and Repair, Department of Neurosurgery, University of Pennsylvania, Philadelphia, Pennsylvania 19104.
John D ArenaCenter for Brain Injury and Repair, Department of Neurosurgery, University of Pennsylvania, Philadelphia, Pennsylvania 19104.
Victoria E JohnsonCenter for Brain Injury and Repair, Department of Neurosurgery, University of Pennsylvania, Philadelphia, Pennsylvania 19104.
John A WolfCenter for Brain Injury and Repair, Department of Neurosurgery, University of Pennsylvania, Philadelphia, Pennsylvania 19104 wolfjo@pennmedicine.upenn.edu.ORCID 0000-0002-6950-2303
California University of Pennsylvania · USVeterans Health Administration · US

Funding

BRIAN INJURY TRAINING GRANTT32NS043126 · NINDS · UNIVERSITY OF PENNSYLVANIA · PI Douglas Hamilton Smith · 2003 to 2026
$5.9M
Network Dysfunction and Neuromodulation following TBIR01NS101108 · NINDS · UNIVERSITY OF PENNSYLVANIA · PI John Allen Wolf · 2017 to 2026
$3.3M
Neuromodulation as a Therapy for PTSD following Chronic TBII01RX002705 · VA · PHILADELPHIA VA MEDICAL CENTER · PI John Allen Wolf · 2018 to 2026
–
Mechanisms of Cortico-Limbic Network Dysfunction Underlying PTSD after TBIIK2RX001479 · VA · PHILADELPHIA VA MEDICAL CENTER · PI WOLF, JOHN ALLEN · 2015 to 2018
–
NINDS NIH HHS R01 NS101108NINDS NIH HHS T32 NS043126RRD VA I01 RX002705RRD VA IK2 RX001479
6 · The paper itself

Abstract

While hippocampal-dependent learning and memory are particularly vulnerable to traumatic brain injury (TBI), the functional status of individual hippocampal neurons and their interactions with oscillations are unknown following injury. Using the most common rodent TBI model and laminar recordings in CA1, we found a significant reduction in oscillatory input into the radiatum layer of CA1 after TBI. Surprisingly, CA1 neurons maintained normal firing rates despite attenuated input, but did not maintain appropriate synchronization with this oscillatory input or with local high-frequency oscillations. Normal synchronization between these coordinating oscillations was also impaired. Simultaneous recordings of medial septal neurons known to participate in theta oscillations revealed increased GABAergic/glutamatergic firing rates postinjury under anesthesia, potentially because of a loss of modulating feedback from the hippocampus. These results suggest that TBI leads to a profound disruption of connectivity and oscillatory interactions, potentially disrupting the timing of CA1 neuronal ensembles that underlie aspects of learning and memory.

Indexed as

Brain Injuries, TraumaticTheta RhythmAction PotentialsHippocampusHumansMemoryNeuronshippocampusmedial septumoscillations rodentssynchronizationTBI

Identifiers

PMID32737188
PMCPMC7477953
OpenAlexW3046587021

What OpenQuestion 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 OpenQuestion graph.