Evidence map›Paper›PMID 26903822›Full record

ArticleFrontiers in systems neuroscience2016

Traumatic Brain Injury Upregulates Phosphodiesterase Expression in the Hippocampus.

Nicole M Wilson, David J Titus, Anthony A Oliva, Concepcion Furones, Coleen M Atkins

Open access · goldAbstract read
In one paragraph

Article in Frontiers in systems neuroscience, 2016. 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
2.1field-weighted citation impact, top 13% 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, 34 citations in OpenAlex.

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  3. The effect of traumatic brain injury on learning and memory: A synaptic focus.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2025
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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

5 authors at 2 institutions in 1 country.

Nicole M WilsonThe Miami Project to Cure Paralysis, Department of Neurological Surgery, University of Miami Miller School of Medicine Miami, FL, USA.
David J TitusThe Miami Project to Cure Paralysis, Department of Neurological Surgery, University of Miami Miller School of Medicine Miami, FL, USA.
Anthony A OlivaThe Miami Project to Cure Paralysis, Department of Neurological Surgery, University of Miami Miller School of Medicine Miami, FL, USA.
Concepcion FuronesThe Miami Project to Cure Paralysis, Department of Neurological Surgery, University of Miami Miller School of Medicine Miami, FL, USA.
Coleen M AtkinsThe Miami Project to Cure Paralysis, Department of Neurological Surgery, University of Miami Miller School of Medicine Miami, FL, USA.
University of Miami · USNeurological Surgery · US

Funding

Cyclic Nucleotide Regulation in Traumatic Brain Injury and Alzheimer's DiseaseR01NS056072 · NINDS · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI ATKINS, COLEEN M., DIETRICH, W DALTON · 2007 to 2018
$4.1M
Rehabilitation Strategies for Memory Dysfunction After Traumatic Brain InjuryR01NS069721 · NINDS · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI ATKINS, COLEEN M. · 2010 to 2019
$3.7M
The Role of Phosphodiesterase 4B in Inflammation after Traumatic Brain InjuryF31NS089351 · NINDS · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI WILSON, NICOLE MARIE · 2014 to 2016
$129k
NINDS NIH HHS F31 NS089351NINDS NIH HHS R01 NS056072NINDS NIH HHS R01 NS069721
6 · The paper itself

Abstract

Traumatic brain injury (TBI) results in significant impairments in hippocampal synaptic plasticity. A molecule critically involved in hippocampal synaptic plasticity, 3',5'-cyclic adenosine monophosphate, is downregulated in the hippocampus after TBI, but the mechanism that underlies this decrease is unknown. To address this question, we determined whether phosphodiesterase (PDE) expression in the hippocampus is altered by TBI. Young adult male Sprague Dawley rats received sham surgery or moderate parasagittal fluid-percussion brain injury. Animals were analyzed by western blotting for changes in PDE expression levels in the hippocampus. We found that PDE1A levels were significantly increased at 30 min, 1 h and 6 h after TBI. PDE4B2 and 4D2 were also significantly increased at 1, 6, and 24 h after TBI. Additionally, phosphorylation of PDE4A was significantly increased at 6 and 24 h after TBI. No significant changes were observed in levels of PDE1B, 1C, 3A, 8A, or 8B between 30 min to 7 days after TBI. To determine the spatial profile of these increases, we used immunohistochemistry and flow cytometry at 24 h after TBI. PDE1A and phospho-PDE4A localized to neuronal cell bodies. PDE4B2 was expressed in neuronal dendrites, microglia and infiltrating CD11b(+) immune cells. PDE4D was predominantly found in microglia and infiltrating CD11b(+) immune cells. To determine if inhibition of PDE4 would improve hippocampal synaptic plasticity deficits after TBI, we treated hippocampal slices with rolipram, a pan-PDE4 inhibitor. Rolipram partially rescued the depression in basal synaptic transmission and converted a decaying form of long-term potentiation (LTP) into long-lasting LTP. Overall, these results identify several possible PDE targets for reducing hippocampal synaptic plasticity deficits and improving cognitive function acutely after TBI.

Indexed as

cAMPCREBfluid-percussionhippocampusinflammationphosphodiesterasetraumatic brain injury

Identifiers

PMID26903822
PMCPMC4742790
OpenAlexW2284243349

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.