Evidence map›Paper›PMID 39316552›Full record

ReviewThe Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry2025

The effect of traumatic brain injury on learning and memory: A synaptic focus.

Eric Eyolfson, Kirsten R B Suesser, Holly Henry, Itziar Bonilla-Del Río, Pedro Grandes, Richelle Mychasiuk, Brian R Christie

Abstract readReview
In one paragraph

Review in The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed, 1 pooled it
–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

9 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Article
  4. Animal Models of Prenatal Alcohol Exposure.Advances in experimental medicine and biology · 2026
    Review
  5. Article
  6. Article
  7. Article
  8. Synaptic Pathology in Traumatic Brain Injury and Therapeutic Insights.International journal of molecular sciences · 2025
    Review
  9. 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.

Eric EyolfsonDivision of Medical Sciences and Institute for Aging and Lifelong Health, University of Victoria, Victoria, BC, Canada.ORCID 0000-0002-2201-5444
Kirsten R B SuesserDivision of Medical Sciences and Institute for Aging and Lifelong Health, University of Victoria, Victoria, BC, Canada.ORCID 0009-0003-7601-1988
Holly HenryDivision of Medical Sciences and Institute for Aging and Lifelong Health, University of Victoria, Victoria, BC, Canada.
Itziar Bonilla-Del RíoDepartment of Neurosciences, Faculty of Medicine and Nursing, University of the Basque Country, Leioa, Spain.
Pedro GrandesDepartment of Neurosciences, Faculty of Medicine and Nursing, University of the Basque Country, Leioa, Spain.
Richelle MychasiukDepartment of Neuroscience, Central Clinical School, Monash University, Melbourne, VIC, Australia.ORCID 0000-0001-5291-5083
Brian R ChristieDivision of Medical Sciences and Institute for Aging and Lifelong Health, University of Victoria, Victoria, BC, Canada.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Deficits in learning and memory are some of the most commonly reported symptoms following a traumatic brain injury (TBI). We will examine whether the neural basis of these deficits stems from alterations to bidirectional synaptic plasticity within the hippocampus. Although the CA1 subregion of the hippocampus has been a focus of TBI research, the dentate gyrus should also be given attention as it exhibits a unique ability for adult neurogenesis, a process highly susceptible to TBI-induced damage. This review examines our current understanding of how TBI results in deficits in synaptic plasticity, as well as how TBI-induced changes in endocannabinoid (eCB) systems may drive these changes. Through the synthesis and amalgamation of existing data, we propose a possible mechanism for eCB-mediated recovery in synaptic plasticity deficits. This hypothesis is based on the plausible roles of CB1 receptors in regulating inhibitory tone, influencing astrocytes and microglia, and modulating glutamate release. Dysregulation of the eCBs may be responsible for deficits in synaptic plasticity and learning following TBI. Taken together, the existing evidence indicates eCBs may contribute to TBI manifestation, pathogenesis, and recovery, but it also suggests there may be a therapeutic role for the eCB system in TBI.

Indexed as

Brain Injuries, TraumaticLearningMemoryNeuronal PlasticitySynapsesAnimalsEndocannabinoidsHippocampusHumansEndocannabinoidsdentate gyruselectrophysiologyendocannabinoidshippocampuslong-term depressionlong-term potentiationsynaptic plasticity

Identifiers

PMID39316552
PMCPMC11909778

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.