Acute Axonal Degeneration Drives Development of Cognitive, Motor, and Visual Deficits after Blast-Mediated Traumatic Brain Injury in Mice

Terry C Yin; Jaymie R Voorhees; Rachel M Genova; Kevin C Davis; Ashley M Madison; Jeremiah K Britt; Coral J Cintrón-Pérez; Latisha McDaniel; Matthew M Harper; Andrew A Pieper

doi:10.1523/ENEURO.0220-16.2016

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Acute Axonal Degeneration Drives Development of Cognitive, Motor, and Visual Deficits after Blast-Mediated Traumatic Brain Injury in Mice

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Peer reviewed

Acute Axonal Degeneration Drives Development of Cognitive, Motor, and Visual Deficits after Blast-Mediated Traumatic Brain Injury in Mice

Terry C Yin, Jaymie R Voorhees, Rachel M Genova, Kevin C Davis, Ashley M Madison, Jeremiah K Britt, Coral J Cintrón-Pérez, Latisha McDaniel, Matthew M Harper and Andrew A Pieper

eNeuro, Vol.3(5), p.ENEURO.0220-16.2016

09/2016

DOI: 10.1523/ENEURO.0220-16.2016

PMCID: PMC5086797

PMID: 27822499

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Abstract

Axonal degeneration is a prominent feature of many forms of neurodegeneration, and also an early event in blast-mediated traumatic brain injury (TBI), the signature injury of soldiers in Iraq and Afghanistan. It is not known, however, whether this axonal degeneration is what drives development of subsequent neurologic deficits after the injury. The Wallerian degeneration slow strain ( ) of mice is resistant to some forms of axonal degeneration because of a triplicated fusion gene encoding the first 70 amino acids of Ufd2a, a ubiquitin-chain assembly factor, that is linked to the complete coding sequence of nicotinamide mononucleotide adenylyltransferase 1 (NMAT1). Here, we demonstrate that resistance of mice to axonal degeneration after blast-mediated TBI is associated with preserved function in hippocampal-dependent spatial memory, cerebellar-dependent motor balance, and retinal and optic nerve-dependent visual function. Thus, early axonal degeneration is likely a critical driver of subsequent neurobehavioral complications of blast-mediated TBI. Future therapeutic strategies targeted specifically at mitigating axonal degeneration may provide a uniquely beneficial approach to treating patients suffering from the effects of blast-mediated TBI.

Visual Perception

Animals

Axons - pathology

Axons - physiology

Blast Injuries - complications

Blast Injuries - pathology

Blast Injuries - physiopathology

Blast Injuries - psychology

Brain Injuries, Traumatic - etiology

Brain Injuries, Traumatic - pathology

Brain Injuries, Traumatic - physiopathology

Brain Injuries, Traumatic - psychology

Cognition

Disease Models, Animal

Male

Maze Learning

Mice, Mutant Strains

Motor Activity

Neuroprotection

Retina - pathology

Retina - physiopathology

Spatial Memory

Ubiquitin-Protein Ligases - genetics

Ubiquitin-Protein Ligases - metabolism

Vision Disorders - etiology

Vision Disorders - pathology

Vision Disorders - physiopathology

Vision Disorders - psychology

Wallerian Degeneration - etiology

Wallerian Degeneration - pathology

Wallerian Degeneration - physiopathology

Wallerian Degeneration - psychology

Details

Title: Subtitle: Acute Axonal Degeneration Drives Development of Cognitive, Motor, and Visual Deficits after Blast-Mediated Traumatic Brain Injury in Mice
Creators: Terry C Yin - University of Iowa
Jaymie R Voorhees - University of Iowa
Rachel M Genova - University of Iowa
Kevin C Davis - University of Iowa
Ashley M Madison - University of Iowa
Jeremiah K Britt - University of Iowa
Coral J Cintrón-Pérez - University of Iowa
Latisha McDaniel - University of Iowa
Matthew M Harper - University of Iowa
Andrew A Pieper - University of Iowa
Resource Type: Journal article
Publication Details: eNeuro, Vol.3(5), p.ENEURO.0220-16.2016
DOI: 10.1523/ENEURO.0220-16.2016
PMID: 27822499
PMCID: PMC5086797
NLM abbreviation: eNeuro
ISSN: 2373-2822
eISSN: 2373-2822
Grant note: I01 RX000952 / RRD VA T32 GM007337 / NIGMS NIH HHS
Language: English
Date published: 09/2016
Academic Unit: Molecular Physiology and Biophysics; Psychiatry; Biology; Ophthalmology and Visual Sciences
Record Identifier: 9984180934502771

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