scholarly journals Blast-induced axonal degeneration in the rat cerebellum in the absence of head movement

2022 ◽  
Vol 12 (1) ◽  
Author(s):  
Robin Bishop ◽  
Seok Joon Won ◽  
Karen-Amanda Irvine ◽  
Jayinee Basu ◽  
Eric S. Rome ◽  
...  
Keyword(s):  
Head Movement ◽  
Axonal Degeneration ◽  
Ocular Trauma ◽  
Axonal Injury ◽  
Direct Effects ◽  
Cerebellar White Matter ◽  
Pattern Of Injury ◽  
Head Displacement ◽  
Blast Exposure ◽  
Lateral Plane

AbstractBlast exposure can injure brain by multiple mechanisms, and injury attributable to direct effects of the blast wave itself have been difficult to distinguish from that caused by rapid head displacement and other secondary processes. To resolve this issue, we used a rat model of blast exposure in which head movement was either strictly prevented or permitted in the lateral plane. Blast was found to produce axonal injury even with strict prevention of head movement. This axonal injury was restricted to the cerebellum, with the exception of injury in visual tracts secondary to ocular trauma. The cerebellar axonal injury was increased in rats in which blast-induced head movement was permitted, but the pattern of injury was unchanged. These findings support the contentions that blast per se, independent of head movement, is sufficient to induce axonal injury, and that axons in cerebellar white matter are particularly vulnerable to direct blast-induced injury.

scholarly journals Blast-Induced Axonal Degeneration In The Rat Cerebellum In The Absence of Head Movement

2021 ◽  
Author(s):  
Robin Bishop ◽  
Seok Joon Won ◽  
Karen-Amanda Irvine ◽  
Jayinee Basu ◽  
Eric S. Rome ◽  
...  
Keyword(s):  
Head Movement ◽  
Axonal Degeneration ◽  
Ocular Trauma ◽  
Axonal Injury ◽  
Direct Effects ◽  
Cerebellar White Matter ◽  
Pattern Of Injury ◽  
Head Displacement ◽  
Blast Exposure ◽  
Lateral Plane

Abstract Blast exposure can injure brain by multiple mechanisms, and injury attributable to direct effects of the blast wave itself have been difficult to distinguish from that caused by rapid head displacement and other secondary processes. To resolve this issue, we used a rat model of blast exposure in which head movement was either strictly prevented or permitted in the lateral plane. Blast was found to produce axonal injury even with strict prevention of head movement. This axonal injury was restricted to the cerebellum, with the exception of injury in visual tracts secondary to ocular trauma. The cerebellar axonal injury was increased in rats in which blast-induced head movement was permitted, but the pattern of injury was unchanged. These findings support the contentions that blast per se, independent of head movement, is sufficient to induce axonal injury, and that axons in cerebellar white matter are particularly vulnerable to direct blast - induced injury.

scholarly journals DDIT3 (CHOP) contributes to retinal ganglion cell somal loss but not axonal degeneration in DBA/2J mice

2019 ◽  
Vol 5 (1) ◽  
Author(s):  
Olivia J. Marola ◽  
Stephanie B. Syc-Mazurek ◽  
Richard T. Libby
Keyword(s):  
Optic Nerve ◽  
Ocular Hypertension ◽  
Optic Nerve Head ◽  
Cellular Response ◽  
Molecular Mechanisms ◽  
Axonal Degeneration ◽  
Axonal Injury ◽  
Retinal Ganglion ◽  
Age Related

Abstract Glaucoma is an age-related neurodegenerative disease characterized by the progressive loss of retinal ganglion cells (RGCs). Chronic ocular hypertension, an important risk factor for glaucoma, leads to RGC axonal injury at the optic nerve head. This insult triggers molecularly distinct cascades governing RGC somal apoptosis and axonal degeneration. The molecular mechanisms activated by ocular hypertensive insult that drive both RGC somal apoptosis and axonal degeneration are incompletely understood. The cellular response to endoplasmic reticulum stress and induction of pro-apoptotic DNA damage inducible transcript 3 (DDIT3, also known as CHOP) have been implicated as drivers of neurodegeneration in many disease models, including glaucoma. RGCs express DDIT3 after glaucoma-relevant insults, and importantly, DDIT3 has been shown to contribute to both RGC somal apoptosis and axonal degeneration after acute induction of ocular hypertension. However, the role of DDIT3 in RGC somal and axonal degeneration has not been critically tested in a model of age-related chronic ocular hypertension. Here, we investigated the role of DDIT3 in glaucomatous RGC death using an age-related, naturally occurring ocular hypertensive mouse model of glaucoma, DBA/2J mice (D2). To accomplish this, a null allele of Ddit3 was backcrossed onto the D2 background. Homozygous Ddit3 deletion did not alter gross retinal or optic nerve head morphology, nor did it change the ocular hypertensive profile of D2 mice. In D2 mice, Ddit3 deletion conferred mild protection to RGC somas, but did not significantly prevent RGC axonal degeneration. Together, these data suggest that DDIT3 plays a minor role in perpetuating RGC somal apoptosis caused by chronic ocular hypertension-induced axonal injury, but does not significantly contribute to distal axonal degeneration.

scholarly journals The problem of axonal injury in the brains of veterans with histories of blast exposure

2014 ◽  
Vol 2 (1) ◽  
Author(s):  
Jiwon Ryu ◽  
Iren Horkayne-Szakaly ◽  
Leyan Xu ◽  
Olga Pletnikova ◽  
Francesco Leri ◽  
...  
Keyword(s):  
Axonal Injury ◽  
Blast Exposure

Mechanisms of Axonal Degeneration and Regeneration

2017 ◽  
pp. 574-592 ◽  
Author(s):  
Jiaxing Li ◽  
Catherine A. Collins
Keyword(s):  
Axonal Degeneration ◽  
Morphological Changes ◽  
Axonal Injury ◽  
Model Organisms ◽  
C Elegans ◽  
The Face ◽  
Invertebrate Model ◽  
Critical Components ◽  
Injury Models ◽  
Shed Light

In the face of acute or chronic axonal damage, neurons and their axons undergo a number of molecular, cellular, and morphological changes. These changes facilitate two types of responses, axonal degeneration and regeneration, both of which are remarkably conserved in both vertebrates and invertebrates. Invertebrate model organisms, including Drosophila and C. elegans, have offered a powerful platform with accessible genetic tools for manipulation and amenable nervous system for visualization. Thus far, several critical components and pathways in axonal degeneration and regeneration have been identified in invertebrate studies, including Sarm and Wallenda/DLK. This article highlights important findings in Drosophila, C. elegans, and other invertebrate injury models that have shed light upon the mechanism in axonal injury response.

Blast Exposure in Rats with Body Shielding Is Characterized Primarily by Diffuse Axonal Injury

2011 ◽  
Vol 28 (6) ◽  
pp. 947-959 ◽  
Author(s):  
Robert H. Garman ◽  
Larry W. Jenkins ◽  
Robert C. Switzer ◽  
Richard A. Bauman ◽  
Lawrence C. Tong ◽  
...  
Keyword(s):  
Axonal Injury ◽  
Diffuse Axonal Injury ◽  
Blast Exposure

scholarly journals DDIT3 (CHOP) contributes to retinal ganglion cell somal loss but not axonal degeneration in DBA/2J mice

2019 ◽  
Author(s):  
Olivia J. Marola ◽  
Stephanie B. Syc-Mazurek ◽  
Richard T. Libby
Keyword(s):  
Optic Nerve ◽  
Ocular Hypertension ◽  
Optic Nerve Head ◽  
Cellular Response ◽  
Molecular Mechanisms ◽  
Axonal Degeneration ◽  
Axonal Injury ◽  
Retinal Ganglion ◽  
Age Related

AbstractGlaucoma is an age-related neurodegenerative disease characterized by the progressive loss of retinal ganglion cells (RGCs). Chronic ocular hypertension, an important risk factor for glaucoma, leads to RGC axonal injury at the optic nerve head. This insult triggers molecularly distinct cascades governing RGC somal apoptosis and axonal degeneration. The molecular mechanisms activated by ocular hypertensive insult that drive both RGC somal apoptosis and axonal degeneration are incompletely understood. The cellular response to endoplasmic reticulum stress and induction of pro-apoptotic DNA damage inducible transcript 3 (DDIT3, also known as CHOP) has been implicated as a driver of neurodegeneration in many disease models, including glaucoma. RGCs express DDIT3 upon glaucoma-relevant insults, and importantly, DDIT3 has been shown to contribute to both RGC somal apoptosis and axonal degeneration after acute induction of ocular hypertension. However, the role of DDIT3 in RGC somal and axonal degeneration has not been critically tested in a model of age-related chronic ocular hypertension. Here, we investigated the role of DDIT3 in glaucomatous RGC death using an age-related, naturally occurring ocular hypertensive mouse model of glaucoma, DBA/2J mice (D2). To accomplish this, a null allele of Ddit3 was backcrossed onto the D2 background. Homozygous Ddit3 deletion did not alter gross retinal or optic nerve head morphology, nor did it change the ocular hypertensive profile of D2 mice. In D2 mice, Ddit3 deletion conferred mild protection to RGC somas but did not significantly prevent RGC axonal degeneration. Together, these data suggest that DDIT3 plays a minor role in perpetuating RGC somal apoptosis caused by chronic ocular hypertension-induced axonal injury, but does not significantly contribute to distal axonal degeneration.

scholarly journals DLK-dependent signaling is important for somal but not axonal degeneration of retinal ganglion cells following axonal injury

2014 ◽  
Vol 69 ◽  
pp. 108-116 ◽  
Author(s):  
Kimberly A. Fernandes ◽  
Jeffrey M. Harder ◽  
Simon W. John ◽  
Peter Shrager ◽  
Richard T. Libby
Keyword(s):  
Retinal Ganglion Cells ◽  
Axonal Degeneration ◽  
Ganglion Cells ◽  
Axonal Injury ◽  
Retinal Ganglion

scholarly journals The Ups and Downs of Head Displacement

2020 ◽  
pp. 1-49
Author(s):  
Karlos Arregi ◽  
Asia Pietraszko
Keyword(s):  
Head Movement ◽  
Head Displacement ◽  
Downward Displacement ◽  
Syntactic Properties ◽  
Mirror Principle ◽  
Crosslinguistic Variation

We propose a theory of head displacement that replaces traditional Head Movement and Lowering with a single syntactic operation of Generalized Head Movement. We argue that upward and downward head displacement have the same syntactic properties: cyclicity, Mirror Principle effects, feeding upward head displacement, and being blocked in the same syntactic configurations. We also study the interaction of head displacement and other syntactic operations, arguing that claimed differences between upward and downward displacement are either spurious or follow directly from our account. Finally, we show that our theory correctly predicts the attested crosslinguistic variation in verb and inflection doubling in predicate clefts.

Traumatic or diffuse axonal injury? Author's response

2000 ◽  
Vol 26 (5) ◽  
pp. 491-491 ◽  
Author(s):  
J. F. Geddes ◽  
H. L. Whitwell ◽  
D. I. Graham
Keyword(s):  
Axonal Injury ◽  
Diffuse Axonal Injury

Motion Analysis of the Cervical Spine

2004 ◽  
Vol 9 (5) ◽  
pp. 1-11
Author(s):  
Patrick R. Luers
Keyword(s):  
Cervical Spine ◽  
Intervertebral Disk ◽  
Radiographic Evaluation ◽  
Ligamentous Injury ◽  
Pattern Of Injury ◽  
Motion Segment ◽  
Single Pattern ◽  
Compensatory Motion ◽  
Loss Of Motion ◽  
Flexion And Extension

Abstract The AMA Guides to the Evaluation of Permanent Impairment (AMA Guides), Fifth Edition, defines a motion segment as “two adjacent vertebrae, the intervertebral disk, the apophyseal or facet joints, and ligamentous structures between the vertebrae.” The range of motion from segment to segment varies, and loss of motion segment integrity is defined as “an anteroposterior motion of one vertebra over another that is greater than 3.5 mm in the cervical spine, greater than 2.5 mm in the thoracic spine, and greater than 4.5 mm in the lumbar spine.” Multiple etiologies are associated with increased motion in the cervical spine; some are physiologic or compensatory and others are pathologic. The standard radiographic evaluation of instability and ligamentous injury in the cervical spine consists of lateral flexion and extension x-ray views, but no single pattern of injury is identified in whiplash injuries. Fluoroscopy or cineradiographic techniques may be more sensitive than other methods for evaluating subtle abnormal motion in the cervical spine. The increased motion thus detected then must be evaluated to determine whether it represents normal physiologic motion, normal compensatory motion, motion related to underlying degenerative disk and/or facet disease, or increased motion related to ligamentous injury. Imaging studies should be performed and interpreted as instructed in the AMA Guides.

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