Repeated Low Intensity Blast Exposure Is Associated with Damaged Endothelial Glycocalyx and Downstream Behavioral Deficits
Current clinical research into mild traumatic brain injury (mTBI) has focused on white matter changes as identified by advanced MRI based imaging techniques. However, perivascular tau accumulation in the brains of individuals diagnosed with mTBI suggests that the vasculature plays a key role in the...
| Main Authors: | , , , , , |
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| Format: | Article |
| Language: | English |
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Frontiers Media S.A.
2017-06-01
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| Series: | Frontiers in Behavioral Neuroscience |
| Subjects: | |
| Online Access: | https://www.frontiersin.org/article/10.3389/fnbeh.2017.00104/full |
| _version_ | 1818445171077939200 |
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| author | Aaron A. Hall Mirian I. Mendoza Hanbing Zhou Michael Shaughness Richard M. McCarron Stephen T. Ahlers |
| author_facet | Aaron A. Hall Mirian I. Mendoza Hanbing Zhou Michael Shaughness Richard M. McCarron Stephen T. Ahlers |
| author_sort | Aaron A. Hall |
| collection | DOAJ |
| description | Current clinical research into mild traumatic brain injury (mTBI) has focused on white matter changes as identified by advanced MRI based imaging techniques. However, perivascular tau accumulation in the brains of individuals diagnosed with mTBI suggests that the vasculature plays a key role in the pathology. This study used a rat model to examine whether the endothelial glycocalyx, a layer of the vasculature responsible for sensing luminal shear forces, is damaged by exposure to repeated low intensity blast, and whether this layer is associated with observed behavioral deficits. The blast exposure used consisted of 12, 40 kPa blast exposures conducted with a minimum of 24 h between blasts. We found that repeated blast exposure reduced glycocalyx length and density in various brain regions indicating damage. This blast exposure paradigm was associated with a mild performance decrement in the Morris water maze (MWM) which assesses learning and memory. Administration of hyaluronidase, an enzyme that binds to and degrades hyaluronan (a major structural component of the glycocalyx) prior to blast exposure reduced the observed behavioral deficits and induced a thickening of the glycocalyx layer. Taken together these findings demonstrate that the endothelial glycocalyx degradation following repeated blast is associated with behavioral decrements which can be prevented by treatment with hyaluronidase. |
| first_indexed | 2024-12-14T19:27:31Z |
| format | Article |
| id | doaj.art-88838d66c1af4f2e876386f9569955dd |
| institution | Directory Open Access Journal |
| issn | 1662-5153 |
| language | English |
| last_indexed | 2024-12-14T19:27:31Z |
| publishDate | 2017-06-01 |
| publisher | Frontiers Media S.A. |
| record_format | Article |
| series | Frontiers in Behavioral Neuroscience |
| spelling | doaj.art-88838d66c1af4f2e876386f9569955dd2022-12-21T22:50:10ZengFrontiers Media S.A.Frontiers in Behavioral Neuroscience1662-51532017-06-011110.3389/fnbeh.2017.00104246526Repeated Low Intensity Blast Exposure Is Associated with Damaged Endothelial Glycocalyx and Downstream Behavioral DeficitsAaron A. HallMirian I. MendozaHanbing ZhouMichael ShaughnessRichard M. McCarronStephen T. AhlersCurrent clinical research into mild traumatic brain injury (mTBI) has focused on white matter changes as identified by advanced MRI based imaging techniques. However, perivascular tau accumulation in the brains of individuals diagnosed with mTBI suggests that the vasculature plays a key role in the pathology. This study used a rat model to examine whether the endothelial glycocalyx, a layer of the vasculature responsible for sensing luminal shear forces, is damaged by exposure to repeated low intensity blast, and whether this layer is associated with observed behavioral deficits. The blast exposure used consisted of 12, 40 kPa blast exposures conducted with a minimum of 24 h between blasts. We found that repeated blast exposure reduced glycocalyx length and density in various brain regions indicating damage. This blast exposure paradigm was associated with a mild performance decrement in the Morris water maze (MWM) which assesses learning and memory. Administration of hyaluronidase, an enzyme that binds to and degrades hyaluronan (a major structural component of the glycocalyx) prior to blast exposure reduced the observed behavioral deficits and induced a thickening of the glycocalyx layer. Taken together these findings demonstrate that the endothelial glycocalyx degradation following repeated blast is associated with behavioral decrements which can be prevented by treatment with hyaluronidase.https://www.frontiersin.org/article/10.3389/fnbeh.2017.00104/fullblastglycocalyxbehavioral deficitstraumatic brain injuryrepeated low intensity |
| spellingShingle | Aaron A. Hall Mirian I. Mendoza Hanbing Zhou Michael Shaughness Richard M. McCarron Stephen T. Ahlers Repeated Low Intensity Blast Exposure Is Associated with Damaged Endothelial Glycocalyx and Downstream Behavioral Deficits Frontiers in Behavioral Neuroscience blast glycocalyx behavioral deficits traumatic brain injury repeated low intensity |
| title | Repeated Low Intensity Blast Exposure Is Associated with Damaged Endothelial Glycocalyx and Downstream Behavioral Deficits |
| title_full | Repeated Low Intensity Blast Exposure Is Associated with Damaged Endothelial Glycocalyx and Downstream Behavioral Deficits |
| title_fullStr | Repeated Low Intensity Blast Exposure Is Associated with Damaged Endothelial Glycocalyx and Downstream Behavioral Deficits |
| title_full_unstemmed | Repeated Low Intensity Blast Exposure Is Associated with Damaged Endothelial Glycocalyx and Downstream Behavioral Deficits |
| title_short | Repeated Low Intensity Blast Exposure Is Associated with Damaged Endothelial Glycocalyx and Downstream Behavioral Deficits |
| title_sort | repeated low intensity blast exposure is associated with damaged endothelial glycocalyx and downstream behavioral deficits |
| topic | blast glycocalyx behavioral deficits traumatic brain injury repeated low intensity |
| url | https://www.frontiersin.org/article/10.3389/fnbeh.2017.00104/full |
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