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Article: Enhanced attention in rats following blast-induced traumatic brain injury.

Navarro, Victor M / Boehme, Nickolas / Wasserman, Edward A / Harper, Matthew M

2024 Volume 10, Issue 4, Page(s) e25661

Abstract: Purpose: To evaluate visuo-cognitive sequelae following blast-induced traumatic brain injury in a rat model.: Methods: Rats were randomly assigned to one of four groups depending on the intensity/quantity of a blast received in a blast chamber: sham ( ...

Abstract	Purpose: To evaluate visuo-cognitive sequelae following blast-induced traumatic brain injury in a rat model. Methods: Rats were randomly assigned to one of four groups depending on the intensity/quantity of a blast received in a blast chamber: sham (no blast), low intensity (22 psi), medium intensity (26 psi), or three medium intensity blasts (26 psi × 3). After recovery, all subjects were given visual discrimination tasks of increasing complexity, until mastery. After behavioral training, visual function was assessed via spectral-domain optical coherence tomography and pattern electroretinogram, and the extent of retinal damage was quantified via immunohistochemistry of retinal ganglion cells. Results: None of the measures assessing visual function revealed significant differences as a function of blast intensity/quantity. Behavioral training did not disclose short-term effects of blast in general motivation or the development of anticipatory responding. No differences in general learning ability and the number of perseverative errors were observed. However, behavioral training found effects of blast in attentional function; relative to controls, subjects that received blasts were faster in learning to attend to informative (over non-informative) cues in the most difficult visual discrimination task. Conclusion: Blast exposure in rats resulted in increased attention following blast, with no appreciable deficits in visual function. These results are contrary to what is often reported for human clinical populations; as such, more research bridging methodological differences is necessary.
Language	English
Publishing date	2024-02-10
Publishing country	England
Document type	Journal Article
ZDB-ID	2835763-2
ISSN	2405-8440
ISSN	2405-8440
DOI	10.1016/j.heliyon.2024.e25661
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Article ; Online: Increasing the number and intensity of shock tube generated blast waves leads to earlier retinal ganglion cell dysfunction and regional cell death.

Harper, Matthew M / Boehme, Nickolas A / Dutca, Laura / Navarro, Victor

Experimental eye research

2023 Volume 239, Page(s) 109754

Abstract: The purpose of this study was to examine the effect of a blast exposure generated from a shock tube on retinal ganglion cell (RGC) function and structure. Mice were exposed to one of three blast conditions using a shock tube; a single blast wave of 20 ... ...

Abstract	The purpose of this study was to examine the effect of a blast exposure generated from a shock tube on retinal ganglion cell (RGC) function and structure. Mice were exposed to one of three blast conditions using a shock tube; a single blast wave of 20 PSI, a single blast wave of 30 PSI, or three blast waves of 30 PSI given on three consecutive days with a one-day inter-blast interval. The structure and function of the retina were analyzed using the pattern electroretinogram (PERG), the optomotor reflex (OMR), and optical coherence tomography (OCT). The in vivo parameters were examined at baseline, and then again 1-week, 4-weeks, and 16-weeks following blast exposure. The number of surviving RGCs was quantified at the end of the study. Analysis of mice receiving a 20 PSI injury showed decreased PERG and OMR responses 16-weeks post blast, without evidence of changed retinal thickness or RGC death. Mice subjected to a 30 PSI injury showed decreased PERG responses 4 weeks and 16 weeks after injury, without changes in the retinal thickness or RGC density. Mice subjected to 30 PSI X 3 blast exposures had PERG deficits 1-week and 4-weeks post exposure. There was also significant change in retinal thickness 1-week and 16-weeks post blast exposure. Mice receiving 30 PSI X 3 blast injuries had regional loss of RGCs in the central retina, but not in the mid-peripheral or peripheral retina. Overall, this study has shown that increasing the number of blast exposures and the intensity leads to earlier functional loss of RGCs. We have also shown regional RGC loss only when using the highest blast intensity and number of blast injuries.
MeSH term(s)	Mice ; Animals ; Retinal Ganglion Cells/metabolism ; Blast Injuries/metabolism ; Retina ; Electroretinography ; Cell Death ; Disease Models, Animal ; Mice, Inbred C57BL
Language	English
Publishing date	2023-12-17
Publishing country	England
Document type	Journal Article
ZDB-ID	80122-7
ISSN	1096-0007 ; 0014-4835
ISSN (online)	1096-0007
ISSN	0014-4835
DOI	10.1016/j.exer.2023.109754
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Article ; Online: Chronic effects of blast injury on the microvasculature in a transgenic mouse model of Alzheimer's disease related Aβ amyloidosis.

Clark, Alexander T / Abrahamson, Eric E / Harper, Matthew M / Ikonomovic, Milos D

Fluids and barriers of the CNS

2022 Volume 19, Issue 1, Page(s) 5

Abstract: Background: Altered cerebrovascular function and accumulation of amyloid-β (Aβ) after traumatic brain injury (TBI) can contribute to chronic neuropathology and increase the risk for Alzheimer's disease (AD). TBI due to a blast-induced shock wave (bTBI) ... ...

Abstract	Background: Altered cerebrovascular function and accumulation of amyloid-β (Aβ) after traumatic brain injury (TBI) can contribute to chronic neuropathology and increase the risk for Alzheimer's disease (AD). TBI due to a blast-induced shock wave (bTBI) adversely affects the neurovascular unit (NVU) during the acute period after injury. However, the chronic effects of bTBI and Aβ on cellular components of the NVU and capillary network are not well understood. Methods: We exposed young adult (age range: 76-106 days) female transgenic (Tg) APP/PS1 mice, a model of AD-like Aβ amyloidosis, and wild type (Wt) mice to a single bTBI (~ 138 kPa or ~ 20 psi) or to a Sham procedure. At 3-months or 12-months survival after exposure, we quantified neocortical Aβ load in Tg mice, and percent contact area between aquaporin-4 (AQP4)-immunoreactive astrocytic end-feet and brain capillaries, numbers of PDGFRβ-immunoreactive pericytes, and capillary densities in both genotypes. Results: The astroglia AQP4-capillary contact area in the Tg-bTBI group was significantly lower than in the Tg-Sham group at 3-months survival. No significant changes in the AQP4-capillary contact area were observed in the Tg-bTBI group at 12-months survival or in the Wt groups. Capillary density in the Tg-bTBI group at 12-months survival was significantly higher compared to the Tg-Sham control and to the Tg-bTBI 3-months survival group. The Wt-bTBI group had significantly lower capillary density and pericyte numbers at 12-months survival compared to 3-months survival. When pericytes were quantified relative to capillary density, no significant differences were detected among the experimental groups, for both genotypes. Conclusion: In conditions of high brain concentrations of human Aβ, bTBI exposure results in reduced AQP4 expression at the astroglia-microvascular interface, and in chronic capillary proliferation like what has been reported in AD. Long term microvascular changes after bTBI may contribute to the risk for developing chronic neurodegenerative disease later in life.
MeSH term(s)	Alzheimer Disease/etiology ; Alzheimer Disease/metabolism ; Alzheimer Disease/physiopathology ; Amyloid beta-Peptides/metabolism ; Animals ; Blast Injuries/complications ; Blast Injuries/metabolism ; Blast Injuries/physiopathology ; Brain Injuries, Traumatic/complications ; Brain Injuries, Traumatic/metabolism ; Brain Injuries, Traumatic/physiopathology ; Disease Models, Animal ; Female ; Humans ; Mice ; Mice, Transgenic ; Microvessels/metabolism ; Microvessels/physiopathology
Chemical Substances	Amyloid beta-Peptides
Language	English
Publishing date	2022-01-10
Publishing country	England
Document type	Journal Article
ZDB-ID	2595406-4
ISSN	2045-8118 ; 2045-8118
ISSN (online)	2045-8118
ISSN	2045-8118
DOI	10.1186/s12987-021-00301-z
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Article ; Online: Author response: Pressure wave dosimetry for "Retinal ganglion cell damage in an experimental rodent model of blast-mediated traumatic brain injury".

Harper, Matthew M

Investigative ophthalmology & visual science

2014 Volume 55, Issue 3, Page(s) 1350–1351

MeSH term(s)	Animals ; Blast Injuries/complications ; Brain Injuries/etiology ; Disease Models, Animal ; Male ; Optic Nerve Injuries/etiology ; Retina/injuries ; Retinal Ganglion Cells/pathology
Language	English
Publishing date	2014-03-06
Publishing country	United States
Document type	Comment ; Letter
ZDB-ID	391794-0
ISSN	1552-5783 ; 0146-0404
ISSN (online)	1552-5783
ISSN	0146-0404
DOI	10.1167/iovs.13-13692
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Article ; Online: The Retinal Ganglion Cell Response to Blast-Mediated Traumatic Brain Injury Is Genetic Background Dependent.

Harper, Matthew M / Boehme, Nickolas / Dutca, Laura M / Anderson, Michael G

Investigative ophthalmology & visual science

2021 Volume 62, Issue 7, Page(s) 13

Abstract: Purpose: The purpose of this study was to examine the influence of genetic background on the retinal ganglion cell (RGC) response to blast-mediated traumatic brain injury (TBI) in Jackson Diversity Outbred (J:DO), C57BL/6J and BALB/cByJ mice.: Methods! ...

Abstract	Purpose: The purpose of this study was to examine the influence of genetic background on the retinal ganglion cell (RGC) response to blast-mediated traumatic brain injury (TBI) in Jackson Diversity Outbred (J:DO), C57BL/6J and BALB/cByJ mice. Methods: Mice were subject to one blast injury of 137 kPa. RGC structure was analyzed by optical coherence tomography (OCT), function by the pattern electroretinogram (PERG), and histologically using BRN3A antibody staining. Results: Comparison of the change in each group from baseline for OCT and PERG was performed. There was a significant difference in the J:DOΔOCT compared to C57BL/6J mice (P = 0.004), but not compared to BALB/cByJ (P = 0.21). There was a significant difference in the variance of the ΔOCT in J:DO compared to both C57BL/6J and BALB/cByJ mice. The baseline PERG amplitude was 20.33 ± 9.32 µV, which decreased an average of -4.14 ± 12.46 µV following TBI. Baseline RGC complex + RNFL thickness was 70.92 ± 4.52 µm, which decreased an average of -1.43 ± 2.88 µm following blast exposure. There was not a significant difference in the ΔPERG between J:DO and C57BL/6J (P = 0.13), although the variances of the groups were significantly different. Blast exposure in J:DO mice results in a density change of 558.6 ± 440.5 BRN3A-positive RGCs/mm2 (mean ± SD). Conclusions: The changes in retinal outcomes had greater variance in outbred mice than what has been reported, and largely replicated herein, for inbred mice. These results demonstrate that the RGC response to blast injury is highly dependent upon genetic background.
MeSH term(s)	Animals ; Blast Injuries/complications ; Brain Injuries, Traumatic/etiology ; Brain Injuries, Traumatic/metabolism ; Brain Injuries, Traumatic/physiopathology ; Electroretinography/methods ; Genetic Variation ; Immunohistochemistry ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Retina/pathology ; Retina/physiology ; Retinal Ganglion Cells/physiology ; Stress, Physiological/physiology ; Tomography, Optical Coherence/methods ; Transcription Factor Brn-3A/genetics
Chemical Substances	Pou4f1 protein, mouse ; Transcription Factor Brn-3A
Language	English
Publishing date	2021-05-26
Publishing country	United States
Document type	Journal Article ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	391794-0
ISSN	1552-5783 ; 0146-0404
ISSN (online)	1552-5783
ISSN	0146-0404
DOI	10.1167/iovs.62.7.13
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Article ; Online: Decreased Expression of Glial-Derived Neurotrophic Factor Receptors in Glaucomatous Human Retinas.

Akurathi, Abhigna / Boese, Erin A / Kardon, Randy H / Ledolter, Johannes / Kuehn, Markus H / Harper, Matthew M

Current eye research

2022 Volume 47, Issue 4, Page(s) 597–605

Abstract: Purpose: The purpose of this study was to examine the expression of glial-derived neurotrophic factor (GDNF), the GDNF receptors GFRα1 and GFRα2, ciliary neurotrophic factor (CNTF), and the CNTF receptor CNTFRα in normal and glaucomatous human tissue.!## ...

Abstract	Purpose: The purpose of this study was to examine the expression of glial-derived neurotrophic factor (GDNF), the GDNF receptors GFRα1 and GFRα2, ciliary neurotrophic factor (CNTF), and the CNTF receptor CNTFRα in normal and glaucomatous human tissue. Methods: Human retinas were collected from 8 donors that had been clinically diagnosed and treated for glaucoma, and also from 9 healthy control donors. Immunohistochemical analysis for each trophic factor and receptor was performed. The percent of each retinal section labeled with each antibody was quantified for the total retinal thickness, and separately for the retinal ganglion cell (RGC) complex + retinal nerve fiber layer (RNFL). The expression of each protein was correlated with measures of the subject's ocular histories. Results: The percentage area immunopositive for GFRα2 was significantly decreased in the total retinal thickness containing all retinal layers and in the combined RGC complex + RNFL in glaucomatous eyes in both the peripapillary region and more peripheral retinal locations. We also observed a decrease in GFRα1 expression in the peripapillary RGC Complex + RNFL in glaucoma patients compared to healthy control patients. We also observed a relationship between GDNF and its receptors with several outcomes obtained from the medical record. No differences in CNTF or CNTFR labeling were observed. Conclusion: Decreases in GDNF receptor expression in glaucomatous tissue may limit the potential for neuroprotective therapy by supplementation with GDNF.
MeSH term(s)	Ciliary Neurotrophic Factor/metabolism ; Ciliary Neurotrophic Factor Receptor alpha Subunit/metabolism ; Glaucoma/diagnosis ; Glaucoma/metabolism ; Glial Cell Line-Derived Neurotrophic Factor/metabolism ; Glial Cell Line-Derived Neurotrophic Factor Receptors/metabolism ; Humans ; Retina/metabolism ; Retinal Ganglion Cells/metabolism
Chemical Substances	Ciliary Neurotrophic Factor ; Ciliary Neurotrophic Factor Receptor alpha Subunit ; GDNF protein, human ; Glial Cell Line-Derived Neurotrophic Factor ; Glial Cell Line-Derived Neurotrophic Factor Receptors
Language	English
Publishing date	2022-04-07
Publishing country	England
Document type	Journal Article ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, Non-U.S. Gov't
ZDB-ID	82079-9
ISSN	1460-2202 ; 0271-3683
ISSN (online)	1460-2202
ISSN	0271-3683
DOI	10.1080/02713683.2021.2002907
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Article ; Online: Immune responses in mice after blast-mediated traumatic brain injury TBI autonomously contribute to retinal ganglion cell dysfunction and death.

Harper, Matthew M / Gramlich, Oliver W / Elwood, Benjamin W / Boehme, Nickolas A / Dutca, Laura M / Kuehn, Markus H

Experimental eye research

2022 Volume 225, Page(s) 109272

Abstract: Purpose: The purpose of this study was to examine the role of the immune system and its influence on chronic retinal ganglion cell (RGC) dysfunction following blast-mediated traumatic brain injury (bTBI).: Methods: C57BL/6J and B6.129S7-Rag1: ... ...

Abstract	Purpose: The purpose of this study was to examine the role of the immune system and its influence on chronic retinal ganglion cell (RGC) dysfunction following blast-mediated traumatic brain injury (bTBI). Methods: C57BL/6J and B6.129S7-Rag1 Results: Analysis of the PERG showed a decreased amplitude two months post-AT that persisted for the duration of the study in AT-TBI mice. We also observed a significant decrease in the retinal thickness of AT-TBI mice two months post-AT compared to sham, but not at four or six months post-AT. The OMR response was significantly decreased in AT-TBI mice 5- and 6-months post-AT. BRN3A staining showed a loss of RGCs in AT-TBI and AT-Rag Conclusion: These results suggest that the immune system contributes to chronic RGC dysfunction following bTBI.
MeSH term(s)	Mice ; Animals ; Retinal Ganglion Cells/pathology ; Mice, Inbred C57BL ; Disease Models, Animal ; Brain Injuries, Traumatic/complications ; Immunity
Language	English
Publishing date	2022-10-06
Publishing country	England
Document type	Journal Article ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	80122-7
ISSN	1096-0007 ; 0014-4835
ISSN (online)	1096-0007
ISSN	0014-4835
DOI	10.1016/j.exer.2022.109272
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Article ; Online: High Correlation between Glaucoma Treatment with Topical Prostaglandin Analogs and BDNF Immunoreactivity in Human Retina.

Harper, Matthew M / Boese, Erin A / Kardon, Randy H / Ledolter, Johannes / Kuehn, Markus H

Current eye research

2020 Volume 46, Issue 5, Page(s) 739–745

Abstract: Purpose: To examine the expression of brain-derived neurotrophic factor (BDNF) and its high-affinity receptor, tropomyosin-related kinase receptor-B (TrkB), in normal and glaucomatous human retinas.: Methods: Human retinas were collected from 8 ... ...

Abstract	Purpose: To examine the expression of brain-derived neurotrophic factor (BDNF) and its high-affinity receptor, tropomyosin-related kinase receptor-B (TrkB), in normal and glaucomatous human retinas. Methods: Human retinas were collected from 8 donors who had been clinically diagnosed and treated for glaucoma, and from 9 control donors. Immunohistochemical analysis for BDNF and TrkB was performed. The percent of each retina expressing BDNF and TrkB was quantified for the total retinal thickness, and separately for the retinal ganglion cell (RGC) complex + retinal nerve fiber layer (RNFL). The expression of each protein was correlated with clinical outcomes obtained from the subject's ocular histories. Results: There was no significant difference in BDNF or TrkB expression when comparing glaucomatous and control retinas. Correlation analysis revealed a significant relationship between BDNF expression and the use of prostaglandin analogs. TrkB expression was highly correlated with the last-measured intraocular pressure (IOP), the use of carbonic anhydrase inhibitors, the use of beta blockers, and the total number of drugs used for the treatment of glaucoma. Conclusion: Topical drugs used to treat glaucoma were associated with an increase in retinal BDNF and TrkB expression in human retina, independent of IOP, which may represent molecular evidence of neuroprotective pathway activation.
MeSH term(s)	Administration, Ophthalmic ; Aged ; Aged, 80 and over ; Antihypertensive Agents/therapeutic use ; Brain-Derived Neurotrophic Factor/metabolism ; Female ; Glaucoma, Open-Angle/drug therapy ; Glaucoma, Open-Angle/metabolism ; Humans ; Immunohistochemistry ; Intraocular Pressure ; Male ; Membrane Glycoproteins/metabolism ; Middle Aged ; Nerve Fibers/metabolism ; Ophthalmic Solutions ; Prostaglandins, Synthetic/therapeutic use ; Receptor, trkB/metabolism ; Retina/metabolism ; Retinal Ganglion Cells/metabolism
Chemical Substances	Antihypertensive Agents ; Brain-Derived Neurotrophic Factor ; Membrane Glycoproteins ; Ophthalmic Solutions ; Prostaglandins, Synthetic ; BDNF protein, human (7171WSG8A2) ; Receptor, trkB (EC 2.7.10.1) ; tropomyosin-related kinase-B, human (EC 2.7.10.1)
Keywords	covid19
Language	English
Publishing date	2020-09-27
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	82079-9
ISSN	1460-2202 ; 0271-3683
ISSN (online)	1460-2202
ISSN	0271-3683
DOI	10.1080/02713683.2020.1822417
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Article ; Online: Characterization of the Jet-Flow Overpressure Model of Traumatic Brain Injury in Mice.

Shin, Min-Kyoo / Vázquez-Rosa, Edwin / Cintrón-Pérez, Coral J / Riegel, William A / Harper, Matthew M / Ritzel, David / Pieper, Andrew A

Neurotrauma reports

2021 Volume 2, Issue 1, Page(s) 1–13

Abstract: The jet-flow overpressure chamber (OPC) has been previously reported as a model of blast-mediated traumatic brain injury (bTBI). However, rigorous characterization of the features of this injury apparatus shows that it fails to recapitulate exposure to ... ...

Abstract	The jet-flow overpressure chamber (OPC) has been previously reported as a model of blast-mediated traumatic brain injury (bTBI). However, rigorous characterization of the features of this injury apparatus shows that it fails to recapitulate exposure to an isolated blast wave. Through combined experimental and computational modeling analysis of gas-dynamic flow conditions, we show here that the jet-flow OPC produces a collimated high-speed jet flow with extreme dynamic pressure that delivers a severe compressive impulse. Variable rupture dynamics of the diaphragm through which the jet flow originates also generate a weak and infrequent shock front. In addition, there is a component of acceleration-deceleration injury to the head as it is agitated in the headrest. Although not a faithful model of free-field blast exposure, the jet-flow OPC produces a complex multi-modal model of TBI that can be useful in laboratory investigation of putative TBI therapies and fundamental neurophysiological processes after brain injury.
Language	English
Publishing date	2021-01-05
Document type	Journal Article
ISSN	2689-288X
ISSN (online)	2689-288X
DOI	10.1089/neur.2020.0020
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Article ; Online: Neprilysin inhibition promotes corneal wound healing.

Genova, Rachel M / Meyer, Kacie J / Anderson, Michael G / Harper, Matthew M / Pieper, Andrew A

Scientific reports

2018 Volume 8, Issue 1, Page(s) 14385

Abstract: Neprilysin (NEP), an ectoenzyme that modulates inflammation by degrading neuropeptides, was recently identified in the human corneal epithelium. The cornea expresses many NEP substrates, but the function of NEP in homeostatic maintenance and wound ... ...

Abstract	Neprilysin (NEP), an ectoenzyme that modulates inflammation by degrading neuropeptides, was recently identified in the human corneal epithelium. The cornea expresses many NEP substrates, but the function of NEP in homeostatic maintenance and wound healing of the cornea is unknown. We therefore investigated the role of this enzyme under naive and injured conditions using NEP-deficient (NEP
MeSH term(s)	Animals ; Burns, Chemical/drug therapy ; Burns, Chemical/genetics ; Burns, Chemical/pathology ; Cornea/drug effects ; Cornea/metabolism ; Cornea/pathology ; Corneal Injuries/drug therapy ; Corneal Injuries/genetics ; Corneal Injuries/pathology ; Gene Deletion ; Male ; Mice ; Mice, Inbred C57BL ; Neprilysin/antagonists & inhibitors ; Neprilysin/genetics ; Protease Inhibitors/therapeutic use ; Thiorphan/therapeutic use ; Wound Healing/drug effects
Chemical Substances	Protease Inhibitors ; Thiorphan (B79L7B5X3Z) ; Neprilysin (EC 3.4.24.11)
Language	English
Publishing date	2018-09-26
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-018-32773-9
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