Repeat low-level blast exposure increases transient receptor potential vanilloid 1 (TRPV1) and endothelin-1 (ET-1) expression in the trigeminal ganglion

Por, Elaine D.; Sandoval, Melody; Thomas-Benson, Chiquita; Burke, Teresa A; Brackley, Allison Doyle; Jeske, Nathaniel Aaron; Cleland, Jeffery; Lund, Brian J.

doi:10.1371/journal.pone.0182102

Cited by 7 publications

(3 citation statements)

References 65 publications

(78 reference statements)

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“…Neutrophil infiltrates were also found in corneal stromal layers following blast injury with concurrent increases in pain and inflammatory signaling mediators such as the transient receptor potential vanilloid 1 (TRPV1) channel, calcitonin gene-related peptide (CGRP), substance P (SP), and endothelin-1 (ET-1). Increases in hematic myeloperoxidase (MPO), a peroxidase enzyme released during the degranulation and activation of neutrophils, were also reported (Por et al, 2017).…”

Section: Inflammatory Over-activation Following Btbimentioning

confidence: 96%

Visual Outcomes in Experimental Rodent Models of Blast-Mediated Traumatic Brain Injury

Evans

Roghair

Gilkes

et al. 2021

Front. Mol. Neurosci.

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Blast-mediated traumatic brain injuries (bTBI) cause long-lasting physical, cognitive, and psychological disorders, including persistent visual impairment. No known therapies are currently utilized in humans to lessen the lingering and often serious symptoms. With TBI mortality decreasing due to advancements in medical and protective technologies, there is growing interest in understanding the pathology of visual dysfunction after bTBI. However, this is complicated by numerous variables, e.g., injury location, severity, and head and body shielding. This review summarizes the visual outcomes observed by various, current experimental rodent models of bTBI, and identifies data showing that bTBI activates inflammatory and apoptotic signaling leading to visual dysfunction. Pharmacologic treatments blocking inflammation and cell death pathways reported to alleviate visual deficits in post-bTBI animal models are discussed. Notably, techniques for assessing bTBI outcomes across exposure paradigms differed widely, so we urge future studies to compare multiple models of blast injury, to allow data to be directly compared.

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Section: Inflammatory Over-activation Following Btbimentioning

confidence: 96%

Visual Outcomes in Experimental Rodent Models of Blast-Mediated Traumatic Brain Injury

Evans

Roghair

Gilkes

et al. 2021

Front. Mol. Neurosci.

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“…Neutrophil infiltration was significant only in multiple exposed animals. A study utilizing the same set of exposure conditions and biomarkers supplemented with ET-A and Ca 2+ imaging, found increased levels of TRPV1 and ET-1 in trigeminal ganglion (31).…”

Section: Repeated Blast Tbi Rodent Models: An Overview Of the Experimmentioning

confidence: 99%

A Comprehensive Review of Experimental Rodent Models of Repeated Blast TBI

et al. 2019

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We reviewed the relevant literature delineating advances in the development of the experimental models of repeated blast TBI (rbTBI). It appears this subject is a relatively unexplored area considering the first work published in 2007 and the bulk of peer-reviewed papers was published post-2011. There are merely 34 papers published to date utilizing rodent rbTBI models. We performed an analysis and extracted basic parameters to capture the characteristics of the exposure conditions (the blast intensity, inter-exposure interval and the number of exposures), the age and weight of the animal models most commonly used in the studies, and their endpoints. Our analysis revealed three strains of rodents are predominantly used: Sprague Dawley and Long Evans rats and wild type (C57BL/6J) mice, and young adult animals 8 to 12-week-old are a preferred choice. Typical exposure conditions are the following: (1) peak overpressure in the 27–145 kPa (4–21 psi) range, (2) number of exposures: 2 (13.9%), 3 (63.9%), 5 (16.7%), or 12 (5.6%) with a single exposure used for a baseline comparison in 41.24% of the studies. Two inter-exposure interval durations were used: (1) short (1–30 min.) and (2) extended (24 h) between consecutive shock wave exposures. The experiments included characterization of repeated blast exposure effects on auditory, ocular and neurological function, with a focus on brain etiology in most of the published work. We present an overview of major histopathological findings, which are supplemented by studies implementing MRI (DTI) and behavioral changes after rbTBI in the acute (1–7 days post-injury), subacute (7–14 days), and chronic (>14 days) phases post-injury.

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“…Tooth pump inflammation showed many GFAP-immunoreactive cells and an increase in TRPV1 immunoreactivity in the second branch region of the trigeminal ganglion and simultaneously decreased the threshold to noxious heat stimuli (Watase et al, 2018 ). Exposure to repetitive tertiary blast resulted in increases in TRPV1, endothelin-1, and GFAP expression in the trigeminal ganglion, and enhanced nociception through a decrease in the desensitization of TRPV1 in the cornea (Por et al, 2017 ). Donegan et al ( 2013 ) suggested that the enhancement of GFAP expression in the ganglion plays a crucial role in the maintenance of neuropathic pain.…”

Section: Discussionmentioning

confidence: 99%

Chronic Tear Deficiency Sensitizes Transient Receptor Potential Vanilloid 1-Mediated Responses in Corneal Sensory Nerves

Masuoka

Yamashita

Nakano

et al. 2020

Front. Cell. Neurosci.

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Chronic tear deficiency enhances the excitability of corneal cold-sensitive nerves that detect ocular dryness, which can lead to discomfort in patients with dry eye disease (DED). However, changes in corneal nerve excitations through the polymodal nociceptor “transient receptor potential vanilloid 1” (TRPV1) and the potential link between this receptor and symptoms of DED remain unclear. In this study, we examined the firing properties of corneal cold-sensitive nerves expressing TRPV1 and possible contributions of chronic tear deficiency to corneal nerve excitability by TRPV1 activation. The bilateral excision of lacrimal glands in guinea pigs decreased the tear volume and increased the frequency of spontaneous eyeblinks 1–4 weeks after surgery. An analysis of the firing properties of the cold-sensitive nerves was performed by single-unit recordings of corneal preparations 4 weeks after surgery in both the sham-operated and gland-excised groups. Perfusion of the TRPV1 agonist, capsaicin (1 μM), transiently increased the firing frequency in approximately 46–48% of the cold-sensitive nerves characterized by low-background activity and high threshold (LB-HT) cold thermoreceptors in both groups. Gland excision significantly decreased the latency of capsaicin-induced firing in cold-sensitive nerves; however, its magnitude was unchanged. Calcium imaging of cultured trigeminal ganglion neurons from both groups showed that intracellular calcium elevation of corneal neurons induced by a low concentration of capsaicin (0.03 μM) was significantly larger in the gland excision group, regardless of responsiveness to cold. An immunohistochemical study of the trigeminal ganglion revealed that gland excision significantly increased the proportion of corneal neurons enclosed by glial fibrillary acidic protein (GFAP)-immunopositive satellite glial cells. Topical application of the TRPV1 antagonist, A784168 (30 μM), on the ocular surface attenuated eye-blink frequency after gland excision. Furthermore, gland excision enhanced blink behavior induced by a low concentration of capsaicin (0.1 μM). These results suggest that chronic tear deficiency sensitizes the TRPV1-mediated response in the corneal LB-HT cold thermoreceptors and cold-insensitive polymodal nociceptors, which may be linked to dry eye discomfort and hyperalgesia resulting from nociceptive stimuli in aqueous-deficient dry eyes.

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Repeat low-level blast exposure increases transient receptor potential vanilloid 1 (TRPV1) and endothelin-1 (ET-1) expression in the trigeminal ganglion

Cited by 7 publications

References 65 publications

Visual Outcomes in Experimental Rodent Models of Blast-Mediated Traumatic Brain Injury

Visual Outcomes in Experimental Rodent Models of Blast-Mediated Traumatic Brain Injury

A Comprehensive Review of Experimental Rodent Models of Repeated Blast TBI

Chronic Tear Deficiency Sensitizes Transient Receptor Potential Vanilloid 1-Mediated Responses in Corneal Sensory Nerves

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