Pressure Hyperalgesia in Hind Limb Suspended Rats

Chowdhury, Parimal; Soulsby, Michael; Jayroe, John; Akel, Nisreen; Gaddy, Dana; Dobretsov, Maxim

doi:10.3357/asem.3063.2011

Cited by 9 publications

(17 citation statements)

References 10 publications

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“…Analysis of filtered data measured in this way have confirmed previous findings (Chowdhury et al. ) of decreased PPT in groups of tail‐HLS animals, and demonstrate for the first time that both tail‐ and pelvic‐HLS rats have similarly decreased PPT (relative to control and relative to baseline PPT level, asterisks in Fig. C).…”

Section: Resultssupporting

confidence: 88%

“…In addition, these findings confirm the recent observation (Chowdhury et al. ) of decreasing PPT of the hindlimb paw in HLS rats. The novel observations of this study are that despite sharply different effects of tail‐ and pelvic‐HLS techniques on mechanical loads experienced by the lower spine of the rat, the above mentioned effects of HLS developed similarly in both models.…”

Section: Discussionsupporting

confidence: 92%

“…Recently, however, we provided the evidence of pressure hyperalgesia developing in tail‐HLS rats, as well as an indication that this could be associated with insulinopenia (Chowdhury et al. ). Here, we determined whether the PPT and associated insulinopenia was comparable in the tail‐HLS and the pelvic‐HLS animals.…”

Section: Resultsmentioning

confidence: 98%

“…; Chowdhury et al. ) with a possible link of this prediabetic state to the development of deep pressure hyperalgesia.…”

Section: Discussionmentioning

confidence: 99%

“…) and muscle pain in tail‐HLS rats (Chowdhury et al. ). These problems may be related to both the back pain and gastrointestinal problems reported by a majority of astronauts and bed‐ridden human patients (Styf et al.…”

Section: Introductionmentioning

confidence: 99%

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Animal model of simulated microgravity: a comparative study of hindlimb unloading via tail versus pelvic suspension

et al. 2013

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The aim of this study was to compare physiological effects of hindlimb suspension (HLS) in tail- and pelvic-HLS rat models to determine if severe stretch in the tail-HLS rats lumbosacral skeleton may contribute to the changes traditionally attributed to simulated microgravity and musculoskeletal disuse in the tail-HLS model. Adult male Sprague-Dawley rats divided into suspended and control-nonsuspended groups were subjected to two separate methods of suspension and maintained with regular food and water for 2 weeks. Body weights, food and water consumption, soleus muscle weight, tibial bone mineral density, random plasma insulin, and hindlimb pain on pressure threshold (PPT) were measured. X-ray analysis demonstrated severe lordosis in tail- but not pelvic-HLS animals. However, growth retardation, food consumption, and soleus muscle weight and tibial bone density (decreased relative to control) did not differ between two HLS models. Furthermore, HLS rats developed similar levels of insulinopenia and mechanical hyperalgesia (decreased PPT) in both tail- and pelvic-HLS groups. In the rat-to-rat comparisons, the growth retardation and the decreased PPT observed in HLS-rats was most associated with insulinopenia. In conclusion, these data suggest that HLS results in mild prediabetic state with some signs of pressure hyperalgesia, but lumbosacral skeleton stretch plays little role, if any, in these pathological changes.

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Section: Resultssupporting

confidence: 88%

Section: Discussionsupporting

confidence: 92%

Section: Resultsmentioning

confidence: 98%

“…; Chowdhury et al. ) with a possible link of this prediabetic state to the development of deep pressure hyperalgesia.…”

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Animal model of simulated microgravity: a comparative study of hindlimb unloading via tail versus pelvic suspension

et al. 2013

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Simulated microgravity‐induced oxidative stress and loss of osteogenic potential of osteoblasts can be prevented by protection of primary cilia

Miao,

Liu,

Sun

et al. 2023

Journal Cellular Physiology

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Oxidative stress has been considered to be closely related to spaceflight‐induced bone loss; however, mechanism is elusive and there are no effective countermeasures. Using cultured rat calvarial osteoblasts exposed to microgravity simulated by a random positioning machine, this study addressed the hypotheses that microgravity‐induced shortening of primary cilia leads to oxidative stress and that primary cilium protection prevents oxidative stress and osteogenesis loss. Microgravity was found to induce oxidative stress (as represented by increased levels of reactive oxygen species (ROS) and malondialdehyde production, and decreased activities of antioxidant enzymes), which was perfectly replicated in osteoblasts growing in NG with abrogated primary cilia (created by transfection of an interfering RNA), suggesting the possibility that shortening of primary cilia leads to oxidative stress. Oxidative stress was accompanied by mitochondrial dysfunction (represented by increased mitochondrial ROS and decreased mitochondrial membrane potential) and intracellular Ca2+ overload, and the latter was found to be caused by increased activity of Ca2+ channel transient receptor potential vanilloid 4 (TRPV4), as also evidenced by TRPV4 agonist GSK1016790A‐elicited Ca2+ influx. Supplementation of HC‐067047, a specific antagonist of TRPV4, attenuated microgravity‐induced mitochondrial dysfunction, oxidative stress, and osteogenesis loss. Although TRPV4 was found localized in primary cilia and expressed at low levels in NG, microgravity‐induced shortening of primary cilia led to increased TRPV4 levels and Ca2+ influx. When primary cilia were protected by miR‐129‐3p overexpression or supplementation with a natural flavonoid moslosooflavone, microgravity‐induced increased TRPV4 expression, mitochondrial dysfunction, oxidative stress, and osteogenesis loss were all prevented. Our data revealed a new mechanism that primary cilia function as a controller for TRPV4 expression. Microgravity‐induced injury on primary cilia leads to increased expression and overactive channel of TRPV4, causing intracellular Ca2+ overload and oxidative stress, and primary cilium protection could be an effective countermeasure against microgravity‐induced oxidative stress and loss of osteogenic potential of osteoblasts.

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The analysis of antioxidant expression during muscle atrophy induced by hindlimb suspension in mice

et al. 2016

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Oxidative stress contributes to acceleration of muscle atrophy. However, it is still not completely understood what triggers the production of reactive oxygen species (ROS) during muscle atrophy. The objective of this study was to investigate redox balance during muscle atrophy. ROS generators and antioxidants were analyzed in atrophied soleus muscles after 2 weeks of hindlimb suspension (HLS) in mice. The HLS group showed an increase in lipid peroxidation, upregulated NOX1 and NOXO1, and downregulated mitochondrial complex I subunits NDUFS5 and NDUFV2. Additionally, HLS mice demonstrated a decrease in Prdx5 and MnSOD, but an increase in GPX2 and GPX3 in both mRNA and protein levels. As expected, MnSOD activity declined in the HLS group, while GPX activity was enhanced. These results suggest that redox imbalance occurs during muscle atrophy through NOX1 activation, mitochondrial complex I deficiency, and disturbance of antioxidants. Antioxidants altered by HLS may represent potential therapeutic targets for the protection against muscle atrophy.

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Pressure Hyperalgesia in Hind Limb Suspended Rats

Cited by 9 publications

References 10 publications

Animal model of simulated microgravity: a comparative study of hindlimb unloading via tail versus pelvic suspension

Animal model of simulated microgravity: a comparative study of hindlimb unloading via tail versus pelvic suspension

Simulated microgravity‐induced oxidative stress and loss of osteogenic potential of osteoblasts can be prevented by protection of primary cilia

The analysis of antioxidant expression during muscle atrophy induced by hindlimb suspension in mice

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