scholarly journals Comment on “Calmangafodipir Reduces Sensory Alterations and Prevents Intraepidermal Nerve Fibers Loss in a Mouse Model of Oxaliplatin Induced Peripheral Neurotoxicity” Antioxidants 2020, 9, 594

Antioxidants ◽  
2020 ◽  
Vol 9 (9) ◽  
pp. 802
Author(s):  
Jan Eric Stehr ◽  
Ingemar Lundström ◽  
Jan Olof G. Karlsson
Keyword(s):  
Mouse Model ◽  
Nerve Fibers ◽  
Peripheral Neurotoxicity

We have with enthusiasm read the article “Calmangafodipir Reduces Sensory Alterations and Prevents Intraepidermal Nerve Fibers Loss in a Mouse Model of Oxaliplatin Induced Peripheral Neurotoxicity” written by Annalisa Canta, Guido Cavaletti and co-workers and published in Antioxidants [...]

scholarly journals Reply to a Comment Paper on the Published Paper by Canta, A. et al: “Calmangafodipir Reduces Sensory Alterations and Prevents Intraepidermal Nerve Fibers Loss in a Mouse Model of Oxaliplatin Induced Peripheral Neurotoxicity”—Antioxidants 2020, 9, 594

Antioxidants ◽  
2020 ◽  
Vol 9 (9) ◽  
pp. 807
Author(s):  
Annalisa Canta ◽  
Alessia Chiorazzi ◽  
Eleonora Pozzi ◽  
Giulia Fumagalli ◽  
Laura Monza ◽  
...  
Keyword(s):  
Mouse Model ◽  
Nerve Fiber ◽  
Protective Action ◽  
Mechanisms Of Action ◽  
Nerve Fibers ◽  
Peripheral Neurotoxicity ◽  
Published Paper ◽  
Intraepidermal Nerve Fiber

The comments sent by Stehr, Lundstom and Karlsson with reference to our article “Calmangafodipir reduces sensory alterations and prevents intraepidermal nerve fiber loss in a mouse model of oxaliplatin-induced peripheral neurotoxicity“ are very interesting, since they suggest possible mechanisms of action of the compound, which might contribute to its protective action [...]

scholarly journals Calmangafodipir Reduces Sensory Alterations and Prevents Intraepidermal Nerve Fibers Loss in a Mouse Model of Oxaliplatin Induced Peripheral Neurotoxicity

Antioxidants ◽  
2020 ◽  
Vol 9 (7) ◽  
pp. 594 ◽  
Author(s):  
Annalisa Canta ◽  
Alessia Chiorazzi ◽  
Eleonora Pozzi ◽  
Giulia Fumagalli ◽  
Laura Monza ◽  
...  
Keyword(s):  
Mouse Model ◽  
Thermal Hyperalgesia ◽  
Nerve Fibers ◽  
Peripheral Neurotoxicity ◽  
Mitochondrial Superoxide ◽  
Key Factor ◽  
Skin Biopsies ◽  
Pre Treatment ◽  
Mitochondrial Superoxide Dismutase ◽  
Intraepidermal Nerve Fiber

Oxaliplatin (OHP) is an antineoplastic compound able to induce peripheral neurotoxicity. Oxidative stress has been suggested to be a key factor in the development of OHP-related peripheral neurotoxicity. Mangafodipir, a contrast agent possessing mitochondrial superoxide dismutase (MnSOD)-mimetic activity, has been tested as a cytoprotector in chemotherapy-induced peripheral neurotoxicity (CIPN). Calmangafodipir (PledOx®) has even better therapeutic activity. We investigated a BALB/c mouse model of OHP-related CIPN and the effects of the pre-treatment of calmangafodipir (2.5, 5, or 10 mg/kg intravenously) on sensory perception, and we performed a pathological study on skin biopsies to assess intraepidermal nerve fiber (IENF) density. At the end of the treatments, OHP alone or in pre-treatment with calmangafodipir 2.5 and 10 mg/kg, induced mechanical allodynia and cold thermal hyperalgesia, but calmangafodipir 5 mg/kg prevented these effects. Accordingly, OHP alone or in pre-treatment with calmangafodipir 2.5 and 10 mg/kg, induced a significant reduction in IENF density, but calmangafodipir 5 mg/kg prevented this reduction. These results confirm a protective effect of calmangafodipir against OHP-induced small fiber neuropathy. Interestingly, these results are in agreement with previous observations suggesting a U-shaped effect of calmangafodipir, with the 10 mg/kg dose less effective than the lower doses.

scholarly journals Early loss of peptidergic intraepidermal nerve fibers in an STZ-induced mouse model of insensate diabetic neuropathy

Pain ◽  
2008 ◽  
Vol 140 (1) ◽  
pp. 35-47 ◽  
Author(s):  
Megan S. Johnson ◽  
Janelle M. Ryals ◽  
Douglas E. Wright
Keyword(s):  
Mouse Model ◽  
Diabetic Neuropathy ◽  
Nerve Fibers ◽  
Early Loss

scholarly journals Acute changes in nerve excitability following oxaliplatin treatment in mice

2020 ◽  
Vol 124 (1) ◽  
pp. 232-244
Author(s):  
Preet G. S. Makker ◽  
Daniel White ◽  
Justin G. Lees ◽  
Jasneet Parmar ◽  
David Goldstein ◽  
...  
Keyword(s):  
Peripheral Neuropathy ◽  
Mouse Model ◽  
Intramuscular Injection ◽  
Motor Nerve ◽  
Channel Activity ◽  
Peripheral Neurotoxicity ◽  
Clinical Observations ◽  
Nerve Excitability ◽  
Oxaliplatin Treatment ◽  
Acute Changes

We present a novel mouse model of acute oxaliplatin-induced peripheral neurotoxicity that is comparable to clinical observations. Intramuscular injection of oxaliplatin produced acute changes in motor nerve excitability that were attributable to alterations in Na+ and K+ channel activity. Conversely, we were unable to show any significant changes in nerve excitability with systemic intraperitoneal injections of oxaliplatin. This study suggests that local intramuscular injection is a valid approach for modelling oxaliplatin-induced peripheral neuropathy in animals.

scholarly journals Exercise rather than fluoxetine promotes oligodendrocyte differentiation and myelination in the hippocampus in a male mouse model of depression

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Jing Tang ◽  
Xin Liang ◽  
Xiaoyun Dou ◽  
Yingqiang Qi ◽  
Chunmao Yang ◽  
...  
Keyword(s):  
Mouse Model ◽  
Preference Test ◽  
Nerve Fibers ◽  
Oligodendrocyte Differentiation ◽  
Myelinated Nerve ◽  
Sugar Water ◽  
Running Exercise ◽  
Fluoxetine Treatment ◽  
Sucrose Preference Test ◽  
G Ratio

AbstractAlthough selective serotonin reuptake inhibitor (SSRI) systems have been meaningfully linked to the clinical phenomena of mood disorders, 15–35% of patients do not respond to multiple SSRI interventions or even experience an exacerbation of their condition. As we previously showed, both running exercise and fluoxetine reversed depression-like behavior. However, whether exercise reverses depression-like behavior more quickly than fluoxetine treatment and whether this rapid effect is achieved via the promotion of oligodendrocyte differentiation and/or myelination in the hippocampus was previously unknown. Sixty male C57BL/6 J mice were used in the present study. We subjected mice with unpredictable chronic stress (UCS) to a 4-week running exercise trial (UCS + RN) or intraperitoneally injected them with fluoxetine (UCS + FLX) to address these uncertainties. At the behavioral level, mice in the UCS + RN group consumed significantly more sugar water in the sucrose preference test (SPT) at the end of the 7th week than those in the UCS group, while those in the UCS + FLX group consumed significantly more sugar water than mice in the UCS group at the end of the 8th week. The unbiased stereological results and immunofluorescence analyses revealed that running exercise, and not fluoxetine treatment, increased the numbers of CC1+ and CC1+/Olig2+/BrdU+ oligodendrocytes in the CA1 subfield in depressed mice exposed to UCS. Moreover, running exercise rather than fluoxetine increased the level of myelin basic protein (MBP) and the G-ratio of myelinated nerve fibers in the CA1 subfield in the UCS mouse model. Unlike fluoxetine, exercise promoted hippocampal myelination and oligodendrocyte differentiation and thus has potential as a therapeutic strategy to reduce depression-like behaviors induced by UCS.

scholarly journals Mechanical Hypersensitivity and Alterations in Cutaneous Nerve Fibers in a Mouse Model of Skin Cancer Pain

2003 ◽  
Vol 91 (2) ◽  
pp. 167-170 ◽  
Author(s):  
Hong-Wei Zhang ◽  
Yuko Iida ◽  
Tsugunobu Andoh ◽  
Hiroshi Nojima ◽  
Jun Murata ◽  
...  
Keyword(s):  
Skin Cancer ◽  
Mouse Model ◽  
Cancer Pain ◽  
Nerve Fibers ◽  
Cutaneous Nerve ◽  
Mechanical Hypersensitivity

scholarly journals Neuroplasticity of sensory and sympathetic nerve fibers in a mouse model of a painful arthritic joint

2012 ◽  
Vol 64 (7) ◽  
pp. 2223-2232 ◽  
Author(s):  
Joseph R. Ghilardi ◽  
Katie T. Freeman ◽  
Juan M. Jimenez-Andrade ◽  
Kathleen A. Coughlin ◽  
Magdalena J. Kaczmarska ◽  
...  
Keyword(s):  
Mouse Model ◽  
Sympathetic Nerve ◽  
Nerve Fibers ◽  
Arthritic Joint ◽  
Sympathetic Nerve Fibers

scholarly journals Nociceptive mechanisms driving pain in a post-traumatic osteoarthritis mouse model

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
C. J. Alves ◽  
M. Couto ◽  
D. M. Sousa ◽  
A. Magalhães ◽  
E. Neto ◽  
...  
Keyword(s):  
Mouse Model ◽  
Sensory Nerve ◽  
Nerve Fibers ◽  
Peripheral Sensitization ◽  
Therapeutic Approaches ◽  
Calcitonin Gene ◽  
Peripheral Pain ◽  
Pain Sensitization ◽  
Post Traumatic ◽  
Sensory Nervous System

Abstract In osteoarthritis (OA), pain is the dominant clinical symptom, yet the therapeutic approaches remain inadequate. The knowledge of the nociceptive mechanisms in OA, which will allow to develop effective therapies for OA pain, is of utmost need. In this study, we investigated the nociceptive mechanisms involved in post-traumatic OA pain, using the destabilization of the medial meniscus (DMM) mouse model. Our results revealed the development of peripheral pain sensitization, reflected by augmented mechanical allodynia. Along with the development of pain behaviour, we observed an increase in the expression of calcitonin gene-related peptide (CGRP) in both the sensory nerve fibers of the periosteum and the dorsal root ganglia. Interestingly, we also observed that other nociceptive mechanisms commonly described in non-traumatic OA phenotypes, such as infiltration of the synovium by immune cells, neuropathic mechanisms and also central sensitization were not present. Overall, our results suggest that CGRP in the sensory nervous system is underlying the peripheral sensitization observed after traumatic knee injury in the DMM model, highlighting the CGRP as a putative therapeutic target to treat pain in post-traumatic OA. Moreover, our findings suggest that the nociceptive mechanisms involved in driving pain in post-traumatic OA are considerably different from those in non-traumatic OA.

scholarly journals Dynamic Changes in the Nigrostriatal Pathway in the MPTP Mouse Model of Parkinson’s Disease

2017 ◽  
Vol 2017 ◽  
pp. 1-7 ◽  
Author(s):  
Dongping Huang ◽  
Jing Xu ◽  
Jinghui Wang ◽  
Jiabin Tong ◽  
Xiaochen Bai ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Mouse Model ◽  
Therapeutic Strategies ◽  
Nerve Fibers ◽  
Substantia Nigra Pars Compacta ◽  
Nigrostriatal Pathway ◽  
Brain Pathology ◽  
Nonmotor Symptoms ◽  
Dynamic Changes

The characteristic brain pathology and motor and nonmotor symptoms of Parkinson’s disease (PD) are well established. However, the details regarding the causes of the disease and its course are much less clear. Animal models have significantly enriched our current understanding of the progression of this disease. Among various neurotoxin-based models of PD, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model is the most commonly studied model. Here, we provide an overview of the dynamic changes in the nigrostriatal pathway in the MPTP mouse model of PD. Pathophysiological events, such as reductions in the striatal dopamine (DA) concentrations and levels of the tyrosine hydroxylase (TH) protein, depletion of TH-positive nerve fibers, a decrease in the number of TH-positive neurons in the substantia nigra pars compacta (SNpc), and glial activation, are addressed. This article will assist with the development of interventions or therapeutic strategies for PD.

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