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VON FREY FILAMENTS
(Model: Bio-VF-M)
A set of 20 monofilaments based on the Semmes Weinstein monofilament set - featuring retractable filaments to protect the filament and allow the investigator to carry a few around in a pocket

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! NEW RESEARCH WORK ! A recent publication by BR Choi, SJ Kang, JL Kim, YJ Lee, SK Ku in "Natural Product Communications" highlights the merits of using Bioseb's Von Frey Filaments: Effects of Pomegranate Concentrate Powder: Eucommiae Cortex: Achyranthis Radix 5: 4: 1 (w/w) Mixed Formula on Monosodium Iodoacetate-Induced Osteoarthritis

Effects of Pomegranate Concentrate Powder: Eucommiae Cortex: Achyranthis Radix 5: 4: 1 (w/w) Mixed Formula on Monosodium Iodoacetate-Induced Osteoarthritis
BR Choi, SJ Kang, JL Kim, YJ Lee, SK Ku
Department of Preventive Medicine, College of Korean Medicine, Daegu Haany University, Republic of Korea.
Published in "Natural Product Communications" (2020-03-30)


We examined the antiosteoarthritis effect of a mixture of powdered pomegranate concentrate, eucommiae cortex, and achyranthis radix (5:4:1 w/w) (PEA-Mix). After the injection of monosodium iodoacetate (MIA), PEA-Mixs were orally administered. To assess pain-related behaviors, a von Frey filament test and open field test were performed. We also examined the knee thickness, maximum knee extension angle, bone mineral density (BMD), and compressive strength of the knee joint and performed a histopathologic analysis. The number of COX-2, tumor necrosis factor (TNF)-alpha, poly (ADP-ribose) polymerase (PARP), and 5-bromo-2_-deoxyuridine immunoreactive cells, the prostaglandin E2 (PGE2) and 5-lipoxygenase (LPO) levels, matrix metalloproteinase (MMP) activity, and mRNA levels of chondrogenesis-related genes were analyzed. PEA-Mix significantly inhibited the MIA-induced decrease in the paw-withdrawal threshold and total distance moved, and the MIA-induced increases in the maximum knee extension angle and knee thickness. Also, the MIA-induced loss of the knee joint articular surface region and decrease in the BMD were significantly suppressed by PEA-Mix. The MIA-induced increases in the 5-LPO, PGE2, MMP-2, MMP-9, COX-2, and TNF-_ mRNA levels were reduced by PEA-Mix. PEA-Mix increased the MIA-mediated reduction in the SOX-9 and aggrecan mRNA levels. The number of PARP-positive cells was smaller in PEA-Mix-administered rats than in MIA-administered rats, while the number of 5-bromo-2_-deoxyuridine-positive cells was larger. Therefore, PEA-Mix relieved the MIA-induced pain-related behaviors, chondrocyte proliferation, and anti-inflammatory activity.
This set of 20 monofilaments is based on the Semmes Weinstein monofilament set, but now features retractable filaments to protect the filament and allow the investigator to carry a few around in a pocket.


The Semmes Weinstein set of monofilaments provide an approximately logarithmic scale of actual force, and a linear scale of perceived intensity. They have a long history of effective use in clinical settings, and can be used to diagnose pathologies of hyper- or hypo-aesthesia. Subsets within the set of 20 probes distinguish pathologies on different parts of the body (foot, hand, lip, cheek, etc.).

The operating principle remains the same: when the tip of a fiber of given length and diameter is pressed against the skin at right angles, the force of application increases as long as the researcher continues to advance the probe, until the fiber bends. After the fiber bends, continued advance creates more bend, but not more force of application. This principle makes it possible for the researcher using a hand held probe to apply a reproducible force, within a wide tolerance, to the skin surface.

Size 1,652,362,442,833,223,613,844,08 4,174,314,564,744,935,075,185,46 5,886,16,456,65
Force (g) 0,0080,020,040,070,160,40,61 1,42468101526 60100180300

Rodents exhibit a paw withdrawal reflex when the paw is unexpectedly touched. The Touch Test™ Sensory Evaluator can be used on the Plantar surfaces of the foot of a rat or mouse, and the animal will indicate sensation by pulling back its paw. Replacement filaments available.

Attention : Because of the physical properties of the material making up the filaments it's recommended to work at temperature between 18°C an 24°C and hygrometry between 60 and 80 %, for a better reliability of the results.

Publications (Click on an article to show details and read the abstract)

• PAIN •
- General pain -
• Genetic ablation of GINIP-expressing primary sensory neurons strongly impairs Formalin-evoked pain. (2017)
Genetic ablation of GINIP-expressing primary sensory neurons strongly impairs Formalin-evoked pain.
Urien L, Gaillard S, Lo Re L, Malapert P, Bohic M, Reynders A, Moqrich A
"Aix-Marseille-Université, Institut de Biologie du Développement de Marseille, Marseille, France "
Published in "Scientific Reports" (2017-02-17)

Primary sensory neurons are heterogeneous by myriad of molecular criteria. However, the functional significance of this remarkable heterogeneity is just emerging. We precedently described the GINIP(+) neurons as a new subpopulation of non peptidergic C-fibers encompassing the free nerve ending cutaneous MRGPRD(+) neurons and C-LTMRs. Using our recently generated ginip mouse model, we have been able to selectively ablate the GINIP(+) neurons and assess their functional role in the somatosensation. We found that ablation of GINIP(+) neurons affected neither the molecular contents nor the central projections of the spared neurons. GINIP-DTR mice exhibited impaired sensation to gentle mechanical stimuli applied to their hairy skin and had normal responses to noxious mechanical stimuli applied to their glabrous skin, under acute and injury-induced conditions. Importantly, loss of GINIP(+) neurons significantly altered formalin-evoked first pain and drastically suppressed the second pain response. Given that MRGPRD(+) neurons have been shown to be dispensable for formalin-evoked pain, our study suggest that C-LTMRs play a critical role in the modulation of formalin-evoked pain.

- Mechanical allodynia & hyperlagesia -
• Beneficial effects of fish oil enriched in omega_3 fatty acids on the development and maintenance of neuropathic pain (2019)
Beneficial effects of fish oil enriched in omega_3 fatty acids on the development and maintenance of neuropathic pain
SR Unda, EA Villegas, ME Toledo, GA Onell, CH Laino
Biotechnology Institute, Research and Technological Innovation Center (CENIIT)_National University of La Rioja, Av. Luis M de la Fuente SN, 5300 La Rioja, Argentina.
Published in "Journal of Pharmacy and Pharmacology" (2019-12-26)

The aim of this work was to assess the preventive effect of an eicosapentaenoic acid/docosahexaenoic acid_concentrate fish oil on neuropathic pain development and regenerative features of sciatic nerve in rats.

• Efficacy of multimodal analgesic treatment of severe traumatic acute pain in mice pretreated with chronic high dose of buprenorphine inducing mechanical allodynia (2019)
Efficacy of multimodal analgesic treatment of severe traumatic acute pain in mice pretreated with chronic high dose of buprenorphine inducing mechanical allodynia
B Coutens, C Derreumaux, F Labaste, V Minville et el
Centre de Recherches sur la Cognition Animale (CRCA), Centre de Biologie Intégrative (CBI), Toulouse, France
Published in "European Journal of Pharmacology" (2019-12-18)

Managing severe acute nociceptive pain in buprenorphine-maintained individuals for opioid use disorder management is challenging owing to the high affinity and very slow dissociation of buprenorphine from _-opioid receptors that hinders the use of full agonist opioid analgesics. In a translational approach, the aim of this study was to use an animal setting to investigate the effects of a chronic high dose of buprenorphine treatment on nociceptive thresholds before and after applying a severe acute nociceptive traumatic surgery stimulus and to screen postoperative pharmacological analgesic strategies. A chronic treatment of mice with a high dose of buprenorphine (BUP HD, 2 × 200 _g/kg/day; i.p.) revealed significant mechanical allodynia. One and two days after having discontinued buprenorphine administration and having induced a severe nociceptive acute pain by a closed tibial fracture, acute administration of morphine at a dose which has analgesic effects in absence of pretreatment (4.5 mg/kg; i.p.), was ineffective to reduce pain in the BUP HD group. However, mimicking multimodal analgesia strategy used in human postoperative context, the combination of morphine (administered at the same dose) with a NMDA receptor antagonist (ketamine) or an NSAID (ketoprofen) produced antinociceptive responses in these animals. The mouse model of closed tibial fracture could be useful to identify analgesic strategies of postoperative pain for patients with chronic exposure to opioids and suffering from hyperalgesia.

• Urinary K+ promotes irritative voiding symptoms and pain in the face of urothelial barrier dysfunction (2019)
Urinary K+ promotes irritative voiding symptoms and pain in the face of urothelial barrier dysfunction
N Montalbetti, SD Stocker, G Apodaca, SI Bastacky et al
Department of Cell Biology, University of Pittsburgh, Pittsburgh, Pennsylvania, USA
Published in "Scientific Reports" (2019-04-02)

The internal surface of the bladder is lined by the urothelium, a stratified epithelium that forms an impermeable barrier to water and urine constituents. Abnormalities in the urothelial barrier have been described in certain forms of cystitis and were hypothesized to contribute to irritative voiding symptoms and pain by allowing the permeation of urinary K+ into suburothelial tissues, which then alters afferent signaling and smooth muscle function. Here, we examined the mechanisms underlying organ hyperactivity and pain in a model of cystitis caused by adenoviral-mediated expression of claudin-2 (Cldn2), a tight junction protein that forms paracellular pores and increases urothelial permeability. We found that in the presence of a leaky urothelium, intravesical K+ sensitizes bladder afferents and enhances their response to distension. Notably, dietary K+ restriction, a maneuver that reduces urinary K+, prevented the development of pelvic allodynia and inflammation seen in rats expressing Cldn2. Most importantly, intravesical K+ causes and is required to maintain bladder hyperactivity in rats with increased urothelial permeability. Our study demonstrates that in the face of a leaky urothelium, urinary K+ is the main determinant of afferent hyperexcitability, organ hyperactivity and pain. These findings support the notion that voiding symptoms and pain seen in forms of cystitis that coexist with urothelial barrier dysfunction could be alleviated by cutting urinary K+ levels.

• Action of MK_7264 (Gefapixant) at human P2X3 and P2X2/3 receptors and in vivo efficacy in models of sensitisation (2019)
Action of MK_7264 (Gefapixant) at human P2X3 and P2X2/3 receptors and in vivo efficacy in models of sensitisation
D Richards, JR Gever, AP Ford, SJ Fountain
Biomedical Research Centre, School of Biological Sciences, University of East Anglia, Norwich, UK
Published in "British Journal of Pharmacology" (2019-03-30)

The P2X3 receptor is an ATP_gated ion channel expressed by sensory afferent neurons and is used as a target to treat chronic sensitisation conditions. The first_in_class, selective P2X3 and P2X2/3 receptor antagonist, the diaminopyrimidine MK_7264 (gefapixant), has progressed to Phase III trials for refractory or unexplained chronic cough. We used patch clamp to elucidate the pharmacology and kinetics of MK_7264 and rat models of hypersensitivity and hyperalgesia to test its efficacy on these conditions.

• 5-HT2A receptor-induced morphological reorganization of PKC_-expressing interneurons gates inflammatory mechanical allodynia in rat (2018)
5-HT2A receptor-induced morphological reorganization of PKC_-expressing interneurons gates inflammatory mechanical allodynia in rat
C Alba-Delgado, S Mountadem, N Mermet-Joret et al

Published in "Journal of Neuroscience" (2018-10-24)

Mechanical allodynia, a widespread pain symptom which still lacks effective therapy, is associated with the activation of a dorsally-directed polysynaptic circuit within spinal (SDH) or medullary dorsal horn (MDH), whereby tactile inputs into deep SDH/MDH can gain access to superficial SDH/MDH, eliciting pain. Inner lamina II (IIi) interneurons expressing the _ isoform of protein kinase C (PKC_+) are key elements for allodynia circuits but how they operate is still unclear. Combining behavioral, ex vivo electrophysiological and morphological approaches in an adult rat model of facial inflammatory pain (Complete Freund's Adjuvant, CFA), we show that the mechanical allodynia observed 1h after CFA injection is associated with i) sensitization (using ERK1/2 phosphorylation as a marker) and ii) reduced dendritic arborizations and enhanced spine density-in exclusively PKC_+ interneurons, but iii) depolarized resting membrane potential (RMP) in all lamina IIi PKC_+/PKC_- interneurons. Blocking MDH 5HT2A receptors (5-HT2AR) prevents facial mechanical allodynia and associated changes in the morphology of PKC_+ interneurons, but not depolarized RMP in lamina IIi interneurons. Finally, activation of MDH 5-HT2AR in naïve animals is enough to reproduce the behavioral allodynia and morphological changes in PKC_+ interneurons, but not the electrophysiological changes in lamina IIi interneurons, induced by facial inflammation. This suggests that inflammation-induced mechanical allodynia involves strong morphological reorganization of PKC_+ interneurons via 5-HT2AR activation that contributes to open the gate for transmission of innocuous mechanical inputs to superficial SDH/MDH pain circuitry. Preventing 5-HT2AR-induced structural plasticity in PKC_+ interneurons might represent new avenues for the specific treatment of inflammation-induced mechanical hypersensitivity.




Model:
Bio-VF-M
Von Frey Filaments
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Accessories :
BIO-PVF
Modular holder cages for rats and mice
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