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COLD HOT PLATE TEST
(Model: BIO-CHP)
For testing animal's thermal sensitivity to pain resulting from exposure to heat or cold: the Cold Hot Plate is an innovative instrument opening new investigation fields for your analgesia and nociception research, and a useful tool for analgesic drug screening using rats or mice models.

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  • HARVARD MEDICAL SCHOOL Charlestown, Etats-Unis
  • INMED Marseille, France
  • BIOCODEX Compiegne, France
  • UNIL Lausanne, Suisse
  • COLLEGE DE FRANCE Paris, France
  • ESPCI Paris, France
  • INSTITUT DE RECHERCHE PIERRE FABRE Castres, France
  • NEUROFIT Illkirch, France
  • ESPCI Paris, France
  • BIOCODEX Compičgne,France
  • INSERM Clermont-Ferrand, Paris, Bordeaux, Marseille,France
  • MEDICAL UNIVERSITY OF SILESIA Katowice, Pologne
  • CNRS Orleans, Caen, Strasbourg, Valbonne, France
  • SANOFI AVENTIS Vitry sur Seine, Montpellier, France
  • UNIVERSITY OF HEIDELBERG Heidelberg, Allemagne
  • PORSOLT AND PARTNERS PHARMACOLOGY Le Genest St Isle,France
  • IGBMC Strasbourg, France
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! NEW RESEARCH WORK ! A recent publication by M Iftinca, L Basso, R Flynn, C Kwok, C Roland et al in "Molecular Brain" highlights the merits of using Bioseb's Cold Hot Plate Test: Chronic morphine regulates TRPM8 channels via MOR-PKCbeta signaling

Chronic morphine regulates TRPM8 channels via MOR-PKCbeta signaling
M Iftinca, L Basso, R Flynn, C Kwok, C Roland et al
Department of Physiology and Pharmacology, Inflammation Research Network-Snyder Institute for Chronic Diseases and Alberta Children
Published in "Molecular Brain" (2020-04-14)


Postoperative shivering and cold hypersensitivity are major side effects of acute and chronic opioid treatments respectively. TRPM8 is a cold and menthol-sensitive channel found in a subset of dorsal root ganglion (DRG) nociceptors. Deletion or inhibition of the TRPM8 channel was found to prevent the cold hyperalgesia induced by chronic administration of morphine. Here, we examined the mechanisms by which morphine was able to promote cold hypersensitivity in DRG neurons and transfected HEK cells. Mice daily injected with morphine for 5 days developed cold hyperalgesia. Treatment with morphine did not alter the expressions of cold sensitive TREK-1, TRAAK and TRPM8 in DRGs. However, TRPM8-expressing DRG neurons isolated from morphine-treated mice exhibited hyperexcitability. Sustained morphine treatment in vitro sensitized TRPM8 responsiveness to cold or menthol and reduced activation-evoked desensitization of the channel. Blocking phospholipase C (PLC) as well as protein kinase C beta (PKCbeta), but not protein kinase A (PKA) or Rho-associated protein kinase (ROCK), restored channel desensitization. Identification of two PKC phosphorylation consensus sites, S1040 and S1041, in the TRPM8 and their site-directed mutation were able to prevent the MOR-induced reduction in TRPM8 desensitization. Our results show that activation of MOR by morphine 1) promotes hyperexcitability of TRPM8-expressing neurons and 2) induces a PKCbeta-mediated reduction of TRPM8 desensitization. This MOR-PKCbeta dependent modulation of TRPM8 may underlie the onset of cold hyperalgesia caused by repeated administration of morphine. Our findings point to TRPM8 channel and PKCbeta as important targets for opioid-induced cold hypersensitivity.
Presentation

Bioseb’s Cold and Hot Plate Test is an innovative instrument opening new investigation fields for your analgesia research by allowing you to test animal's sensitivity to pain resulting from exposure to heat or cold.

This innovative Analgesia Meter is based on a metal plate which can be heated to 55°C and cooled to -2°C (with an ambient temperature between 20°C and 25°C). An electronic thermostat maintains the plate's temperature and a front panel digital thermometer displays the current plate temperature.

The Bioseb Cold and Hot Plate is designed to be very simple to use and very fast to reach the set temperature (as example From ambient to 4°C, the most used threshold value, it takes less than 10 minutes, and from 4°C to 55°C it takes only 5 minutes). Metrology wise, is accurate to less than 0,5°C (EEC metrology standard) and perfectly constant in the animal holder system. The preset temperature will not change for more than 0,1°C when a 400g rat is placed on the plate, and return to the set temperature is almost immediate.

Bioseb's Cold Hot Plate Test - Software screenshot
Optional software - Screenshot
Operation Principle

The animal's pain sensitivity resulting from exposure to heat or cold is tested by placing the animal (mouse or rat) on the surface of the plate and starting a built-in timer. The operator stops the timer at the instant the animal lifts its paw from the plate, reacting to the discomfort. The front panel timer then displays the number of seconds it took the animal to react. Animal reaction time is a measurement of animal resistance to pain and is used to measure efficacy of analgesics.

The operator can start and stop the timer with the front panel start/stop switch or with the included footswitch, which allows "hands-free" operation.

Dedidcated software

Though it is functional as a stand-alone instrument, the Cold Hot Plate Test Analgesia Meter can also be used with our dedicated optional software, allowing the user to define temperature "ramps" and “loops”. This feature is mainly used for studies with telemetry implants. In addition to displaying the reaction time, the Cold/Hot Plate Analgesia Meter is able to send the same information via USB interface to a computer.

Key features

• Simple to use, fast and accurate
• Can be used as a stand-alone instrument
• Allows testing of sensitivity to both hot and cold stimulus
• Unmatched temperature stability and control for both heat and cold
• Fast reach to set temperatures
• Homogeneous temperature surface
• Practical foot switch timing operation
• Optional Ramp software will allow the user to define temperature ramps and loops (slope in °C/min, start and end points) and store results
Domains of application

• Analgesic drug screening
• Basal pain sensitivity phenotyping
• Integrated supraspinal responses
• Pain sensitivity alterations induced by a specific experimental context change
• Pain sensitivity alterations induced by genetic manipulations
• Animal Models of Nociception (rats and mice)

! METHOD VALIDATION ! Publication

Bioseb team presents its respectful thanks to research team of Prof. Poisbeau (Institut des Neurosciences Cellulaires et Intégratives de Strasbourg), who validated the temperature ramps method used by the Cold and Hot Plate Test during in following study:

Differentiating Thermal Allodynia and Hyperalgesia Using Dynamic Hot and Cold Plate in Rodents, by I. Yalcin, A. Charlet, MJ. Freund-Mercier, M. Barrot and P. Poisbeau, in The Journal of Pain, 2009
(Click here to download this article as a PDF file)


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

PAIN
- General pain -
Effect of 1-Hydroxy-1,1-thylidendiphosphone Acid, Bis(2-Pyridyl-1,2,4-Triazolyl-3)Propane and their adduct on the pain sensitivty of Rats (2019)
Effect of 1-Hydroxy-1,1-thylidendiphosphone Acid, Bis(2-Pyridyl-1,2,4-Triazolyl-3)Propane and their adduct on the pain sensitivty of Rats
IV Cheretaev, MY Ravaeva, ER Dzheldubaeva et al
V. I. Vernadsky Crimean Federal University, Simferopol, Crimea, Russia
Published in "Biology Chemistry" (2019-07-01)

The aim of the work is to evaluate the effect of 1-hydroxy-1,1ethylidenediphosphonic acid, bis(2-pyridyl-1,2,4-triazolyl-3)propane and their adduct on the pain sensitivity of male rats in the dose range from 5 to 200 mg/kg.

Docking and pharmacodynamic studies on hGAT1 inhibition activity in the presence of selected neuronal and astrocytic inhibitors (2018)
Docking and pharmacodynamic studies on hGAT1 inhibition activity in the presence of selected neuronal and astrocytic inhibitors
Nowaczyk A, Fija_kowski _, Zar_ba P, Sa_at K
Department of Pharmacodynamics, Chair of Pharmacodynamics, Jagiellonian University Medical College, 9 Medyczna St., 30 - 688, Krakow, Poland
Published in "Journal of Molecular Graphics and Modelling" (2018-10-01)

Inhibition of 4-aminobutanoic acid (GABA) uptake is a strategy for enhancing GABA transmission. The utility of this approach is demonstrated by the successful development of such agents for the treatment of epilepsy and pain. Existing reports on acute brain slice preparations indicate the intersecting of complementary channels and receptors sets between astrocytes and neurons cells. Thorough analysis of astroglial cells by means of molecular and functional studies demonstrated their active modulatory role in intercellular communication. The chemical interactions between sixteen GABA analogues and isoform of hGAT1 is outlined in the light of molecular docking results. In the in vivo part antinociceptive properties of racemic nipecotic acid, its R and S enantiomers and isonipecotic acid, each administered intraperitoneally at 3 fixed doses (10, 30 and 100_mg/kg), were assessed in a thermally-induced acute pain model i.e. the mouse hot plate test. Docking analyses provided complex binding energies, specific h-bond components, and h-bond properties, such as energies, distances and angles. In vivo tests revealed statistically significant antinociceptive properties of isonipecotic acid (10 and 30_mg/kg), R-nipecotic acid (30 and 100_mg/kg) and S-nipecotic acid (100_mg/kg) in mice. The docking data endorse the hypothesis of correlation between the strength of their chemical interactions with hGAT1 and analgesic action of studied compounds.

Induction of brain Nrf2-HO-1 pathway and antinociception after different physical training paradigms in mice (2018)
Induction of brain Nrf2-HO-1 pathway and antinociception after different physical training paradigms in mice
AbdulkarimTutakhailaQand AghaNazarybDelilaLebsiraSaadiaKerdine-RomercFranŤoisCoudore
CESP/National Institute of Health and Medical Research INSERM UMR-S 1178, Paris-Sud University, Faculty of Pharmacy, Paris-Saclay University, France
Published in "Life Sciences" (2018-09-15)

Aim Activation of the Nrf2-antioxidant response element signaling pathway is a major mechanism in the cellular defense against oxidative or electrophilic stress through conjugative reactions and by enhancing cellular antioxidant capacity. Although exercise training up-regulates antioxidant defenses system, while information regarding the intensity levels of physical exercise that acts on the cellular protection systems is limited.
Main methodsKey findings This study confirmed that only vigorous and longer duration aerobic exercise increased Nrf2 protein level in the hippocampus and HO-1 protein level in the cortex and reduced pain perception. Mechanical and thermal hypoalgesia were only observed in exercise groups after 7_weeks of physical training.
Significance The overall findings in this study confirm that only the long duration intensive forced exercise reduced inflammatory pain by induction of Nrf2/HO-1 antioxidant signaling pathway.

Novel analgesic effects of melanin-concentrating hormone on persistent neuropathic and inflammatory pain in mice (2018)
Novel analgesic effects of melanin-concentrating hormone on persistent neuropathic and inflammatory pain in mice
J-H Jang, J-Y Park, J-Y Oh, S-J Bae, H Jang, S Jeon, J Kim, H-J Park
Department of Korean Medical Science, Graduate School of Korean Medicine, Kyung Hee University, Seoul, Republic of Korea
Published in "Scientific Reports" (2018-01-15)

The melanin-concentrating hormone (MCH) is a peptidergic neuromodulator synthesized by neurons in the lateral hypothalamus and zona incerta. MCHergic neurons project throughout the central nervous system, indicating the involvements of many physiological functions, but the role in pain has yet to be determined. In this study, we found that pMCH_/_ mice showed lower baseline pain thresholds to mechanical and thermal stimuli than did pMCH+/+ mice, and the time to reach the maximum hyperalgesic response was also significantly earlier in both inflammatory and neuropathic pain. To examine its pharmacological properties, MCH was administered intranasally into mice, and results indicated that MCH treatment significantly increased mechanical and thermal pain thresholds in both pain models. Antagonist challenges with naltrexone (opioid receptor antagonist) and AM251 (cannabinoid 1 receptor antagonist) reversed the analgesic effects of MCH in both pain models, suggesting the involvement of opioid and cannabinoid systems. MCH treatment also increased the expression and activation of CB1R in the medial prefrontal cortex and dorsolateral- and ventrolateral periaqueductal grey. The MCH1R antagonist abolished the effects induced by MCH. This is the first study to suggest novel analgesic actions of MCH, which holds great promise for the application of MCH in the therapy of pain-related diseases.

Brain natriuretic peptide-expressing sensory neurons are not involved in acute, inflammatory, or neuropathic pain (2017)
Brain natriuretic peptide-expressing sensory neurons are not involved in acute, inflammatory, or neuropathic pain
S. Pitake, J. DeBrecht, S.K. Mishra
College of Veterinary Medicine, North Carolina State University, Raleigh, NC
Published in "Molecular Pain" (2017-09-08)

Background: We recently demonstrated that brain natriuretic peptide is expressed in the dorsal root ganglia, and that brain natriuretic peptide is required for normal detection of pruritogens. We further showed that the receptor for brain natriuretic peptide, natriuretic peptide receptor A, is present in the spinal cord, and elimination of these neurons profoundly attenuates scratching to itch-inducing compounds. However, the potential modulatory roles of brain natriuretic peptide in nociception, inflammation, and neuropathic mechanisms underlying the sensation of pain have not been investigated in detail.
Findings: To demonstrate the involvement of brain natriuretic peptide in pain, we compared the behavioral responses of brain natriuretic peptide knockout mice with their wild-type littermates. First, we showed that brain natriuretic peptide is not required in chemically induced pain responses evoked by the administration of capsaicin, allyl isothiocyanate, adenosine 50-triphosphate, or inflammatory soup. We further measured pain behaviors and found no involvement of brain natriuretic peptide in hot, cold, or mechanical nociceptive responses in mice, nor did we find evidence for the involvement of brain natriuretic peptide in neuroinflammatory sensitization elicited by complete Freund?s adjuvant or in neuropathic pain.
Conclusions: These results demonstrate that brain natriuretic peptide is not essential for pain-related behaviors.

Methods Used to Evaluate Pain Behaviors in Rodents (2017)
Methods Used to Evaluate Pain Behaviors in Rodents
J.R. Deuis, L.S. Dvorakova, I. Vetter
Centre for Pain Research, Institute for Molecular Bioscience, The University of Queensland, QLD, Australia
Published in "Frontiers in molecular Neuroscience" (2017-09-06)

Rodents are commonly used to study the pathophysiological mechanisms of pain as studies in humans may be difficult to perform and ethically limited. As pain cannot be directly measured in rodents, many methods that quantify “pain-like” behaviors or nociception have been developed. These behavioral methods can be divided into stimulus-evoked or non-stimulus evoked (spontaneous) nociception, based on whether or not application of an external stimulus is used to elicit a withdrawal response. Stimulus-evoked methods, which include manual and electronic von Frey, Randall- Selitto and the Hargreaves test, were the first to be developed and continue to be in widespread use. However, concerns over the clinical translatability of stimulus-evoked nociception in recent years has led to the development and increasing implementation of non-stimulus evoked methods, such as grimace scales, burrowing, weight bearing and gait analysis. This review article provides an overview, as well as discussion of the advantages and disadvantages of the most commonly used behavioral methods of stimulus-evoked and non-stimulus-evoked nociception used in rodents.



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Temp range -2 degrees C. to 55 degrees C (in 20 to 25 degree C. ambient environment, 50% RH)
Temp accuracy +/- 0.5 degrees C.
Temperature uniformity on plate +/- 0.5 degrees C.
Power requirements 110V/220V automatic, 100W
Plate Dimensions 165 x 165 mm
Control unit dimensions 305 x 280 x 158 mm
Weight 6,650 kg

Model:
BIO-CHP
Cold Hot Plate Test
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