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Home > Catalog > Pain - Thermal allodynia / Hyperalgesia
(Model: BIO-T2CT)
An operator independent test to study pain thresholds in rodents (mouse and rat) by assessing temperature preference (thermal comfort zone) - a new tool for your analgesia/nociception research opening new fields of investigation, and an ideal solution for nociceptive and analgesic drugs screening. Now comes with a brand new software, allowing tracking activity and faster temperature transitions!

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  • NIH Bethesda, USA
  • GRUNENTHAL Aachen, Allemagne
  • SANOFI AVENTIS Montpellier, France
  • NIH Bethesda, USA
  • FACULTE DE MEDECINE Clermont Ferrand, France
  • UNIVERSITE DE PARIS SUD Châtenay Malabry, France
  • GRUNENTHAL Aachen, Allemagne
  • Swiss Federal Institute of Technolo Lausanne, Suisse
  • MERCK West Point, USA
  • KU LEUVEN Leuven, Belgium
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! NEW RESEARCH WORK ! A recent publication by M Bohic, I Marics, C Santos, P Malapert, N Ben-Arie et al in "Cell Reports" highlights the merits of using Bioseb's Thermal Place Preference, 2 Temperatures Choice Nociception Test: Loss of bhlha9 Impairs Thermotaxis and Formalin-Evoked Pain in a Sexually Dimorphic Manner

Loss of bhlha9 Impairs Thermotaxis and Formalin-Evoked Pain in a Sexually Dimorphic Manner
M Bohic, I Marics, C Santos, P Malapert, N Ben-Arie et al
Aix-Marseille Université, CNRS, Institut de Biologie du Développement de Marseille, Marseille, France
Published in "Cell Reports" (2020-01-21)

C-LTMRs are known to convey affective aspects of touch and to modulate injury-induced pain in humans and mice. However, a role for these neurons in temperature sensation has been suggested, but not fully demonstrated. Here, we report that deletion of C-low-threshold mechanoreceptor (C-LTMR)-expressed bhlha9 causes impaired thermotaxis behavior and exacerbated formalin-evoked pain in male, but not female, mice. Positive modulators of GABAA receptors failed to relieve inflammatory formalin pain and failed to decrease the frequency of spontaneous excitatory post-synaptic currents (sEPSCs) selectively in bhlha9 knockout (KO) males. This could be explained by a drastic change in the GABA content of lamina II inner inhibitory interneurons contacting C-LTMR central terminals. Finally, C-LTMR-specific deep RNA sequencing revealed more genes differentially expressed in male than in female bhlha9 KO C-LTMRs. Our data consolidate the role of C-LTMRs in modulation of formalin pain and provide in vivo evidence of their role in the discriminative aspects of temperature sensation.

Bioseb's Thermal Place Preference, 2 Temperatures Choice Nociception Test
Overview of the Temperature Choice Test System
Bioseb’s Thermal Place Preference Test, or 2 Temperatures Choice Nociception Test, is an operator independant test to study pain thresholds in rodents (mouse and rat) by assessing temperature preference (comfort zone) - a brand new tool opening new fields of investigation for your analgesia/nociception research.

As advised by A. MOQRICH, and published in Moqrich et al (Science 2005, 307: 1468-72), the Thermal Place Preference Test allows researchers to work on unrestrained animals (mice and rats) let free to choose their preferred position (comfort zone) between 2 compartments set at different temperatures. This behavioural assay will allow monitoring temperature preferences, nociceptive thresholds and state in the role of a given gene or a compound on these pain thresholds associated to cold and hot stimulation.

Unlike the cold/hot plate test, it is investigator-independent: using the traditional plates, an operator can measure the reaction time of an animal (mouse or rat) exposed to a certain temperature. The "two Temperatures Choice Test" will return a nociceptive response without any action from the operator, and the obtained value is a temperature or a temperature range indicating the sensitivity of the animal (mouse or rat) resulting to the exposure to different stimulations (cold or heat).

You have the possibility to either observe one rat at a time or two mice simultaneously and independently, making the Thermal Place Preference system remarkably attractive for your analgesia research.

Dedicated software

The optional, dedicated T2CT software is a convenient tool allowing the operator to define the temperature of each zone, and easily, automatically obtain the position & presence time of each animal (mouse or rat). Results can be transferred directly as an Excel file or as a txt format. Software is compatible with Windows 7/8, in both 32 and 64 bits, and comes with 3 USB cables and a webcam.

T2CT software v2 is now available!
• New algorithm for tracking activity and detecting zone transitions
• A single window for all settings
• New improved electronics are more stable and result in faster temperature transitions

Parameters measured include :
• Time spent in each temperature zone (abs. and %)
• Time of each zone trespassing
• Temperature of each zone
• Activity time of the animal (total or by zone)
• Distance run by the animal (total or by zone)
Key features

• Innovative test opening new fields of investigation
• Easy to set-up
• Operator-independent
• Operated on unrestrained, freely moving animals
• Automatic if using the optional software
• Windows 7/8 32/64bits compatible
• Transition lists can be managed or imported from xls/csv file
• Ability to resume an interrupted session
• Replay experimental videos, incl. animal detection
• Display and export results for custom time periods
• Customized results exports
• Results grouping for animal groups
• Results can be displayed as table or graph format

Domains of application

• Drug screening
• Phenotyping

Operating principle

This test is easy to setup:

Bioseb's Thermal Place Preference, 2 Temperatures Choice Nociception Test - New Software Screenshot Using the optional automatic detection software: the operator defines the temperature of each zone. Once the temperatures are stabilized, animals are placed and the acquisition can be launched. The operator doesn't have to be present any more during the nociceptive experiment.

If not using the automatic detection software, temperatures have to be defined manually, and the operator has to measure the time himself.

During the thermal analgesia experience, the operator can visualize the position and movements of each animal on the screen. Raw data acquisition files are stored in a proprietary format to match GLP norms, while a .txt version of the file can be used for further analysis in MS Excel.


Automatic detection software to measure the position and presence time of the animal (mouse or rat) in each zone, comes with 3 USB cables and a webcam.

Modular design: Using available custom accessories and tools, Bioseb's Thermal Place Preference, 2 Temperatures Choice Nociception Test can be used to run Cold Hot Plate tests, and even Temperature gradient tests. Please contact us to know more!

!New! Publication:

Bioseb team presents its respectful thanks to research teams of Prof. Lazdunski (Université de Nice-Sophia Antipolis, France) and Prof. Eschalier (Clermont Université, Clermont-Ferrand, France), who used the Two-Temperatures Choice Test during their recent studies:

The mechano-activated Kþ channels TRAAK and TREK-1 control both warm and cold perception, by J. Noe, K. Zimmermann, J. Busserolles, E. Deval, A. Alloui,S. Diochot, N. Guy, M. Borsotto,P. Reeh, A. Eschalier and M. Lazdunski, EMBO Journal, 2009
(Click here to download this article as a PDF file)

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

- General pain -
Significant determinants of mouse pain behaviour (2014)
Significant determinants of mouse pain behaviour
Minett MS, Eijkelkamp N, Wood JN
Molecular Nociception Group, Wolfson Institute for Biomedical Research, University College London, Gower Street, London, United Kingdom.
Published in "PLoS One." (2014-08-07)

Transgenic mouse behavioural analysis has furthered our understanding of the molecular and cellular mechanisms underlying damage sensing and pain. However, it is not unusual for conflicting data on the pain phenotypes of knockout mice to be generated by reputable groups. Here we focus on some technical aspects of measuring mouse pain behaviour that are often overlooked, which may help explain discrepancies in the pain literature. We examined touch perception using von Frey hairs and mechanical pain thresholds using the Randall-Selitto test. Thermal pain thresholds were measured using the Hargreaves apparatus and a thermal place preference test. Sodium channel Nav1.7 knockout mice show a mechanical deficit in the hairy skin, but not the paw, whilst shaving the abdominal hair abolished this phenotype. Nav1.7, Nav1.8 and Nav1.9 knockout mice show deficits in noxious mechanosensation in the tail, but not the paw. TRPA1 knockout mice, however, have a loss of noxious mechanosensation in the paw but not the tail. Studies of heat and cold sensitivity also show variability depending on the intensity of the stimulus. Deleting Nav1.7, Nav1.8 or Nav1.9 in Nav1.8-positive sensory neurons attenuates responses to slow noxious heat ramps, whilst responses to fast noxious heat ramps are only reduced when Nav1.7 is lost in large diameter sensory neurons. Deleting Nav1.7 from all sensory neurons attenuates responses to noxious cooling but not extreme cold. Finally, circadian rhythms dramatically influence behavioural outcome measures such as von Frey responses, which change by 80% over the day. These observations demonstrate that fully characterising the phenotype of a transgenic mouse strain requires a range of behavioural pain models. Failure to conduct behavioural tests at different anatomical locations, stimulus intensities, and at different points in the circadian cycle may lead to a pain behavioural phenotype being misinterpreted, or missed altogether.

Antinociceptive effects of fluoxetine in a mouse model of anxiety/depression (2012)
Antinociceptive effects of fluoxetine in a mouse model of anxiety/depression
Hache G, Guiard BP, Le Dantec Y, Orvoën S, David DJ, Gardier AM, Coudoré F.
Lab NeuroPharmacology, Faculty of Pharmacy, Paris Sud University, Paris, France
Published in "Neuroreport." (2012-06-20)

Pain was reported by 60-90% of patients with depression, and chronic pain states are often linked to depression. Animal models of pain/depression are generally lacking for the identification of centrally active drugs. In the present study, pain sensitivity was assessed in a mouse model of anxiety/depression on the basis of chronic corticosterone (CORT) administration through the drinking water (CORT model). We measured thermal hyperalgesia as shown by a decrease in the latency to hind paw licking in the hot plate test and cold allodynia reflected by a decrease in the time spent on the plate set at 20°C in the thermal preference plate test. Subsequently, we determined the effect of chronic administration of the selective serotonin reuptake inhibitor fluoxetine (an antidepressant known to reverse anxiety/depressive-like state in CORT-treated mice) on pain relief. Fluoxetine administration reduced both heat hyperalgesia and cold allodynia, thus unveiling a putative link between mood and nociception in the CORT model. This hypothesis is consistent with previous clinical studies reporting the analgesic efficacy of fluoxetine in depressed patients suffering from pain disorders. Together, these results suggest that the CORT model, with pain/anxiety/depressive-like state, is a good candidate for translational research.

Distinct nav 1.7-dependent pain sensations require different sets of sensory and sympathetic neurons (2012)
Distinct nav 1.7-dependent pain sensations require different sets of sensory and sympathetic neurons
Michael S. Minett, Mohammed A. Nassar, Anna K. Clark, Gayle Passmore, Anthony H. Dickenson, Fan Wang, Marzia Malcangio, and John N. Wooda
Molecular Nociception Group, WIBR UCL, London, UK
Published in "Nat Commun." (2012-04-24)

Human acute and inflammatory pain requires the expression of voltage-gated sodium channel Nav1.7 but its significance for neuropathic pain is unknown. Here we show that Nav1.7 expression in different sets of mouse sensory and sympathetic neurons underlies distinct types of pain sensation. Ablating Nav1.7 gene (SCN9A) expression in all sensory neurons using Advillin-Cre abolishes mechanical pain, inflammatory pain and reflex withdrawal responses to heat. In contrast, heat-evoked pain is retained when SCN9A is deleted only in Nav1.8-positive nociceptors. Surprisingly, responses to the hotplate test, as well as neuropathic pain, are unaffected when SCN9A is deleted in all sensory neurons. However, deleting SCN9A in both sensory and sympathetic neurons abolishes these pain sensations and recapitulates the pain-free phenotype seen in humans with SCN9A loss-of-function mutations. These observations demonstrate an important role for Nav1.7 in sympathetic neurons in neuropathic pain, and provide possible insights into the mechanisms that underlie gain-of-function Nav1.7-dependent pain conditions.

- Mechanical allodynia & hyperlagesia -
Differential Spinal and Supraspinal Activation of Glia in a Rat Model of Morphine Tolerance (2018)
Differential Spinal and Supraspinal Activation of Glia in a Rat Model of Morphine Tolerance
V Jokinen, Y Sidorova, H Viisanen, I Suleymanova, H Tiilikainen, Z Li, T O Lilius, K Matlik, J E Anttila, M Airavaara, L Tian, P V Rauhala, E A Kalso
Department of Pharmacology, Faculty of Medicine, Haartmaninkatu 8 (Biomedicum), 00014 University of Helsinki, Helsinki, Finland
Published in "Neuroscience" (2018-02-06)

Development of tolerance is a well known pharmacological characteristic of opioids and a major clinical problem. In addition to the known neuronal mechanisms of opioid tolerance, activation of glia has emerged as a potentially significant new mechanism. We studied activation of microglia and astrocytes in morphine tolerance and opioid-induced hyperalgesia in rats using immunohistochemistry, flow cytometry and RNA sequencing in spinal- and supraspinal regions. Chronic morphine treatment that induced tolerance and hyperalgesia also increased immunoreactivity of spinal microglia in the dorsal and ventral horns. Flow cytometry demonstrated that morphine treatment increased the proportion of M2-polarized spinal microglia, but failed to impact the number or the proportion of M1-polarized microglia. In the transcriptome of microglial cells isolated from the spinal cord (SC), morphine treatment increased transcripts related to cell activation and defense response. In the studied brain regions, no activation of microglia or astrocytes was detected by immunohistochemistry, except for a decrease in the number of microglial cells in the substantia nigra. In flow cytometry, morphine caused a decrease in the number of microglial cells in the medulla, but otherwise no change was detected for the count or the proportion of M1- and M2-polarized microglia in the medulla or sensory cortex. No evidence for the activation of glia in the brain was seen. Our results suggest that glial activation associated with opioid tolerance and opioid-induced hyperalgesia occurs mainly at the spinal level. The transcriptome data suggest that the microglial activation pattern after chronic morphine treatment has similarities with that of neuropathic pain.

A Polyamine-Deficient Diet Prevents Oxaliplatin-Induced Acute Cold and Mechanical Hypersensitivity in Rats (2013)
A Polyamine-Deficient Diet Prevents Oxaliplatin-Induced Acute Cold and Mechanical Hypersensitivity in Rats
J.Ferrier, M.Bayet-Robert, B.Pereira, L.Daulhac
Published in "PLOS ONE" (2013-11-30)

Oxaliplatin is an anticancer drug used for the treatment of advanced colorectal cancer, but it can also cause painful peripheral neuropathies. The pathophysiology of these neuropathies has not been yet fully elucidated, but may involve spinal N-methyl-D-aspartate (NMDA) receptors, particularly the NR2B subunit. As polyamines are positive modulators of NMDA-NR2B receptors and mainly originate from dietary intake, the modulation of polyamines intake could represent an interesting way to prevent/modulate neuropathic pain symptoms by opposing glutamate neurotransmission.
The effect of a polyamine deficient diet was investigated in an animal model of oxaliplatin-induced acute pain hypersensitivity using behavioral tests (mechanical and cold hypersensitivity). The involvement of spinal glutamate neurotransmission was monitored by using a proton nuclear magnetic resonance spectroscopy based metabolomic approach and by assessing the expression and phosphorylation of the NR2B subunit of the NMDA receptor.
A 7-day polyamine deficient diet totally prevented oxaliplatin-induced acute cold hypersensitivity and mechanical allodynia. Oxaliplatin-induced pain hypersensitivity was not associated with an increase in NR2B subunit expression or phosphorylation, but with an increase of glutamate level in the spinal dorsal horn which was completely prevented by a polyamine deficient diet. As a validation that the oxaliplatin-induced hypersensitivity could be due to an increased activity of the spinal glutamate system, an intrathecal administration of the specific NR2B antagonist, ifenprodil, totally reversed oxaliplatin-induced mechanical and cold hypersensitivity.
A polyamine deficient diet could represent a promising and valuable nutritional therapy to prevent oxaliplatin-induced acute pain hypersensitivity.

- Inflammatory pain -
Conditional knockout of NaV1.6 in adult mice ameliorates neuropathic pain (2018)
Conditional knockout of NaV1.6 in adult mice ameliorates neuropathic pain
L. Chen, J. Huang, P. Zhao. AK Persson, FB Dib-Hajj, X Cheng, A Tan, S Wanman, SD Dib-Hajj
Yale University School of Medicine, New Haven, CT, USA
Published in "Scientific Reports" (2018-02-19)

Voltage-gated sodium channels NaV1.7, NaV1.8 and NaV1.9 have been the focus for pain studies because their mutations are associated with human pain disorders, but the role of NaV1.6 in pain is less understood. In this study, we selectively knocked out NaV1.6 in dorsal root ganglion (DRG) neurons, using NaV1.8-Cre directed or adeno-associated virus (AAV)-Cre mediated approaches, and examined the specific contribution of NaV1.6 to the tetrodotoxin-sensitive (TTX-S) current in these neurons and its role in neuropathic pain. We report here that NaV1.6 contributes up to 60% of the TTX-S current in large, and 34% in small DRG neurons. We also show NaV1.6 accumulates at nodes of Ranvier within the neuroma following spared nerve injury (SNI). Although NaV1.8-Cre driven NaV1.6 knockout does not alter acute, inflammatory or neuropathic pain behaviors, AAV-Cre mediated NaV1.6 knockout in adult mice partially attenuates SNI-induced mechanical allodynia. Additionally, AAV-Cre mediated NaV1.6 knockout, mostly in large DRG neurons, significantly attenuates excitability of these neurons after SNI and reduces NaV1.6 accumulation at nodes of Ranvier at the neuroma. Together, NaV1.6 in NaV1.8-positive neurons does not influence pain thresholds under normal or pathological conditions, but NaV1.6 in large NaV1.8-negative DRG neurons plays an important role in neuropathic pain.


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Temperature range -2°C to +55°C (room temperature 20 to 25 °C)
For more information about thermal specificities, please check the product page of our Cold+Hot Plate
Accuracy Better than +/- 0.5°C.
Max Overshoot 0,5°C
Electrical power 150 watts
Size 32 x 57 x 45.5 cm (L x w x H including cage)
Weight 14 kG
Animal cage 330 x 165 x 300 mm, plexiglass
Time and position measurement 1s accuracy, video analysis
Software optional, requires Windows 7/8, and a PC with 512 MO RAM with 3 USB ports

Thermal Place Preference, 2 Temperatures Choice Nociception Test
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