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 Masaru Sato, Mariko Ito, Masashi Nagase, Yae K Sugimura, Yukari Takahashi, Ayako M Watabe and Fusao Kato in "Molecular Brain" highlights the merits of using Bioseb's Thermal Place Preference, 2 Temperatures Choice Nociception Test: The lateral parabrachial nucleus is actively involved in the acquisition of fear memory in mice

The lateral parabrachial nucleus is actively involved in the acquisition of fear memory in mice
Masaru Sato, Mariko Ito, Masashi Nagase, Yae K Sugimura, Yukari Takahashi, Ayako M Watabe and Fusao Kato
Department of Neuroscience, Jikei University School of Medicine, Tokyo 105-8461, Japan
Published in "Molecular Brain" (2015-03-27)

Background: Pavlovian fear conditioning is a form of learning accomplished by associating a conditioned stimulus (CS) and an unconditioned stimulus (US). While CS–US associations are generally thought to occur in the amygdala, the pathway mediating US signal processing has only been partially identified. The external part of the pontine lateral parabrachial nucleus (elPB) is well situated for providing US nociceptive information to the central amygdala (CeA), which was recently revealed to play a primary role in fear acquisition. Therefore, we manipulated the elPB activity to examine its role in the regulation of fear learning.

Results: First, we transiently inactivate the elPB during the acquisition of fear memory. Mice received bilateral elPB injections of the GABAA agonist muscimol (MUS) or phosphate-buffered saline (drug control), with bilateral misplacement of MUS defined as a placement control group. After the injection, mice were conditioned with a pure tone and foot-shock. On a memory retrieval test on day 2, the freezing ratio was significantly lower in the MUS group compared with that in the drug control or placement control groups. A second retrieval test using a pip tone on day 4 following de novo training on day 3, resulted in significant freezing with no group differences, indicating integrity of fear learning and a temporary limited effect of MUS. Next, we examined whether selectively activating the elPB-CeC pathway is sufficient to induce fear learning when paired with CS. Mice with channelrhodopsin2 (ChR2) expressed in the elPB received a pure tone (CS) in association with optical stimulation in the CeA (CS-LED paired group). On the retrieval test, CS-LED paired mice exhibited significantly higher freezing ratios evoked by CS presentation compared with both control mice receiving optical stimulation immediately after being placed in the shock chamber and exposed to the CS much later (immediate shock group) and those expressing only GFP (GFP control group). These results suggest that selective stimulation of the elPB-CeC pathway substitutes for the US to induce fear learning.

Conclusions: The elPB activity is necessary and sufficient to trigger fear learning, likely as a part of the pathway transmitting aversive signals to the CeA.

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 -
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.

- Neuropathic pain -
Oxaliplatin-induced cold hypersensitivity is due to remodelling of ion channel expression in nociceptors. (2011)
Oxaliplatin-induced cold hypersensitivity is due to remodelling of ion channel expression in nociceptors.
J. Descoeur, V. Pereira, A. Pizzoccaro, A. Francois, B. Ling et al. (Team of Dr Bourinet)
Institut de Génomique Fonctionnelle, CNRS, UMR-5203, Département de Physiologie, Montpellier, France.
Published in "EMBO Molecular Medicine" (2011-05-24)

Cold hypersensitivity is the hallmark of oxaliplatin-induced neuropathy, which develops in nearly all patients under this chemotherapy. To date, pain management strategies have failed to alleviate these symptoms, hence development of adapted analgesics is needed. Here, we report that oxaliplatin exaggerates cold perception in mice as well as in patients. These symptoms are mediated by primary afferent sensory neurons expressing the thermoreceptor TRPM8. Mechanistically, oxaliplatin promotes over-excitability by drastically lowering the expression of distinct potassium channels (TREK1, TRAAK) and by increasing the expression of pro-excitatory channels such as the hyperpolarization-activated channels (HCNs). These findings are corroborated by the analysis of TREK1-TRAAK mice and use of the specific HCN inhibitor ivabradine, which abolishes the oxaliplatin-induced cold hypersensibility. These results suggest that oxaliplatin exacerbates cold perception by modulating the transcription of distinct ionic conductances that together shape sensory neuron responses to cold. The translational and clinical implication of these findings would be that ivabradine may represent a tailored treatment for oxaliplatin-induced neuropathy.

- Chronic pain -
Studying ongoing and spontaneous pain in rodents – challenges and opportunities (2014)
Studying ongoing and spontaneous pain in rodents – challenges and opportunities
A. Tappe-Theodor, R. Kuner
Institute of Pharmacology, Heidelberg University, Heidelberg, Germany
Published in "European Journal of Neurosciences" (2014-04-01)

The measurement of spontaneous ongoing pain in rodents is a multiplex issue and a subject of extensive and longstanding debate. Considering the need to align available rodent models with clinically relevant forms of pain, it is of prime importance to thoroughly characterize behavioral outcomes in rodents using a portfolio of measurements that are not only stimulus-dependent but also encompass voluntary behavior in unrestrained animals. Moreover, the temporal course and duration of behavioral tests should be taken into consideration when we plan our studies to measure explicit chronic pain, with a particular emphasis on performing longitudinal studies in rodents. While using rodents as model organisms, it is also worth considering their circadian rhythm and the influence of the test conditions on the behavioral results, which are affected by social paradigms, stress and anxiety. In humans, general wellbeing is closely related to pain perception, which also makes it necessary in rodents to consider modulators as well as readouts of overall wellbeing. Optimizing the above parameters in study design and the new developments that are forthcoming to test the affective motivational components of pain hold promise in solving inconsistencies across studies and improving their broad applicability in translational research. In this review, we critically discuss a variety of behavioral tests that have been developed and reported in recent years, attempt to weigh their benefits and potential limitations, and discuss key requirements and challenges that lie ahead in measuring ongoing pain in rodent models.


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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 (Modif.)
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