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THERMAL GRADIENT TEST
(Model: BIO-TGT2 - Lanes - Mice: 2 / Rats: 1)
This Operator Independant Thermal Gradient Test is a new analgesia/nociceptive research instrument to demonstrate place preference / temperature comfort threshold on rodents (mouse and rat)

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  • CNRS Marseille, France
  • UNIL Lausanne, Suisse
  • UNIVERSIDAD MIGUEL HERNANDEZ CSIC San Juan de Alicante, Espagne
  • SWISS FEDERAL INTITUTE OF TECHNOLOGY Lausanne, Suisse
  • PFIZER Sandwich, USA
  • CNRS Montpellier, France
  • HARVARD MEDICAL SCHOOL Boston, USA
  • PFISER Sandwich, UK
  • KU LEUVEN Leuven, Belgium
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! NEW RESEARCH WORK ! A recent publication by Urien L, Gaillard S, Lo Re L, Malapert P, Bohic M, Reynders A, Moqrich A in "Scientific Reports" highlights the merits of using Bioseb's Thermal Gradient Test: Genetic ablation of GINIP-expressing primary sensory neurons strongly impairs Formalin-evoked pain.

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.
Presentation

The Thermal Gradient Test has been described in Moqrich et al. 2005, and is one of the very few thermal nociception tests to be operator independant on freely moving rodents (mice and rat). A continuous temperature gradient (-4 to 65°C) is established over a 120 cm long base plate, on which the animal is free to walk. After the exploration period the rodent (mouse or rat) shows a distinct zone preference
, or comfort zone.
Bioseb has defined an automated instrument for your research on analgesia and nociception (especially suitable for research on alodynia), with a temperature gradient stable over the surface and over time, allowing to identify the prefered temperature zone. Two instruments models will test independantly and simultaneously 2 mice or small rats (1 adult rat).


Software

The accompanying software, coupled to a video camera, displays for each animal the time spent per time period in each temperature zone, together with overall travelled distance.
The encrypted datas and the video images are recorded synchroneously in real time during the nociception experiments. This allows the operator to replay and check the animal behaviour at any time and remotely, and also to comply with Good Laboratory Practice (GLP).


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 -
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.

- Neuropathic pain -
Impaired Thermosensation in Mice Lacking TRPV3, a Heat and Camphor Sensor in the Skin (2015)
Impaired Thermosensation in Mice Lacking TRPV3, a Heat and Camphor Sensor in the Skin
Aziz Moqrich, Sun Wook Hwang, Taryn J. Earley et al.
Department of Cell Biology, Scripps Research Insti- tute, La Jolla, CA 92037, USA
Published in "Science" (2015-03-04)

Environmental temperature is thought to be directly sensed by neurons through their projections in the skin. A subset of the mammalian transient receptor potential (TRP) family of ion channels has been implicated in this process. These ‘‘thermoTRPs’’ are activated at distinct temperature thresholds and are typically expressed in sensory neurons. TRPV3 is activated by heat (933-C) and, unlike most thermoTRPs, is expressed in mouse keratinocytes. We found that TRPV3 null mice have strong deficits in responses to innocuous and noxious heat but not in other sensory modalities; hence, TRPV3 has a specific role in thermosensation. The natural compound camphor, which modulates sensations of warmth in humans, proved to be a specific activator of TRPV3. Camphor activated cultured primary keratinocytes but not sensory neurons, and this activity was abolished in TRPV3 null mice. Therefore, heat-activated receptors in keratinocytes are important for mammalian thermosensation.

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.

SENSORY SYSTEM
- Hot & Cold Perception -
Impaired Thermosensation in Mice Lacking TRPV3, a Heat and Camphor Sensor in the Skin (2015)
Impaired Thermosensation in Mice Lacking TRPV3, a Heat and Camphor Sensor in the Skin
Aziz Moqrich, Sun Wook Hwang, Taryn J. Earley et al.
Department of Cell Biology, Scripps Research Insti- tute, La Jolla, CA 92037, USA
Published in "Science" (2015-03-04)

Environmental temperature is thought to be directly sensed by neurons through their projections in the skin. A subset of the mammalian transient receptor potential (TRP) family of ion channels has been implicated in this process. These ‘‘thermoTRPs’’ are activated at distinct temperature thresholds and are typically expressed in sensory neurons. TRPV3 is activated by heat (933-C) and, unlike most thermoTRPs, is expressed in mouse keratinocytes. We found that TRPV3 null mice have strong deficits in responses to innocuous and noxious heat but not in other sensory modalities; hence, TRPV3 has a specific role in thermosensation. The natural compound camphor, which modulates sensations of warmth in humans, proved to be a specific activator of TRPV3. Camphor activated cultured primary keratinocytes but not sensory neurons, and this activity was abolished in TRPV3 null mice. Therefore, heat-activated receptors in keratinocytes are important for mammalian thermosensation.

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.



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Gradient Models TGT2 (2/1 lanes)
Power supply 220 / 110 Volts
Number of Lanes TGT2 Model - Mouse: 2 / Rat: 1
Temperature range °C (at plate surface)
@ environnement 20 to 25°C & %RH 45 to 55%RH
-4 to 65
Temp. stability °C
(surface, over time)
1°C
Supplied with 2 thermal units and controlers, Cage and Base plate.
Materials Base Plate: Aluminum alloy
Walls: Grey ppc
Cover: Transparent ppc
Software TGS Allows to measure per animal: up to 20 temperature zones, time spent/temp.Zone/ time period, overall distance travelled.
Results: .xls type, presented per time periods. Raw datas encrypted (glp) with video recording (synchronous).
Replay: at any time
Sotware requirement PC 1GO Ram, Fast processor, Windows 7 or higher, 3x USB port,
Supplied with: webcam , mini usb cables
Option Infra Red Thermometer / temp control IRB153

Model:
BIO-TGT2
Thermal Gradient Test (Modif.)
Lanes - Mice: 2 / Rats: 1 Contact us

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