The Sciatic Nerve Cuffing Model of Neuropathic Pain in Mice

Yalçın, İpek; Megat, Salim; Barthas, Florent; Waltisperger, Elisabeth; Kremer, Mélanie; Salvat, Éric; Barrot, Michel

doi:10.3791/51608

Cited by 63 publications

(92 citation statements)

References 51 publications

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“…The sciatic nerve cuffing model was used to induce mechanical and thermal hyperalgesia in the hind paw of mice, as described by Yalcin et al (2014). Mice were housed individually to avoid stress derived from the surgery and to prevent injury.…”

Section: Cuff-induced Neuropathic Pain Modelmentioning

confidence: 99%

TRESK background K⁺ channel deletion selectively uncovers enhanced mechanical and cold sensitivity

Castellanos

Pujol-Coma

Andrés‐Bilbé

et al. 2020

The Journal of Physiology

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Key points TRESK background K+ channel is expressed in sensory neurons and acts as a brake to reduce neuronal activation. Deletion of the channel enhances the excitability of nociceptors. Skin nociceptive C‐fibres show an enhanced activation by cold and mechanical stimulation in TRESK knockout animals. Channel deletion selectively enhances mechanical and cold sensitivity in mice, without altering sensitivity to heat. These results indicate that the channel regulates the excitability of specific neuronal subpopulations involved in mechanosensitivity and cold‐sensing. Abstract Background potassium‐permeable ion channels play a critical role in tuning the excitability of nociceptors, yet the precise role played by different subsets of channels is not fully understood. Decreases in TRESK (TWIK‐related spinal cord K+ channel) expression/function enhance excitability of sensory neurons, but its role in somatosensory perception and nociception is poorly understood. Here, we used a TRESK knockout (KO) mouse to address these questions. We show that TRESK regulates the sensitivity of sensory neurons in a modality‐specific manner, contributing to mechanical and cold sensitivity but without any effect on heat sensitivity. Nociceptive neurons isolated from TRESK KO mice show a decreased threshold for activation and skin nociceptive C‐fibres show an enhanced activation by cold and mechanical stimulation that was also observed in behavioural tests in vivo. TRESK is also involved in osmotic pain and in early phases of formalin‐induced inflammatory pain, but not in the development of mechanical and heat hyperalgesia during chronic pain. In contrast, mice lacking TRESK present cold allodynia that is not further enhanced by oxaliplatin. In summary, genetic removal of TRESK uncovers enhanced mechanical and cold sensitivity, indicating that the channel regulates the excitability of specific neuronal subpopulations involved in mechanosensitivity and cold‐sensing, acting as a brake to prevent activation by innocuous stimuli.

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Section: Cuff-induced Neuropathic Pain Modelmentioning

confidence: 99%

TRESK background K⁺ channel deletion selectively uncovers enhanced mechanical and cold sensitivity

Castellanos

Pujol-Coma

Andrés‐Bilbé

et al. 2020

The Journal of Physiology

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show abstract

“…The sciatic nerve cuffing model was used to induce mechanical and thermal hyperalgesia in the hind paw of mice, as described in (Yalcin et al 2014). Mice were housed individually to avoid stress derived from the surgery and to prevent injury.…”

Section: Cuff-induced Neuropathic Pain Modelmentioning

confidence: 99%

TRESK background K⁺ channel deletion selectively uncovers enhanced mechanical and cold sensitivity

Castellanos

Pujol-Coma

Andrés‐Bilbé

et al. 2019

Preprint

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Changes in TRESK K + channel expression/function enhance sensory neurons excitability, but its role in somatosensory perception and nociception is poorly understood. We show that TRESK regulates the sensitivity to mechanical and cold stimuli but not the perception of heat. TRESK knockout mice nociceptive neurons present an enhanced excitability; skin nociceptive C-fibers show an increased activation by lower intensity cold or mechanical stimulation and mice lacking TRESK present mechanical and cold hypersensitivity. TRESK is also involved in osmotic pain and in early phases of formalin-induced inflammatory pain, but not in the development of mechanical and heat hyperalgesia during chronic pain. In contrast, mice lacking TRESK present cold allodynia that is not further enhanced by oxaliplatin. In summary, genetic removal of TRESK uncovers enhanced mechanical and cold sensitivity, indicating that it regulates the excitability of specific neuronal subpopulations involved in mechanosensitivity and cold-sensing, acting as a brake to prevent activation by low-intensity stimuli.

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“…To induce neuropathic pain, rats were anesthetized (ketamine, 87 mg/kg; xylazine, 13 mg/kg), and a 2 mm cuff of PE-90 polyethylene tubing was placed around the main branch of the right sciatic nerve (Yalcin et al, 2014;Benbouzid et al, 2008). The sham group underwent the same surgery without cuff implantation.…”

Section: Aversive Proceduresmentioning

confidence: 99%

Response of the Tail of the Ventral Tegmental Area to Aversive Stimuli

Sánchez-Catalán

Faivre

Yalçın

et al. 2016

Neuropsychopharmacol

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The GABAergic tail of the ventral tegmental area (tVTA), also named rostromedial tegmental nucleus (RMTg), exerts an inhibitory control on dopamine neurons of the VTA and substantia nigra. The tVTA has been implicated in avoidance behaviors, response to drugs of abuse, reward prediction error, and motor functions. Stimulation of the lateral habenula (LHb) inputs to the tVTA, or of the tVTA itself, induces avoidance behaviors, which suggests a role of the tVTA in processing aversive information. Our aim was to test the impact of aversive stimuli on the molecular recruitment of the tVTA, and the behavioral consequences of tVTA lesions. In rats, we assessed Fos response to lithium chloride (LiCl), β-carboline, naloxone, lipopolysaccharide (LPS), inflammatory pain, neuropathic pain, foot-shock, restraint stress, forced swimming, predator odor, and opiate withdrawal. We also determined the effect of tVTA bilateral ablation on physical signs of opiate withdrawal, and on LPS-and LiCl-induced conditioned taste aversion (CTA). Naloxone-precipitated opiate withdrawal induced Fos in μ-opioid receptor-positive (15%) and -negative (85%) tVTA cells, suggesting the presence of both direct and indirect mechanisms in tVTA recruitment during withdrawal. However, tVTA lesion did not impact physical signs of opiate withdrawal. Fos induction was also present with repeated, but not single, foot-shock delivery. However, such induction was mostly absent with other aversive stimuli. Moreover, tVTA ablation had no impact on CTA. Although stimulation of the tVTA favors avoidance behaviors, present findings suggest that this structure may be important to the response to some, but not all, aversive stimuli.

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The Sciatic Nerve Cuffing Model of Neuropathic Pain in Mice

Cited by 63 publications

References 51 publications

TRESK background K⁺ channel deletion selectively uncovers enhanced mechanical and cold sensitivity

TRESK background K⁺ channel deletion selectively uncovers enhanced mechanical and cold sensitivity

TRESK background K⁺ channel deletion selectively uncovers enhanced mechanical and cold sensitivity

Response of the Tail of the Ventral Tegmental Area to Aversive Stimuli

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The Sciatic Nerve Cuffing Model of Neuropathic Pain in Mice

Cited by 63 publications

References 51 publications

TRESK background K+ channel deletion selectively uncovers enhanced mechanical and cold sensitivity

TRESK background K+ channel deletion selectively uncovers enhanced mechanical and cold sensitivity

TRESK background K+ channel deletion selectively uncovers enhanced mechanical and cold sensitivity

Response of the Tail of the Ventral Tegmental Area to Aversive Stimuli

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TRESK background K⁺ channel deletion selectively uncovers enhanced mechanical and cold sensitivity

TRESK background K⁺ channel deletion selectively uncovers enhanced mechanical and cold sensitivity

TRESK background K⁺ channel deletion selectively uncovers enhanced mechanical and cold sensitivity