Antidepressants suppress neuropathic pain by a peripheral β2-adrenoceptor mediated anti-TNFα mechanism

Bohren, Yohann; Tessier, Luc-Henri; Megat, Salim; Petitjean, Hugues; Hugel, Sylvain; Daniel, Dorothée; Kremer, Mélanie; Fournel, Sylvie; Hein, Lutz; Schlichter, Rémy; Freund-Mercier, Marie José; Yalçın, İpek; Barrot, Michel

doi:10.1016/j.nbd.2013.08.012

Cited by 61 publications

(82 citation statements)

References 63 publications

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“…Similar to clinical observations: gabapentinoids display both an acute short-lasting analgesic action at high dose and a delayed sustained relieving action that is observed after a few days of treatment, tricyclic antidepressants and selective serotonin and noradrenaline reuptake inhibitors have no acute analgesic effect at relevant dose but they display a delayed sustained relieving action that requires 1 to 2 weeks of treatment, and the selective serotonin reuptake inhibitor fluoxetine is ineffective 16 . The model is thus appropriate to study the molecular mechanism underlying these treatments [16][17][18]44,45,47 , which may reveal new therapeutic targets to test in patients [48][49][50][51] .…”

Section: Discussionmentioning

confidence: 99%

“…The possibility to use genetically modified animals 17,18,[44][45][46][47]52 , the long-lasting allodynia, the response to clinically used treatments and the time-dependent development of anxiodepressive symptoms make this model appropriate for the study of the various aspects and consequences of neuropathic pain and its treatments, which have already brought valuable information to this field of research.…”

Section: Discussionmentioning

confidence: 99%

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The Sciatic Nerve Cuffing Model of Neuropathic Pain in Mice

Yalçın

Megat

Barthas

et al. 2014

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Neuropathic pain arises as a consequence of a lesion or a disease affecting the somatosensory system. This syndrome results from maladaptive changes in injured sensory neurons and along the entire nociceptive pathway within the central nervous system. It is usually chronic and challenging to treat. In order to study neuropathic pain and its treatments, different models have been developed in rodents. These models derive from known etiologies, thus reproducing peripheral nerve injuries, central injuries, and metabolic-, infectious-or chemotherapy-related neuropathies. Murine models of peripheral nerve injury often target the sciatic nerve which is easy to access and allows nociceptive tests on the hind paw. These models rely on a compression and/or a section. Here, the detailed surgery procedure for the "cuff model" of neuropathic pain in mice is described. In this model, a cuff of PE-20 polyethylene tubing of standardized length (2 mm) is unilaterally implanted around the main branch of the sciatic nerve. It induces a long-lasting mechanical allodynia, i.e., a nociceptive response to a normally non-nociceptive stimulus that can be evaluated by using von Frey filaments. Besides the detailed surgery and testing procedures, the interest of this model for the study of neuropathic pain mechanism, for the study of neuropathic pain sensory and anxiodepressive aspects, and for the study of neuropathic pain treatments are also discussed.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

The Sciatic Nerve Cuffing Model of Neuropathic Pain in Mice

Yalçın

Megat

Barthas

et al. 2014

JoVE

Self Cite

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“…Neurotransmitters such as serotonin (5-hydroxytryptamine; 5-HT) and noradrenaline (NA) have been implicated in pain modulation and many antidepressants that increase the synaptic cleft levels of these neurotransmitters are considered first-line treatment for certain types of chronic pain. 3,9,20,56 It is well established that increases in the levels of 5-HT and NA in the spinal cord can potentiate antinociception. 26,30,52,55,66 The neurotransmitter g-aminobutyric acid (GABA) is also critical for regulating pain processing.…”

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confidence: 99%

Manipulation of Neurotransmitter Levels Has Differential Effects on Formalin-Evoked Nociceptive Behavior in Male and Female Mice

Mifflin

Benson

Thorburn

et al. 2016

The Journal of Pain

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“…This salbutamol-induced antinociceptive effect is most likely mediated by β 2 AR stimulation as evidenced by the observation that the non-selective beta blocker, namely propranolol, rather than the selective beta blocker, namely atenolol, significantly decreased salbutamol-induced anti-nociceptive 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 56 57 58 59 60 61 62 63 64 effect. Thus, the adrenergic system, because of its reported implication in pain mechanism, may be a potential target for chronic pain treatment (Bohren et al, 2013). Currently, antidepressants are one of the first line drug options in neuropathic pain management.…”

Section: Discussionmentioning

confidence: 99%