Effects of tapentadol on mechanical hypersensitivity in rats with ligatures of the infraorbital nerve versus the sciatic nerve

Michot, B.; Bourgoin, S.; Kayser, V.; Hamon, Michel

doi:10.1002/j.1532-2149.2012.00259.x

Cited by 17 publications

(15 citation statements)

References 41 publications

(69 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Compared with SDH, the MDH displays a broader density of IB4-positive fibers which cross laminae I and outer and inner part of lamina II (IIo and IIi) (Ambalavanar and Morris, 1992;Sugimoto et al, 1997). With respect to pharmacology, the efficacy of antinociceptive drugs is different at the trigeminal versus spinal level (Latr emolière et al, 2008;Kayser et al, 2010;Michot et al, 2013Michot et al, , 2014Michot et al, , 2015. Therefore, data gleaned from studies in SDH cannot be directly extrapolated to MDH. In this context, developmental changes affecting the PKCc interneurons within the MDH were studied.…”

Section: Introductionmentioning

confidence: 99%

Lamina specific postnatal development of PKCγ interneurons within the rat medullary dorsal horn

Mermet-Joret

Chatila

Pereira³

et al. 2016

Developmental Neurobiology

View full text Add to dashboard Cite

Protein kinase C gamma (PKCγ) interneurons, located in the superficial spinal (SDH) and medullary dorsal horns (MDH), have been shown to play a critical role in cutaneous mechanical hypersensitivity. However, a thorough characterization of their development in the MDH is lacking. Here, it is shown that the number of PKCγ-ir interneurons changes from postnatal day 3 (P3) to P60 (adult) and such developmental changes differ according to laminae. PKCγ-ir interneurons are already present at P3-5 in laminae I, IIo, and III. In lamina III, they then decrease from P11-P15 to P60. Interestingly, PKCγ-ir interneurons appear only at P6 in lamina IIi, and they conversely increase to reach adult levels at P11-15. Analysis of neurogenesis using bromodeoxyuridine (BrdU) does not detect any PKCγ-BrdU double-labeling in lamina IIi. Quantification of the neuronal marker, NeuN, reveals a sharp neuronal decline (∼50%) within all superficial MDH laminae during early development (P3-15), suggesting that developmental changes in PKCγ-ir interneurons are independent from those of other neurons. Finally, neonatal capsaicin treatment, which produces a permanent loss of most unmyelinated afferent fibers, has no effect on the development of PKCγ-ir interneurons. Together, the results show that: (i) the expression of PKCγ-ir interneurons in MDH is developmentally regulated with a critical period at P11-P15, (ii) PKCγ-ir interneurons are developmentally heterogeneous, (iii) lamina IIi PKCγ-ir interneurons appear less vulnerable to cell death, and (iv) postnatal maturation of PKCγ-ir interneurons is due to neither neurogenesis, nor neuronal migration, and is independent of C-fiber development. © 2016 Wiley Periodicals, Inc. Develop Neurobiol 77: 102-119, 2017.

show abstract

Section: Introductionmentioning

confidence: 99%

Lamina specific postnatal development of PKCγ interneurons within the rat medullary dorsal horn

Mermet-Joret

Chatila

Pereira³

et al. 2016

Developmental Neurobiology

View full text Add to dashboard Cite

show abstract

“…Regarding the first goal of our investigations, i.e., comparison of anti-allodynic effects in CCI-SN versus CCI-ION rats, ‘agomelatine + gabapentin’ markedly differs from other pain alleviating drugs, especially tricyclic antidepressants ( Idänpään-Heikkila and Guilbaud, 1999 ), because this drug combination was effective in both models. In this regard, it closely resembles tapentadol, a mixed μ opioid receptor agonist and NA reuptake inhibitor, which exerts potent anti-allodynic effects at both cephalic and extra-cephalic levels ( Michot et al, 2013 ). As ‘agomelatine + gabapentin,’ like tapentadol, also acts through NA neurotransmission, it can be asked whether a concomitant action through opioidergic mechanisms might contribute to its effective anti-allodynic effects in both CCI-SN and CCI-ION rats.…”

Section: Discussionmentioning

confidence: 99%

“…As for the CCI-ION rats, a time interval of at least 3 s allowed the rat to recover its initial resting state between two filament applications. The minimal force filament for which animals presented a nocifensive response to at least 2 out of the 3 stimulations allowed determination of the mechanical response threshold ( Latrémolière et al, 2008 ; Michot et al, 2012a , 2013 ). The 60 g filament was chosen as the cut-off threshold.…”

Section: Methodsmentioning

confidence: 99%

α2- and β2-Adrenoreceptor-Mediated Efficacy of the Atypical Antidepressant Agomelatine Combined With Gabapentin to Suppress Allodynia in Neuropathic Rats With Ligated Infraorbital or Sciatic Nerve

et al. 2018

View full text Add to dashboard Cite

Previous data showed that neuropathic pain induced by mechanical lesion of peripheral nerves has specific characteristics and responds differently to alleviating drugs at cephalic versus extracephalic level. This is especially true for tricyclic antidepressants currently used for alleviating neuropathic pain in humans which are less effective against cephalic neuropathic pain. Whether this also applies to the antidepressant agomelatine, with its unique pharmacological properties as MT1/MT2 melatonin receptor agonist and 5-HT2B/5-HT2C serotonin receptor antagonist, has been investigated in two rat models of neuropathic pain. Acute treatments were performed 2 weeks after unilateral chronic constriction (ligation) injury to the sciatic nerve (CCI-SN) or the infraorbital nerve (CCI-ION), when maximal mechanical allodynia had developed in ipsilateral hindpaw or vibrissal pad, respectively, in Sprague–Dawley male rats. Although agomelatine (45 mg/kg i.p.) alone was inactive, co-treatment with gabapentin, at an essentially ineffective dose (50 mg/kg i.p.) on its own, produced marked anti-allodynic effects, especially in CCI-ION rats. In both CCI-SN and CCI-ION models, suppression of mechanical allodynia by ‘agomelatine + gabapentin’ could be partially mimicked by the combination of 5-HT2C antagonist (SB 242084) + gabapentin, but not by melatonin or 5-HT2B antagonist (RS 127445, LY 266097), alone or combined with gabapentin. In contrast, pretreatment by idazoxan, propranolol or the β2 antagonist ICI 118551 markedly inhibited the anti-allodynic effect of ‘agomelatine + gabapentin’ in both CCI-SN and CCI-ION rats, whereas pretreatment by the MT1/MT2 receptor antagonist S22153 was inactive. Altogether these data indicate that ‘agomelatine + gabapentin’ is a potent anti-allodynic combination at both cephalic and extra-cephalic levels, whose action implicates α2- and β2-adrenoreceptor-mediated noradrenergic neurotransmission.

show abstract

“…We also showed a differential overexpression of the neuroinflammatory mediators interleukin-6 and brain-derived neurotrophic factor 3,8 , suggesting that mechanisms underlying glial activation are different after infraorbital nerve ligation or sciatic nerve ligation. Indeed, the microglial inhibitor minocycline, reduced neuropathic pain in sciatic nerve ligated rats but was inefficient in trigeminal nerve ligated rats 3 .…”

mentioning

confidence: 81%

“…Using models of chronic constriction injury of either the infraorbital nerve (trigeminal system) or the sciatic nerve (spinal system) we showed that the time course of pain development and the pain duration are different in these models 7 . We also showed a differential overexpression of the neuroinflammatory mediators interleukin-6 and brain-derived neurotrophic factor 3,8 , suggesting that mechanisms underlying glial activation are different after infraorbital nerve ligation or sciatic nerve ligation. Indeed, the microglial inhibitor minocycline, reduced neuropathic pain in sciatic nerve ligated rats but was inefficient in trigeminal nerve ligated rats 3 .…”

mentioning

confidence: 81%

Commentary: Immunohistochemical comparison of astrocytic mGluR5 upregulation in infraorbital nerve- versus sciatic nerve-ligated rat

Michot¹

2017

J Neurol Neuromedicine

View full text Add to dashboard Cite

Neuropathic pain is described as a pain caused by nerve injury or disease that affects the somatosensory system. It is the most difficult to treat, available treatments such as antidepressants, anticonvulsants and opioids have a relative efficacy and dose limiting side effects. Understanding the underlying mechanisms of neuropathic pain is critical to find more efficient and more tolerable treatments.In the past two decades, neuroinflammation has been shown to play an important role in the development and the maintenance of neuropathic pain. Central neuroinflammatory processes are mainly mediated by two glial cells, microglia and astrocytes, which inhibition reduced neuropathic pain [1][2][3] . However, depending on the type of neuropathic pain, glial inhibitors have differential efficacy that would be related to different neuroinflammatory mechanisms. It was shown that neuropathic pain induced by anticancer drugs involves neuroinflammatory processes mediated by astrocytes but not microglia 4 , on the contrary neuropathic pain induced by nerve constriction involves both astrocytes and microglia activation 3 . Moreover, depending on the nerve injured, glial inhibitors have differential effects; propentofylline, which inhibit both astrocytes and microglia activation, reduced pain in L5 spinal nerve ligation model but was totally inefficient to reduced pain after crush of tibial and peroneal nerves 1,5 . Similarly, our previous works showed that neuropathic pain affecting the trigeminal system have specific pharmacological and physiopathological characteristics compared to pain affecting the spinal system 3,6 . Using models of chronic constriction injury of either the infraorbital nerve (trigeminal system) or the sciatic nerve (spinal system) we showed that the time course of pain development and the pain duration are different in these models 7. We also showed a differential overexpression of the neuroinflammatory mediators interleukin-6 and brain-derived neurotrophic factor 3,8 , suggesting that mechanisms underlying glial activation are different after infraorbital nerve ligation or sciatic nerve ligation. Indeed, the microglial inhibitor minocycline, reduced neuropathic pain in sciatic nerve ligated rats but was inefficient in trigeminal nerve ligated rats 3 . Because commonly used glial inhibitors are non-selective drugs, which effects on glial cells is poorly understood and depends on the type of neuropathic pain, studies aiming at understand specific mechanisms underlying glial dysregulation are particularly important in the pain field.Among glial cells involved in neuroinflammatory processes, astrocytes are particularly important in the regulation of neuronal communication. Astrocytes uptake glutamate form the synaptic cleft and release neurotransmitters such as glutamate and D-serine. Previous studies

show abstract

Effects of tapentadol on mechanical hypersensitivity in rats with ligatures of the infraorbital nerve versus the sciatic nerve

Abstract: The dual synergistic pharmacological properties of tapentadol, which result in clear-cut anti-neuropathic pain effects at both cephalic and extra-cephalic levels, probably involve mechanisms downstream of nerve injury-induced neuroinflammatory reaction.

Cited by 17 publications

References 41 publications

Lamina specific postnatal development of PKCγ interneurons within the rat medullary dorsal horn

Lamina specific postnatal development of PKCγ interneurons within the rat medullary dorsal horn

α2- and β2-Adrenoreceptor-Mediated Efficacy of the Atypical Antidepressant Agomelatine Combined With Gabapentin to Suppress Allodynia in Neuropathic Rats With Ligated Infraorbital or Sciatic Nerve

Commentary: Immunohistochemical comparison of astrocytic mGluR5 upregulation in infraorbital nerve- versus sciatic nerve-ligated rat

Contact Info

Product

Resources

About