Botulinum toxin type A and gabapentin attenuate postoperative pain and NK1 receptor internalization in rats

Li, Xueyang; Guo, Renhua; Sun, Yuqing; Li, Huili; Ma, Dong; Zhang, Chen; Guan, Yun; Li, Junfa; Wang, Yun

doi:10.1016/j.neuint.2018.03.010

Cited by 10 publications

(6 citation statements)

References 38 publications

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“…A significant decrease in CGRP expression occurred both at spinal cord and dorsal root ganglia. Finally, in a model of postoperative pain induced by plantar incision in rats, Li et al [124] found that i.th. pretreatment with BoNT/A (0.5 U/rat of Botox ® ), induced a prolonged decrease in pain scores and mechanical hypersensitivity.…”

Section: Central Effects Of Bonts After Direct Injection On Cnsmentioning

confidence: 99%

“…injection of BoNT/B was investigated in different pain model [125,126]. Huang et al [124] found that i.th. pretreatment with BoNT/B (0.5 U/mouse of Myobloc ® ) produced a long-lasting reduction in the release of substance P from spinal afferent nociceptors, the spinal c-Fos expression, and the nociceptive behavior in the model of formalin pain in mice.…”

Section: Central Effects Of Bonts After Direct Injection On Cnsmentioning

confidence: 99%

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Botulinum Neurotoxins in Central Nervous System: An Overview from Animal Models to Human Therapy

Luvisetto

2021

Toxins

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Botulinum neurotoxins (BoNTs) are potent inhibitors of synaptic vesicle fusion and transmitter release. The natural target of BoNTs is the peripheral neuromuscular junction (NMJ) where, by blocking the release of acetylcholine (ACh), they functionally denervate muscles and alter muscle tone. This leads them to be an excellent drug for the therapy of muscle hyperactivity disorders, such as dystonia, spasticity, and many other movement disorders. BoNTs are also effective in inhibiting both the release of ACh at sites other than NMJ and the release of neurotransmitters other than ACh. Furthermore, much evidence shows that BoNTs can act not only on the peripheral nervous system (PNS), but also on the central nervous system (CNS). Under this view, central changes may result either from sensory input from the PNS, from retrograde transport of BoNTs, or from direct injection of BoNTs into the CNS. The aim of this review is to give an update on available data, both from animal models or human studies, which suggest or confirm central alterations induced by peripheral or central BoNTs treatment. The data will be discussed with particular attention to the possible therapeutic applications to pathological conditions and degenerative diseases of the CNS.

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Section: Central Effects Of Bonts After Direct Injection On Cnsmentioning

confidence: 99%

Section: Central Effects Of Bonts After Direct Injection On Cnsmentioning

confidence: 99%

Botulinum Neurotoxins in Central Nervous System: An Overview from Animal Models to Human Therapy

Luvisetto

2021

Toxins

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“…For example, an intraplantar administration of 3.5 and 7 U/kg, but not of 1 U/kg of onabotulinumtoxinA (onaBoNT-A) in rats resulted in similar, near-maximal and enduring (up to 10 days) reversal of mechanical hyperalgesia induced by the gastrocnemius muscle cut 21 . Also, onaBoNT-A given via intraplanar or intrathecal routes, 24 or 48 h before the surgery, respectively, reversed allodynia in the rat (“Brennan”) model of post-surgical pain for 5 days 22 .…”

Section: Discussionmentioning

confidence: 99%

“…The effects of BoNT-A on measures of non-evoked, resting pain have been described in other models of post-surgical pain. For example, in rats, intraplantar or intrathecal injection of onaBoNT-A significantly reduced the cumulative post-surgical pain score–a measure of non-evoked pain based on the position of the operated paw in relation to the cage floor 22 . Also, aboBoNT-A reduced non-evoked postoperative pain and need for rescue analgesia in dogs undergoing radical bilateral mastectomy 23 .…”

Section: Discussionmentioning

confidence: 99%

Intraoperative abobotulinumtoxinA alleviates pain after surgery and improves general wellness in a translational animal model

Cornet

Carré

Limana

et al. 2022

Sci Rep

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Pain after surgery remains a significant healthcare challenge. Here, abobotulinumtoxinA (aboBoNT-A, DYSPORT) was assessed in a post-surgical pain model in pigs. Full-skin-muscle incision and retraction surgery on the lower back was followed by intradermal injections of either aboBoNT-A (100, 200, or 400 U/pig), vehicle (saline), or wound infiltration of extended-release bupivacaine. We assessed mechanical sensitivity, distress behaviors, latency to approach the investigator, and wound inflammation/healing for 5–6 days post-surgery. We followed with immunohistochemical analyses of total and cleaved synaptosomal-associated protein 25 kD (SNAP25), glial fibrillary acidic protein (GFAP), ionized calcium-binding adaptor protein-1(Iba1), calcitonin gene-related peptide (CGRP) and substance P (SP) in the skin, dorsal root ganglia (DRG) and the spinal cord of 400 U aboBoNT-A- and saline-treated animals. At Day 1, partial reversal of mechanical allodynia in aboBoNT-A groups was followed by a full reversal from Day 3. Reduced distress and normalized approaching responses were observed with aboBoNT-A from 6 h post-surgery. Bupivacaine reversed mechanical allodynia for 24 h after surgery but did not affect distress or approaching responses. In aboBoNT-A-treated animals cleaved SNAP25 was absent in the skin and DRG, but present in the ipsilateral dorsal horn of the spinal cord. In aboBoNT-A- versus saline-treated animals there were significant reductions in GFAP and Iba1 in the spinal cord, but no changes in CGRP and SP. Analgesic efficacy of aboBoNT-A appears to be mediated by its activity on spinal neurons, microglia and astrocytes. Clinical investigation to support the use of aboBoNT-A as an analgesic drug for post-surgical pain, is warranted.

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“…Measuring the concentration of NK1 receptors in postsynaptic dorsal horn neurons has been used to indicate the release of SP into the spinal cord. 32 SP is the main excitatory neurotransmitter of afferent C-fibers and contributes to the development and maintenance of neuropathic pain. 33,34 SP is an important molecule in the neurogenic inflammation pathway and plays a key role in eliciting pain sensation in the central and peripheral nervous system.…”

Section: Discussionmentioning

confidence: 99%

<p>The Antiallodynic Effect of Nefopam on Vincristine-Induced Neuropathy in Mice</p>

Lee

Sim

Cho

et al. 2020

JPR

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Background: Chemotherapy-induced neuropathic pain is a disabling condition following cancer treatment. Vincristine has more neurotoxicity than other vinca alkaloid agents. This study evaluated the correlation of different doses of nefopam with antiallodynic effects in a mouse vincristine neuropathy model. Methods: A peripheral neuropathic mouse model was made by intraperitoneal injection of vincristine (0.1 mg/kg/day; 5-day-on, 2-day-off schedule over 12 days). After the development of allodynia, mice were injected intraperitoneally with 0.9% normal saline (NS group) or various doses (10, 30, 60 mg/kg) of nefopam (Nefopam group). We examined allodynia using von Frey hairs pre-administration and at 30, 60, 90, 120, 180, 240 mins, and 24 hrs after drug administration. We also measured the neurokinin-1 receptor concentrations in the spinal cord to confirm the antiallodynic effect of nefopam after drug administration. Results: The peripheral neuropathic mouse model showed prominent mechanical allodynia. Intraperitoneal nefopam produced a clear dose-dependent increase in paw withdrawal threshold compared with pre-administration values and versus the NS group. The concentration of neurokinin-1 receptor was significantly decreased in the Nefopam group (P<0.05). Conclusion: Intraperitoneally administered nefopam yielded a dose-dependent attenuation of mechanical allodynia and decreased neurokinin-1 receptor concentration, suggesting that the neurokinin-1 receptor is involved in the antiallodynic effects of nefopam in vincristine neuropathy.

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Botulinum toxin type A and gabapentin attenuate postoperative pain and NK1 receptor internalization in rats

Cited by 10 publications

References 38 publications

Botulinum Neurotoxins in Central Nervous System: An Overview from Animal Models to Human Therapy

Botulinum Neurotoxins in Central Nervous System: An Overview from Animal Models to Human Therapy

Intraoperative abobotulinumtoxinA alleviates pain after surgery and improves general wellness in a translational animal model

<p>The Antiallodynic Effect of Nefopam on Vincristine-Induced Neuropathy in Mice</p>

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