Effects of intrathecal administration of newer antidepressants on mechanical allodynia in rat models of neuropathic pain

Ikeda, Tetsuya; Ishida, Yoshiteru; Naono, Rumi; Takeda, Ryuichiro; Abe, Hiroshi; Nakamura, Tadashi; Nishimori, Toshikazu

doi:10.1016/j.neures.2008.10.002

Cited by 45 publications

(47 citation statements)

References 30 publications

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“…It was then modified to implant a single cuff 7,8 , even though some research groups still use multiple cuff insertion [19][20][21][22] . It was then adapted to mice 9,23 , which opened the possibility to use transgenic animals.…”

Section: Discussionmentioning

confidence: 99%

The Sciatic Nerve Cuffing Model of Neuropathic Pain in Mice

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Megat

Barthas

et al. 2014

JoVE

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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%

The Sciatic Nerve Cuffing Model of Neuropathic Pain in Mice

Yalçın

Megat

Barthas

et al. 2014

JoVE

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“…There have been several reports indicating that milnacipran and fluvoxamine have significant antinociceptive effects against nociceptive and inflammatory pain (20,22,27,28,30). Furthermore, milnacipran was more effective than SSRIs such as fluvoxamine, paroxetine, and citalopram in attenuating persistent pain (30) and neuropathic pain (9), and more effective than amitriptyline (TCAs) in attenuating cold allodynia (4°C cold plate stimuli) (1). However, the efficacy of milnacipran and fluvoxamine in attenuating paclitaxel-induced mechanical allodynia (tactile stimuli) is poorly understood.…”

Section: Discussionmentioning

confidence: 99%

“…One typical SSRI, fluvoxamine, attenuated licking behavior in the late phase of the formalin test (22,30) and also in the hot-plate test (27), but it failed to attenuate mechanical allodynia in a neuropathic pain model (chronic constriction injury model) (9). Moreover, fluvoxamine showed an antiallodynic effect in a streptozotocin-induced diabetic neuropathy model (9). Similar to the research on SSRIs, the analgesic effects of SNRIs have also been examined using a variety of animal models of pain (18).…”

Section: Time Course and Dose-response Of Paclitaxel-induced Mechanicmentioning

confidence: 98%

“…One typical SNRI, milnacipran, has been shown to be efficacious for the prevention and/or reversal of pain in several preclinical models of acute and chronic pain in rodents. Yokogawa et al demonstrated that milnacipran significantly attenuated late phase paw licking behavior in the formalin test (30) and also reversed mechanical allodynia in the chronic constriction injury model or spinal nerve ligation model of neuropathic pain (9,28). In addition, milnacipran had an antiallodynic effect on the streptozotocin-induced diabetic neuropathy model (9) and potentiated the antihyperalgesic effect of tramadol (opioid analgesic) (21).…”

Section: Time Course and Dose-response Of Paclitaxel-induced Mechanicmentioning

confidence: 99%

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Effects of repeated milnacipran and fluvoxamine treatment on mechanical allodynia in a mouse paclitaxel-induced neuropathic pain model

et al. 2013

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Paclitaxel is widely used in cancer chemotherapy for the treatment of solid tumors, but it frequently causes peripheral neuropathy. Milnacipran, a serotonin/noradrenaline reuptake inhibitor and fluvoxamine, a selective serotonin reuptake inhibitor, have shown efficacy against several chronic pain syndromes. In this study, we investigated the attenuation of paclitaxel-induced mechanical allodynia in mice by milnacipran and fluvoxamine. Paclitaxel was administered once per day (2 mg/kg, intraperitoneally (i.p.)) for 5 days to mice. Mechanical allodynia was evaluated by measuring the withdrawal response to stimulation with a von Frey filament. In paclitaxel-treated mice, mechanical allodynia was observed on days 3-15 of paclitaxel administration. A single administration of milnacipran (20 mg/kg, i.p.) or fluvoxamine (40 mg/kg, i.p.) had no effect on paclitaxel-induced mechanical allodynia. However, repeated administration of milnacipran (10, 20 mg/kg, once per day, i.p.) for 5 days significantly reduced paclitaxel-induced mechanical allodynia. In contrast, repeated fluvoxamine administration (40 mg/kg, once per day, i.p.) for 5 days resulted in a weak attenuation of paclitaxel-induced mechanical allodynia. These results suggest that chronic paclitaxel administration induces mechanical allodynia, and that repeated milnacipran administration may be an effective therapeutic approach for the treatment of neuropathic pain caused by paclitaxel treatment for cancer.Peripheral neurotoxicity induced by antineoplastic drugs (taxanes, vinca-alkaloids and platin-based compounds) is a clinically significant complication that can be dose-limiting and can substantially diminish quality of life. Paclitaxel is commonly used for the treatment of solid tumors and ovarian and breast cancers. Paclitaxel induces antimitotic actions by impeding the cell cycle in the late phases of mitosis, stabilizing microtubule formation, and ultimately inducing apoptosis (26). However, paclitaxelinduced peripheral neuropathy is a side-effect of chemotherapeutic treatment which often manifests as bilateral pain in the extremities in a stocking and glove-type distribution (6), sometimes greatly impairing the patients' quality of life and their ability to perform normal activities of daily living. To date, therapeutic drugs have been evaluated using various animal models of paclitaxel-induced allodynia. Ethosuximide (7), gabapentin (14), thalidomide and minocycline (3), neurotropin (11) and acetyl-L-carnitine (8) have been examined against the paclitaxelinduced neuropathic pain model, although studies regarding their efficacy have not been conclusive. Supplementary analgesics (antidepressants and anticonvulsants) have suppressive effects on opioid-resistant neuropathic pain (16,24), and antidepressants are widely used for the treatment of neuropathic pain. Antidepressants, especially tricyclic antidepressants (TCAs), are regarded as first-line drugs for the treatment of neuropathic pain (16). Recently, more selective monoamine reuptake inhibitors...

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“…79 Intrathecal milnacipran, a newer reuptake inhibitor, was antiallodynic. 80 Comparatively high doses of amitriptyline block mechanical hyperalgesia. 81 Intrathecal administration of a chi-conopeptide, Xen2174, reversed mechanoallodynia through a related mechanism as it blocked the norepinephrine transporter.…”

Section: Chronic Loose Ligationmentioning

confidence: 99%

Behavioral Models of Pain States Evoked by Physical Injury to the Peripheral Nerve

Sorkin

Yaksh

2009

Neurotherapeutics

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Summary:Physical injury or compression of the root, dorsal root ganglion, or peripheral sensory axon leads to welldefined changes in biology and function. Behaviorally, humans report ongoing painful dysesthesias and aberrations in function, such that an otherwise innocuous stimulus will yield a pain report. These behavioral reports are believed to reflect the underlying changes in nerve function after injury, wherein increased spontaneous activity arises from the neuroma and dorsal root ganglion and spinal changes increase the response of spinal projection neurons. These pain states are distinct from those associated with tissue injury and pose particular problems in management. To provide for developing an understanding of the underlying mechanisms of these pain states and to promote development of therapeutic agents, preclinical models involving section, compression, and constriction of the peripheral nerve or compression of the dorsal root ganglion have been developed. These models give rise to behaviors, which parallel those observed in the human after nerve injury. The present review considers these models and their application.

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Effects of intrathecal administration of newer antidepressants on mechanical allodynia in rat models of neuropathic pain

Cited by 45 publications

References 30 publications

The Sciatic Nerve Cuffing Model of Neuropathic Pain in Mice

The Sciatic Nerve Cuffing Model of Neuropathic Pain in Mice

Effects of repeated milnacipran and fluvoxamine treatment on mechanical allodynia in a mouse paclitaxel-induced neuropathic pain model

Behavioral Models of Pain States Evoked by Physical Injury to the Peripheral Nerve

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