The antinociceptive effect of fluvoxamine

Schreiber, Shaul; Backer, Maria M; Yanai, Joseph; Pick, Chaim G.

doi:10.1016/s0924-977x(96)00031-4

Cited by 70 publications

(35 citation statements)

References 15 publications

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“…Milnacipran and fluvoxamine are used for the treatment of acute and neuropathic pain as a supplementary analgesic (16,21). 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).…”

Section: Discussionmentioning

confidence: 99%

“…The antinociceptive effects of SSRIs have been reported in a number of animal experiments (12,13,25). 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).…”

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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Section: Discussionmentioning

confidence: 99%

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

confidence: 99%

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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“…Antidepressant drugs including tricyclic antidepressants and SSRIs show analgesic activity (Messing et al, 1975;Lin et al, 1980;Schreiber et al, 1996;Korzeniewska-Rybicka and Plaznik, 2000;Galeotti et al, 2001). Studies using GIRK2-deficient mice and weaver mutant mice, which have mutant GIRK2 channels insensitive to G proteins and ethanol, have shown that the analgesic effects induced by opioids or ethanol are remarkably reduced in these mice, suggesting that the GIRK channel activation induces analgesia (Kobayashi et al, 1999;Ikeda et al, 2000Ikeda et al, , 2002Blednov et al, 2003;Mitrovic et al, 2003).…”

Section: Discussionmentioning

confidence: 99%

Inhibition of G Protein-Activated Inwardly Rectifying K+ Channels by Various Antidepressant Drugs

Kobayashi

Washiyama

Ikeda

2004

Neuropsychopharmacol

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G protein-activated inwardly rectifying K þ channels (GIRK, also known as Kir3) are activated by various G protein-coupled receptors. GIRK channels play an important role in the inhibitory regulation of neuronal excitability in most brain regions and the heart rate. Modulation of GIRK channel activity may affect many brain functions. Here, we report the inhibitory effects of various antidepressants: imipramine, desipramine, amitriptyline, nortriptyline, clomipramine, maprotiline, and citalopram, on GIRK channels. In Xenopus oocytes injected with mRNAs for GIRK1/GIRK2, GIRK2 or GIRK1/GIRK4 subunits, the various antidepressants tested, except fluvoxamine, zimelidine, and bupropion, reversibly reduced inward currents through the basal GIRK activity at micromolar concentrations. The inhibitions were concentration-dependent with various degrees of potency and effectiveness, but voltage-and time-independent. In contrast, Kir1.1 and Kir2.1 channels in other Kir channel subfamilies were insensitive to all of the drugs. Furthermore, GIRK current responses activated by the cloned A 1 adenosine receptor were similarly inhibited by the tricyclic antidepressant desipramine. The inhibitory effects of desipramine were not observed when desipramine was applied intracellularly, and were not affected by extracellular pH, which changed the proportion of the uncharged to protonated desipramine, suggesting its action from the extracellular side. The GIRK currents induced by ethanol were also attenuated in the presence of desipramine. Our results suggest that inhibition of GIRK channels by the tricyclic antidepressants and maprotiline may contribute to some of the therapeutic effects and adverse side effects, especially seizures and atrial arrhythmias in overdose, observed in clinical practice.

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“…Two cohorts of NmU Tg mice (n=11 and 14) and wild-type littermates (n=14 and 15) were maintained on chow and tested in a behavioral battery including the following: the primary observational screen from the SHIRPA protocol (Rogers et al 1999), locomotor activity (LMA; Coulbourn Tru-Scan, 60 min), elevated plus maze (transparent closed arms, 5 min), accelerating rotarod (Accuscan SmartRod, eight trials, acceleration rate: 20 r.p.m./60 s), spatial Y-maze (Dellu et al 2000), motor coordination battery (Lalonde et al 1994, Klein et al 1996, Carter et al 1999, Contet et al 2001, hotplate (Schreiber et al 1996), tail suspension (Steru et al 1985), forced swim (Redrobe & Bourin 1998), warm water tail flick (Janssen 1963), auditory startle threshold (Varty et al 2001), prepulse inhibition of auditory startle (Varty et al 2001), passive avoidance (one-trial step-through, 2 s 0·6 mA, 24-h retention, 300 s maximum) and pentylenetetrazole-induced seizure threshold (Nutt et al 1986). The group housed mice began testing when they were 12-24 weeks and ended when they were 20-31 weeks of age.…”

Section: Behavioral Studiesmentioning

confidence: 99%

Transgenic overexpression of neuromedin U promotes leanness and hypophagia in mice

Kowalski¹,

Spar²,

Markowitz³

et al. 2005

Journal of Endocrinology

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Recent work has shown that neuromedin U (NmU), a peptide initially identified as a smooth muscle contractor, may play a role in regulating food intake and energy homeostasis. To further evaluate this putative function, we measured food intake, body weight, energy expenditure and glucose homeostasis in transgenic mice that ubiquitously overexpress murine proNmU. NmU transgenic mice were lighter and had less somatic and liver fat, were hypophagic, and had improved insulin sensitivity as judged by an intraperitoneal insulin tolerance test. Transgenic mice had higher levels of hypothalamic NPY, POMC and MCH mRNA. There was no difference in O 2 consumption between genotypes; however, NmU transgenic mice displayed a modest increase in respiratory quotient during food deprivation and refeeding. There were no behavioral disturbances in the NmU transgenic mice that could account for the results (e.g. changes in locomotor activity). When placed on a high-fat diet, transgenic mice remained lighter than wild-type mice and ate less, but gained weight at a rate similar to wild-type mice. Despite the increased weight gain with high-fat feeding, glucose tolerance was significantly improved in the transgenic mice. These findings support the hypothesized role of NmU as an endogenous anorexigenic peptide.

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The antinociceptive effect of fluvoxamine

Cited by 70 publications

References 15 publications

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

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

Inhibition of G Protein-Activated Inwardly Rectifying K+ Channels by Various Antidepressant Drugs

Transgenic overexpression of neuromedin U promotes leanness and hypophagia in mice

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