S Iwai

Wakayama Medical University, Wakayama, Wakayama, Japan

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Publications (3)1.94 Total impact

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    ABSTRACT: Tolerance to morphine analgesia following repeated administration disturbs the continuation of opioid therapy for severe pain. Emerging evidence suggests that the development of morphine tolerance may be antagonized by painful stimuli. To clarify the detailed mechanisms of these phenomena, we examined the effects of several pain stimuli on morphine-induced tolerance. Subcutaneous (s.c.) injection of morphine (10 mg/kg) produced an analgesic effect, which was evaluated by tail-pinch test. Morphine-induced analgesia was diminished by repeated administration of morphine (10 mg/kg, s.c.) once a day for 5 days, demonstrating the development of tolerance. Morphine analgesic tolerance was suppressed by nerve injury-induced neuropathic pain and formalin- or carrageenan-induced inflammatory pain. Tolerance to serum corticosterone elevation by morphine (10 mg/kg), which was evaluated by fluorometric assay, was also suppressed by formalin-induced inflammatory pain. Moreover, morphine analgesia induced by intracerebroventricular (10 nmol) or intrathecal (5 nmol) injection was diminished by repeated administration of morphine s.c., and this was also suppressed by carrageenan-induced inflammatory pain. These results suggest that morphine tolerance is inhibited by several pain stimuli, including neuropathic and inflammatory pain, through central mechanisms.
    No preview · Article · Feb 2012 · Drug discoveries & therapeutics
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    ABSTRACT: To test the possibility of a peroxisome proliferator activated receptor (PPAR) γ agonist to treat neuropathic pain, we examined the effects of pioglitazone, a PPARγ agonist, on tactile allodynia and expression of activated microglia in the dorsal horn of spinal cord using neuropathic pain model. The unilateral sciatic nerve was partially ligated (PSL) in male ICR mice. Pioglitazone (1-25 mg/kg p.o.) was administrated to mice once daily for five days immediately after PSL. We stimulated the footpad of the hind paw of mice using a von Frey filament to estimate tactile allodynia on day 5 of PSL. The activated microglia in the lumbar spinal cord was observed by immunohistochemistry with anti-Iba1 antibody, a marker for activated microglia. The number of Iba1-immunoreactive cells was counted in the dorsal horn spinal cord. On day 5, significant allodynia was developed in PSL mice. Pioglitazone significantly attenuated the tactile allodynia in a dose of 1-25 mg/kg. However, these doses of pioglitazone did not affect nociceptive responses in sham mice. Moreover, on day 6, the number of activated microglia was significantly increased in the ipsilateral dorsal horn of mice. The increase in the number of activated microglia induced by PSL was significantly suppressed by pioglitazone (1-25 mg/kg p.o.). Pioglitazone did not affect the number of activated microglia in sham mice. These results suggest that PPARγ activation inhibits the development of tactile allodynia and the expression of activated microglia in the dorsal horn of spinal cord in mice with PSLinduced peripheral nerve injury.
    Full-text · Article · Dec 2008 · Drug discoveries & therapeutics

  • No preview · Article · Dec 2007 · Neuroscience Research