Footshock- and Psychological-Stress Prevent the Development of Tolerance to Spinal but Not Supraspinal Morpine.

Takahashi, Masakatsu; Kaneto, Hiroshi

doi:10.1254/jjp.56.121

Cited by 9 publications

(2 citation statements)

References 15 publications

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“…In a previous report, we demonstrated that the effect of morphine given daily i.t. was suppressed by the concomitant exposure to socio-psychological stress (30) or a subanalgesic dose of U-50,488H (27,28), both of which were antagonized by nor-binaltorphimine, implicating the k -receptor mechanism in the spine. The result shown here that SNL mice showed a persistent antinociceptive effect of U-50,488H when it was given i.t.…”

Section: Discussionmentioning

confidence: 95%

Disability of Development of Tolerance to Morphine and U-50,488H, a Selective κ-Opioid Receptor Agonist, in Neuropathic Pain Model Mice

et al. 2004

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Abstract. We examined the analgesic and anti-allodynic effects of morphine and U-50,488H (trans-(±)-3,4-dichloro-N-methyl-N-(2-[1-pyrrolidinyl]-cyclohexyl)-benzeneacetamide methanesulfonate salt), a selective k-opioid receptor agonist, and the development of tolerance to their effects in neuropathic pain model mice induced by sciatic nerve ligation (SNL). In the tail-pinch method, morphine at 10 mg / kg, s.c. produced a weak analgesic effect in SNL mice; however, U-50,488H at 5 mg / kg, s.c. produced an analgesic effect equipotent to that in normal mice. In contrast, morphine produced an adequate analgesic effect when given either intracerebroventricularly (i.c.v.) or intrathecally (i.t.), but U-50,488H only produced analgesia when given i.t. Repeated administration of morphine (either i.c.v. or i.t.) or U-50,488H (either s.c. or i.t.), did not induce tolerance to the effect. In the static allodynia test with an application of von Frey filaments, both compounds given s.c. suppressed the allodynic effect, but in the dynamic allodynia test involving lightly stroking the plantar surface with a cotton bud, only U-50,488H produced an anti-allodynic effect. Repeated administrations of both compounds did not develop tolerance to these anti-allodynic effects. Thus, U-50488H was found to be a highly effective at blocking hyperalgesia and allodynia in nerve injury, and these findings suggest that k-opioid receptor agonists are attractive pharmacological targets for the control of patients with neuropathic pain.

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Section: Discussionmentioning

confidence: 95%

Disability of Development of Tolerance to Morphine and U-50,488H, a Selective κ-Opioid Receptor Agonist, in Neuropathic Pain Model Mice

et al. 2004

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“…Stressors such as pain (Melzack, 1990;Solan and Melzack, 1999;Javan et al, 2005), psychological stress (Takahashi et al, 1988(Takahashi et al, , 1992Tokuyama et al, 1989;Takahashi and Kaneto, 1991) and forced swim stress (Ghiafeh-Davoodi et al, 2005) prevent morphine tolerance.…”

Section: Introductionmentioning

confidence: 99%

Chronic forced swim stress inhibits ultra-low dose morphine-induced hyperalgesia in rats

Fereidoni

Javan

Semnanian

et al. 2007

Behavioural Pharmacology

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Ultra-low doses of morphine (UL-morphine) induce hyperalgesia, which is assumed to be mediated by stimulatory G proteins (G(alphas)) signaling pathway. G(alphas) pathway inhibition and chronic stress both attenuate development of tolerance to analgesic effect of morphine. This study evaluated the effect of chronic stress on UL-morphine-induced hyperalgesia to find out if chronic stress interacts with the G(alphas) signaling pathway. Repeated daily forced swim stress was applied to induce chronic stress. UL-morphine (1 microg/kg, intraperitoneal)-induced hyperalgesia was assessed using the tail-flick test on day 6, in male rats that during days 1-5 received different treatments of swim stress, dexamethasone, swim stress following adrenalectomy (ADX) or swim stress after sham operation. Chronic stress by itself induced hyperalgesia in control and sham-operated rats but inhibited UL-morphine-induced hyperalgesia. In ADX animals, chronic stress did not produce hyperalgesia and could not inhibit UL-morphine-induced hyperalgesia. Chronic dexamethasone produced hyperalgesia but did not change the UL-morphine-induced hyperalgesia. Inhibition of UL-morphine hyperalgesia by chronic stress suggests that chronic stress interacts with the G(alphas) signaling pathway, which is responsible for UL-morphine-induced hyperalgesia. The absence of this effect in the ADX-rats or after repetitive dexamethasone administration demonstrates that hypothalamic-pituitary-adrenal (HPA) axis activation is necessary for controlling UL-morphine-induced hyperalgesia. Finally, the interaction of stress with the G(alphas) signaling pathway may provide an explanation for the inhibitory effect of stress on development of tolerance to the analgesic effect of morphine.

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Does chronic nociceptive stimulation alter the development of morphine tolerance?

1995

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Footshock- and Psychological-Stress Prevent the Development of Tolerance to Spinal but Not Supraspinal Morpine.

Cited by 9 publications

References 15 publications

Disability of Development of Tolerance to Morphine and U-50,488H, a Selective κ-Opioid Receptor Agonist, in Neuropathic Pain Model Mice

Disability of Development of Tolerance to Morphine and U-50,488H, a Selective κ-Opioid Receptor Agonist, in Neuropathic Pain Model Mice

Chronic forced swim stress inhibits ultra-low dose morphine-induced hyperalgesia in rats

Does chronic nociceptive stimulation alter the development of morphine tolerance?

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