Rapid development of tolerance to morphine in the formalin test

Connell, Barry J.; Barnes, Julie C.; Blatt, Tasha; Tasker, R. Andrew

doi:10.1097/00001756-199403000-00020

Cited by 12 publications

(2 citation statements)

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“…Most notably, various different procedures to induce pain have been used: cold-water immersion (e.g., Conley et al, 1997), neuropathic stimulation (e.g., Backonja, Miletic, & Miletic, 1995), mechanical stimulation (e.g., Colpaert, Niemegeers, & Janssen, 1978), ischemia (e.g., Yu et al, 1997), injected acetic acid (e.g., Rahman, Takahashi, & Kaneto, 1993), and inflammation. Inflammatory pain may be induced with formalin (e.g., Connell, Barnes, Blatt, & Tasker, 1994), carrageen (e.g., Suzuki et al, 1996), or complete Freund's adjuvant (e.g., Rahman et al, 1993).…”

mentioning

confidence: 99%

The role of formalin-induced pain in morphine tolerance, withdrawal, and reward.

Bardin¹,

Kim²,

Siegel³

2000

Experimental and Clinical Psychopharmacology

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The effect of a commonly used experimental pain-induction procedure (formalin injection into a hindpaw site) on morphine tolerance, withdrawal, and reward was examined in rats. Results suggest that the effects of morphine are different in the organism that is experiencing pain at the time it receives the drug than in the organism that is pain free. The presence of pain at the time of each morphine administration decreased analgesic tolerance, decreased naloxone-precipitated withdrawal, and enhanced the rewarding effect of the opiate. These findings, together with those of previous studies, suggest that theories of opiate tolerance, withdrawal, and reward should incorporate the effects of pain.

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mentioning

confidence: 99%

The role of formalin-induced pain in morphine tolerance, withdrawal, and reward.

Bardin¹,

Kim²,

Siegel³

2000

Experimental and Clinical Psychopharmacology

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“…Demonstrating morphine antinociceptive tolerance in the formalin test has been more challenging (Abbott et al, 1981;Abbott et al, 1982;Connell et al, 1994;Detweiler et al, 1995). We were able to detect modest morphine tolerance in the second phase but not the first phase of the test.…”

Section: Discussionmentioning

confidence: 75%

Comparison of morphine, oxycodone and the biased MOR agonist SR-17018 for tolerance and efficacy in mouse models of pain

Pantouli¹,

Grim²,

Schmid³

et al. 2020

Preprint

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The mu opioid receptor-selective agonist, SR-17018, preferentially activates GTPS binding over beta-arrestin2 recruitment in cellular assays. In mice, SR-17018 stimulates GTPgammaS binding in brainstem and produces antinociception with potencies similar to morphine. However, it produces much less respiratory suppression and mice do not develop antinociceptive tolerance in the hot plate assay upon repeated dosing. Herein we evaluate the effects of acute and repeated dosing of SR-17018, oxycodone and morphine in additional models of pain-related behaviors. In the mouse warm water tail immersion assay, an assessment of spinal reflex to thermal nociception, repeated administration of SR-17018 produces tolerance as does morphine and oxycodone. SR-17018 retains efficacy in a formalin-induced inflammatory pain model upon repeated dosing, while oxycodone does not. In a chemotherapeutic-induced neuropathy pain model SR-17018 is more potent and efficacious than morphine or oxycodone, moreover, this efficacy is retained upon repeated dosing of SR-17018. These findings demonstrate that, with the exception of the tail flick test, SR-17018 retains efficacy upon chronic treatment across several pain models.

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Formalin pretreatment attenuates tail-flick inhibition induced by β-endorphin administered intracerebroventricularly or intrathecally in mice

et al. 2005

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We examined the effect of the subcutaneous (s.c.) pretreatment of formalin into both hind paws of mice on the antinociception induced by the intracerebroventricularly (i.c.v.) or intrathecally (i.t.) administration of beta-endorphin using the tail-flick test. Pretreatment with formalin (5%) for 5 h had no affect on the i.c.v. administered beta-endorphin-induced tail-flick response. However, pretreatment with formalin for 40 h attenuated the tail-flick inhibition induced by i.c.v. administered beta-endorphin. This antinociceptive tolerance to i.c.v. beta-endorphin continued up to 1 week, but to a lesser extent. Pretreatment with formalin for 5 and 40 h significantly reduced the i.t. beta-endorphin-induced inhibition of the tail-flick response, which continued up to 1 week. The s.c. formalin treatment increased the hypothalamic pro-opiomelanocortin (POMC) mRNA level at 2 h, but this returned to the basal level after 40 h. Our results suggest that the increase in the POMC mRNA level in the hypothalamus appears to be involved in the supraspinal or spinal beta-endorphin-induced antinociceptive tolerance in formalin-induced inflammatory pain.

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Rapid development of tolerance to morphine in the formalin test

Cited by 12 publications

References 0 publications

The role of formalin-induced pain in morphine tolerance, withdrawal, and reward.

The role of formalin-induced pain in morphine tolerance, withdrawal, and reward.

Comparison of morphine, oxycodone and the biased MOR agonist SR-17018 for tolerance and efficacy in mouse models of pain

Formalin pretreatment attenuates tail-flick inhibition induced by β-endorphin administered intracerebroventricularly or intrathecally in mice

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