Formalin- and carrageenan-induced inflammation attenuates place preferences produced by morphine, methamphetamine and cocaine

Suzuki, Tsutomu; Kishimoto, Yayoi; Misawa, Miwa

doi:10.1016/0024-3205(96)00498-5

Cited by 69 publications

(38 citation statements)

References 18 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…When opioids are used for the management of clinical pain, they may help the patient to achieve an affective state normally experienced when free of pain, but not the extreme positive affect that might support addiction. Supporting this view are reports that the capacity of morphine to serve as a reinforcer is attenuated when given to rats that are in a chronic/tonic pain state, 50 , and that morphine tolerance and dependence fails to develop in rats when administered during a pain state, 52 . The neurobiology that relates reinforcement with analgesia is of obvious clinical importance and warrants further study.…”

Section: Discussionmentioning

confidence: 95%

Affective Analgesia Following Muscarinic Activation of the Ventral Tegmental Area in Rats

Kender

Harte

Munn

et al. 2008

The Journal of Pain

View full text Add to dashboard Cite

Cholinergic stimulation of dopamine neurons in the ventral tegmental area (VTA) underlies activation of the brain reward circuitry. Activation of this circuit is proposed to preferentially suppress the affective reaction to noxious stimulation. Vocalization afterdischarges (VADs) are a validated model of the affective response of rats to noxious tailshock. The antinociceptive action of the acetylcholine agonist carbachol microinjected into the VTA on VAD threshold was compared to its effect on the thresholds of other tailshock-elicited responses (VDS = vocalizations during shock, and SMR = spinal motor reflexes). Whereas VADs are organized within the forebrain, VDSs and SMRs are organized at medullary and spinal levels of the neuraxis, respectively. Carbachol (1 μg, 2 μg, and 4 μg) injected into VTA produced dose-dependent increases in VAD and VDS thresholds, although increases in VAD threshold were significantly greater than increases in VDS threshold. Administration of carbachol into VTA failed to elevate SMR threshold. Elevations in vocalization thresholds produced by intra-VTA carbachol were reversed in a dose-dependent manner by local administration of the muscarinic receptor antagonist atropine sulfate (30 μg and 60 μg). These results provide the first demonstration of the involvement of the VTA in muscarinic-induced suppression of pain affect.Perspective-Cholinergic activation of the brain reward circuit produced a preferential suppression of rats' affective reaction to noxious stimulation. The neurobiology that relates reinforcement to suppression of pain affect may provide insights into new treatments for pain and its associated affective disorders.

show abstract

Section: Discussionmentioning

confidence: 95%

Affective Analgesia Following Muscarinic Activation of the Ventral Tegmental Area in Rats

Kender

Harte

Munn

et al. 2008

The Journal of Pain

View full text Add to dashboard Cite

show abstract

“…We also reported that morphine failed to induce rewarding effects under an inflammatory pain-like state produced by formalin or carrageenan (Suzuki et al, 1996(Suzuki et al, , 1999. However, there is, if any, direct evidence regarding possible changes at the supraspinal level after inflammation.…”

Section: Introductionmentioning

confidence: 82%

“…One compartment was white with a textured floor and the other was black with a smooth floor. Conditioning sessions (two for morphine : two for saline) were started on the first day after formalin and vehicle injection into the rat paw, and conditioning was conducted once daily for 4 days (Suzuki et al, 1996(Suzuki et al, , 1999. Immediately after i.p.…”

mentioning

confidence: 99%

Direct Evidence for the Involvement of the Mesolimbic κ-Opioid System in the Morphine-Induced Rewarding Effect Under an Inflammatory Pain-Like State

Narita

Kishimoto

Ise

et al. 2004

Neuropsychopharmacol

Self Cite

120

View full text Add to dashboard Cite

Recent clinical studies have demonstrated that when morphine is used to control pain in cancer patients, psychological dependence is not a major concern. The present study was undertaken to ascertain the modulation of psychological dependence on morphine under a chronic pain-like state in rats. The prototypical m-opioid receptor agonist morphine (8 mg/kg, i.p.) induced a dose-dependent place preference. In the present study, we found that an inflammatory pain-like state following formalin injection significantly suppressed the morphine-induced rewarding effect. This effect was almost reversed by s.c. pretreatment with the k-opioid receptor antagonist norbinaltorphimine (nor-BNI, 5 mg/kg). Furthermore, the morphine-induced increase in dopamine (DA) turnover in the limbic forebrain was significantly inhibited by treatment with formalin. This inhibition was also suppressed by pretreatment with nor-BNI. In addition, in vivo microdialysis studies clearly showed that the morphine-induced increase in the extracellular levels of DA and its metabolites, 3,4-dihydroxyphenylacetic acid and homovanillic acid, in the nucleus accumbens (N.Acc.) was significantly decreased in rats that had been pretreated with formalin. This effect was in turn reversed by the microinjection of a specific dynorphin A antibody into the N.Acc. These findings suggest that the inflammatory pain-like state induced by formalin injection may have caused a sustained activation of the kopioidergic system within the N.Acc., resulting in suppression of the morphine-induced rewarding effect in rats. The present study provides further evidence of the clinical usefulness of morphine in patients suffering from severe pain. Neuropsychopharmacology (2005) 30, 111-118, advance online publication, 14 July 2004; doi:10.1038/sj.npp.1300527Keywords: opioid; inflammatory pain-like state; morphine dependence; nucleus accumbens; rat INTRODUCTIONThe World Health Organization publication Cancer Pain Relief (WHO, 1996) proposed a method for the relief of cancer pain based on a small number of relatively inexpensive drugs, including morphine. This approach is now used worldwide.Recent clinical experience has shown that when morphine is used to control pain in cancer patients, psychological dependence is not a major concern (WHO, 1996). However, undue anxiety about psychological dependence on morphine in cancer patients has caused physicians and patients to use inadequate doses of opioids. Nociceptive stimuli produced physiological changes in the levels of some proteins and neuropeptides in dorsal horn neurons (Dubner and Ruda, 1992;Narita et al, 2000). We reported previously that morphine failed to induce rewarding effects under a neuropathic pain-like state induced by sciatic nerve ligation in the rat and mouse (Ozaki et al, 2002(Ozaki et al, , 2003. Furthermore, this pain-like state leads to a reduction in m-receptor function in the ventral tegmental area (VTA; Ozaki et al, 2002Ozaki et al, , 2003, which is the origin of the mesolimbic dopaminergic system and the major ...

show abstract

“…We previously reported that morphine failed to induce rewarding effects in rats that had been injected with formalin or carrageenan into the hind paw (Suzuki et al, 1996(Suzuki et al, , 2001Narita et al, 2005a). Furthermore, it has been documented that chronic pain attenuates the development of tolerance to the antinociceptive effect of morphine in rats (Vaccarino et al, 1993).…”

Section: Introductionmentioning

confidence: 99%

Comparative Pharmacological Profiles of Morphine and Oxycodone under a Neuropathic Pain-Like State in Mice: Evidence for Less Sensitivity to Morphine

Narita

Nakamura

Masahiko

et al. 2007

Neuropsychopharmacol

Self Cite

102

View full text Add to dashboard Cite

The present study was undertaken to investigate pharmacological actions induced by morphine and oxycodone under a neuropathic pain-like state. In the m-opioid receptor (MOR) binding study and G-protein activation, we confirmed that both morphine and oxycodone showed MOR agonistic activities. Mice with sciatic nerve ligation exhibited the marked neuropathic pain-like behavior. Under these conditions, antinociception induced by subcutaneously (s.c.) injected morphine was significantly decreased by sciatic nerve ligation, whereas s.c. injection of oxycodone produced a profound antinociception in sciatic nerve-ligated mice. There were no significant differences in spinal or supraspinal antinociception of morphine and oxycodone between sham operation and nerve ligation. Moreover, either morphine-or oxycodone-induced increase in guanosine-5 0 -o-(3-thio) triphosphate ([ 35 S]GTPgS) binding in the spinal cord, periaqueductal gray matter and thalamus in sciatic nerve-ligated mice was similar to that in sham-operated mice. Antinociception induced by s.c., intrathecal, or intracerebroventricular injection of the morphine metabolite morphine-6-glucuronide (M-6-G) was significantly decreased by sciatic nerve ligation. Furthermore, the increase in the G-protein activation induced by M-6-G was eliminated in sciatic nerve ligation. In addition, either morphine-or oxycodone-induced rewarding effect was dramatically suppressed under a neuropathic pain-like state. The increased [ 35 S]GTPgS binding by morphine or oxycodone was significantly lower in the lower midbrain of mice with sciatic nerve ligation compared with that in control mice. These findings provide further evidence that oxycodone shows a profound antinociceptive effect under a neuropathic pain-like state with less of a rewarding effect. Furthermore, the reduction in G-protein activation induced by M-6-G may, at least in part, contribute to the suppression of the antinociceptive effect produced by morphine under a neuropathic pain-like state.

show abstract

Formalin- and carrageenan-induced inflammation attenuates place preferences produced by morphine, methamphetamine and cocaine

Cited by 69 publications

References 18 publications

Affective Analgesia Following Muscarinic Activation of the Ventral Tegmental Area in Rats

Affective Analgesia Following Muscarinic Activation of the Ventral Tegmental Area in Rats

Direct Evidence for the Involvement of the Mesolimbic κ-Opioid System in the Morphine-Induced Rewarding Effect Under an Inflammatory Pain-Like State

Comparative Pharmacological Profiles of Morphine and Oxycodone under a Neuropathic Pain-Like State in Mice: Evidence for Less Sensitivity to Morphine

Contact Info

Product

Resources

About