Opioids and addiction: Emerging pharmaceutical strategies for reducing reward and opponent processes

Bryant, Camron D.; Zaki, Paulette A.; Carroll, F. Ivy; Evans, Christopher J.

doi:10.1016/j.cnr.2005.08.006

Cited by 14 publications

(14 citation statements)

References 147 publications

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“…In Table 2, in naïve mice, in examining changes in baseline latencies after repeated administration, there was a main effect of treatment [F(3,80) ϭ 12.8; P Ͻ 0.0001] and sex [F(1,80) ϭ 16.5; P Ͻ 0.001]. In comparing mor mice with control mice, morphine-induced hyperalgesia developed in males and females [F(3,80) ϭ 6.0; P Ͻ 0.05; F(3,80) ϭ 9.9; P Ͻ 0.01, respectively] as previously reported with this same protocol in males (11). However, in comparing mor mice with MKϩmor mice, the development of morphine-induced hyperalgesia was potentiated by repeated coadministration of MK-801 in males [F(3,80) ϭ 4.6; P Ͻ 0.05], but not females ( Table 2).…”

Section: Resultssupporting

confidence: 64%

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NMDA receptor antagonism disrupts the development of morphine analgesic tolerance in male, but not female C57BL/6J mice

Bryant

Eitan²,

Sinchak

et al. 2006

American Journal of Physiology-Regulatory, Integrative and Comp

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Multiple studies demonstrate that coadministration of N-methyl-D-aspartate (NMDA) receptor antagonists with the opioid agonist morphine attenuates the development of analgesic tolerance. Sex differences in the effects of noncompetitive, but not competitive NMDA receptor antagonists on acute morphine analgesia, have been reported in mice, yet the role of sex in modulation of morphine tolerance by NMDA receptor antagonists has yet to be addressed. Therefore, we tested whether there is a sex difference in the effect of NMDA receptor antagonists on the development of morphine analgesic tolerance in C57BL/6J mice. Acutely, at a dose required to affect morphine tolerance in male mice, the noncompetitive NMDA receptor antagonist dizocilpine (MK-801) prolonged morphine analgesia similarly in both sexes in the hot plate and tail withdrawal assays. In the hot plate assay, coadministration of MK-801 or the competitive antagonist 3-(2-carboxpiperazin-4-yl)propyl-1-phosphanoic acid (CPP) with morphine attenuated the development of tolerance in male mice, while having no effect in females. Like normal and sham females, ovariectomized mice were similarly insensitive to the attenuation of morphine tolerance by MK-801 in the hot plate assay. Surprisingly, in the tail withdrawal assay, MK-801 facilitated the development of morphine-induced hyperalgesia and tolerance in males but not females. The results demonstrate that male mice are more sensitive to modulation of nociception and morphine analgesia after repeated coadministration of NMDA receptor antagonists. Furthermore, the underlying mechanisms are likely to be different from those mediating the sex difference in the modulation of acute morphine analgesia that has previously been reported.

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Section: Resultssupporting

confidence: 64%

“…11). Adaptations, such as hyperalgesia can have an associative learning component, which contributes to tolerance (58).…”

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confidence: 99%

NMDA receptor antagonism disrupts the development of morphine analgesic tolerance in male, but not female C57BL/6J mice

Bryant

Eitan²,

Sinchak

et al. 2006

American Journal of Physiology-Regulatory, Integrative and Comp

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“…Previous studies have suggested the induction of hyperalgesia as a contributing factor in the development of acute opioid tolerance (see McNaull et al, 2007). Many mechanisms have been proposed to mediate opioid-induced hyperalgesia (Lee et al, 2011;Angst and Clark, 2006) and involve the activation of opponent processes (Bryant et al, 2005). A single dose of morphine (Goldfarb et al, 1978) or heroin (Celerier et al, 2001) can generate naloxone-precipitated hyperalgesia that has been replicated in non-addicted humans following a single injection of morphine (Compton et al, 2003).…”

Section: Discussionmentioning

confidence: 99%

Stereo-selective inhibition of spinal morphine tolerance and hyperalgesia by an ultra-low dose of the alpha-2-adrenoceptor antagonist efaroxan

Milne

Jhamandas

Sutak

et al. 2013

European Journal of Pharmacology

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a b s t r a c tUltra-low doses of alpha-2 (a 2 )-adrenoceptor antagonists augment spinal morphine antinociception and inhibit tolerance, but the role of receptor specificity in these actions is unknown. We used the stereo-isomers of the a 2 adrenoceptor antagonist, efaroxan to evaluate the effect of receptor specificity on the induction of spinal morphine tolerance and hyperalgesia. Tail flick and paw pressure tests were first used to evaluate high dose efaroxan (12.6 mg) and its stereo-isomers on clonidine analgesia in intrathecally catheterized rats. Ultra-low doses of individual isomers (1.3 ng) were then coadministered with morphine (15 mg) to determine their effects on acute antinociceptive tolerance and hyperalgesia induced by low dose spinal morphine (0.05 ng). Results demonstrate that high dose ( þ) efaroxan antagonized clonidine-induced antinociception, while ( À ) efaroxan had minimal effect. In addition, an ultra-low dose of (þ ) efaroxan (1.3 ng), substantially lower than required for receptor blockade, inhibited the development of acute morphine tolerance, while ( À ) efaroxan was less effective. Racemic (7 ) efaroxan effects were similar to those of (þ ) efaroxan. Furthermore, low dose morphine (0.05 ng) produced sustained hyperalgesia in the tail flick test and this was blocked by coinjection of ( þ) but not ( À ) efaroxan (1.3 ng). Given the isomer-specific efaroxan effects and their different receptor potencies, we suggest that inhibition of opioid tolerance by ultra-low dose efaroxan involves a specific interaction with spinal a 2 -adrenoceptors in this model. Likewise, inhibitory effects of adrenoceptor antagonists on morphine tolerance may be due to blockade of opioid-induced hyperalgesia.

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“…However, in the past, using C57BL/6J mice, we have constructed cumulative dose-response curves following a number of different chronic morphine regimens and cumulative dosing procedures and have never observed large shifts in the dose-response curve or ED 50 values. Although using separate mice for each dose might alleviate the problem, due to the exponential costs that this would require, we frequently report a difference in analgesic efficacy following a single morphine challenge dose (Bryant et al 2006;Bryant 2005;Eitan et al 2003).…”

Section: Discussionmentioning

confidence: 99%

“…We replicated the strain-specific spontaneous hyperalgesia resulting from chronic morphine that occurs in the tail withdrawal assay in C57BL/6J, but not 129P3/J mice (Bryant et al 2006;Bryant 2005;Kest et al 2002) (Table 1). Additionally, C57BL/6J, but not 129P3/J mice, exhibited a large increase in the frequency of tail flicks during the first second following the first baseline nociceptive response ( Figure 5A).…”

Section: Discussionmentioning

confidence: 99%

Morphine analgesic tolerance in 129P3/J and 129S6/SvEv mice

Bryant¹,

Roberts²,

Byun³

et al. 2006

Pharmacology Biochemistry and Behavior

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Morphine analgesic tolerance is heritable in both humans and rodents, with some individuals and strains exhibiting little and others exhibiting robust tolerance. 129S6/SvEv and 129P3/J mice reportedly do not demonstrate tolerance to morphine analgesia. Using our laboratory's standard morphine tolerance regimen and a between-subjects design, tolerance developed in the hot plate and tail withdrawal assays as indicated by a change in analgesic efficacy following a morphine challenge dose. Furthermore, the non-competitive NMDA receptor antagonist MK-801 (dizocilipine) blocked morphine tolerance in 129S6/SvEv and CD-1 mice in the hot plate assay. As previously reported, when a within-subjects design and cumulative dosing was employed, no tolerance was observed in the 129P3/J strain. However, using the same morphine regimen and a between-subjects design, comparable tolerance developed between 129P3/J and C57BL/6J strains following a single challenge dose of morphine. Spontaneous hyperalgesia was observed in the tail withdrawal assay following chronic morphine in C57BL/6J, but not 129P3/J mice. Additionally, morphine-tolerant C57BL/6J mice, but not 129P3/J mice, exhibited a large increase in the frequency of tail flicks during the first second following the baseline nociceptive response which may facilitate detection of the response during the tolerant state. We conclude that the method of tolerance assessment affects the ability to detect tolerance and thus, may affect the degree and pattern of heritability of this trait and this could have implications for gene mapping studies.

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Opioids and addiction: Emerging pharmaceutical strategies for reducing reward and opponent processes

Cited by 14 publications

References 147 publications

NMDA receptor antagonism disrupts the development of morphine analgesic tolerance in male, but not female C57BL/6J mice

NMDA receptor antagonism disrupts the development of morphine analgesic tolerance in male, but not female C57BL/6J mice

Stereo-selective inhibition of spinal morphine tolerance and hyperalgesia by an ultra-low dose of the alpha-2-adrenoceptor antagonist efaroxan

Morphine analgesic tolerance in 129P3/J and 129S6/SvEv mice

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