Opioid and non-opioid stress analgesia: assessment of tolerance and cross-tolerance with morphine

Jw, Lewis; Je, Sherman; Liebeskind, John C.

doi:10.1523/jneurosci.01-04-00358.1981

Cited by 205 publications

(79 citation statements)

References 15 publications

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“…Repeated once-daily exposure to intermittent footshock stress for two weeks results in tolerance to an opioid-dependent, but not an opioid-independent, form of stress antinociception (Lewis et al, 1981;Terman et al, 1986). Similarly, we showed that chronic treatment with the cannabinoid agonist WIN55,212-2 attenuated endocannabinoid-mediated stress antinociception .…”

Section: Introductionsupporting

confidence: 60%

“…Repeated once daily exposure to intermittent footshock stress (20 min at 0.2 Hz × 14 days) induces tolerance to opioid-mediated stress antinociception (Lewis et al, 1981;Terman et al, 1986). Thus, it is noteworthy that repeated daily exposure to brief, continuous footshock stress (3 min × 15 days) does not induce tolerance to opioid-mediated stress antinociception (Lewis et al, 1981;Terman et al, 1986) and produced no deficit in endocannabinoid-mediated stress antinociception in our study. Moreover, WIN55,212-2 produced similar antinociceptive effects in rats exposed repeatedly to the footshock stressor and rats not subjected to footshock.…”

Section: Discussionsupporting

confidence: 44%

“…Thus, it is noteworthy that CB 1 antagonists have found therapeutic applications in reducing recidivism in smokers (Cohen et al, 2005;Tucci et al, 2006) and other substance abusers (Maldonado et al, 2006). Repeated once daily exposure to intermittent footshock stress (20 min at 0.2 Hz × 14 days) induces tolerance to opioid-mediated stress antinociception (Lewis et al, 1981;Terman et al, 1986). Thus, it is noteworthy that repeated daily exposure to brief, continuous footshock stress (3 min × 15 days) does not induce tolerance to opioid-mediated stress antinociception (Lewis et al, 1981;Terman et al, 1986) and produced no deficit in endocannabinoid-mediated stress antinociception in our study.…”

Section: Discussionmentioning

confidence: 99%

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Cross-sensitization and cross-tolerance between exogenous cannabinoid antinociception and endocannabinoid-mediated stress-induced analgesia

et al. 2008

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SummaryFootshock stress induces both endocannabinoid mobilization and antinociception. The present studies investigated behavioral plasticity in cannabinoid antinociceptive mechanisms following repeated activation using the tail-flick test. A secondary objective was to ascertain whether blockade of stress antinociception by the CB 1 antagonist rimonabant could be attributed to changes in locomotor activity. The cannabinoid agonist WIN55,212-2 induced hypoactivity in the open field relative to vehicle-treated controls. By contrast, rimonabant, administered at a dose that virtually eliminated endocannabinoid-mediated stress antinociception, failed to alter locomotor behavior (i.e. time resting, ambulatory counts, distance traveled) in rats subjected to the same stressor. Rats exposed acutely to footshock were hypersensitive to the antinociceptive effects of WIN55,212-2 and Δ 9 -tetrahydrocannabinol (Δ 9 -THC). The converse was also true; acute Δ 9 -THC and WIN55,212-2 administration potentiated stress antinociception, suggesting a bidirectional sensitization between endocannabinoid-mediated stress antinociception and exogenous cannabinoid antinociception. Stress antinociception was also attenuated following chronic relative to acute treatment with WIN55,212-2 or Δ 9 -THC. Repeated exposure to footshock (3 min/day for 15 days), however, failed to attenuate antinociception induced by either footshock stress or WIN55,212-2. Our results demonstrate that endocannabinoid-mediated stress antinociception cannot be attributed to motor suppression. Our results further identify a functional plasticity of the cannabinoid system in response to repeated activation. The existence of cross-sensitization between endocannabinoid-mediated stress antinociception and exogenous cannabinoid antinociception suggests that these phenomena are mediated by a common mechanism. The observation of stress-induced hypersensitivity to effects of exogenous cannabinoids may have clinical implications for understanding marijuana abuse liability in humans.

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Section: Introductionsupporting

confidence: 60%

Section: Discussionsupporting

confidence: 44%

Section: Discussionmentioning

confidence: 99%

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Cross-sensitization and cross-tolerance between exogenous cannabinoid antinociception and endocannabinoid-mediated stress-induced analgesia

et al. 2008

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“…Further, an increase in the toradiography in discrete regions of the brain of arthritic rats, activity of serotoninergic networks may underlie the potentiated such as the periaqueductal gray, stimulation of which elicits the antinociceptive action of morphine induced by acute stress (Kelly and Franklin, 1984). In analogy to arthritis, other models of chronic pain (footshock or mechanical stimulation) evoke an increased antinociceptive response to morphine (Lewis et al, 1981;Appelbaum and Holtzman, 1984;Sherman et al, 1984;Williams et al, 1984;Girardot and Holloway, 1985). It has been contended that this may reflect classical conditioning; that is, cues associated with exposure to stress summate with morphine to produce an enhanced antinociception.…”

Section: Endogenous and Exogenous Opioid Control Of Nociception In Armentioning

confidence: 99%

A model of chronic pain in the rat: functional correlates of alterations in the activity of opioid systems

Millan¹,

Członkowski²,

Pilcher³

et al. 1987

J. Neurosci.

111

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Intradermal inoculation of rats at the tail base with Mycobacterium butyricum led to the gradual development of an arthritic swelling of the limbs which peaked at 3 weeks and subsided thereafter. Arthritic rats displayed a loss of body weight, hypophagia, and hypodipsia in addition to a disruption of the diurnal rhythms of ingestive behavior and of core temperature. The activity of adenohypophyseal beta- endorphin-(beta-EP) secreting corticotrophs, in contrast to prolactin- (PRL) secreting lactotrophs, was increased in arthritic rats. Indeed, hypertrophy of the adrenal glands was seen. Arthritic rats also showed an elevation in spinal cord levels of immunoreactive dynorphin (DYN), an endogenous ligand of the kappa-opioid receptor. The paws and tail of arthritic rats showed lower thresholds in response to noxious pressure (hyperalgesia), higher thresholds in response to noxious heat (hypoalgesia), and no change in their response to noxious electrical stimulation. Neither naloxone nor ICI-154, 129 (a preferential delta- receptor antagonist) modified the responses of the paw or tail to pressure. However, MR 2266 (an antagonist with higher activity at kappa- receptors) decreased thresholds to pressure in arthritic, but not control, rats; that is, it potentiated the hyperalgesia. This action was stereospecific. None of the antagonists modified the response to heat. MR 2266 did not affect the response to pressure in rats with acute inflammation produced by yeast. Thus, the potentiation of pressure hyperalgesia by MR 2266 in chronic arthritic rats is highly selective. Arthritic rats showed a reduced response to the analgesic effect of a kappa-agonist (U-50,488H), whereas the response to a mu- agonist (morphine) was enhanced. These effects were specific to nociception in that their influence upon endocrine secretion (PRL and beta-EP) was otherwise changed. The secretion of beta-EP and PRL was stimulated by both morphine and U-50,488H, and the influence of U- 50,488H upon the release of beta-EP (from the adenohypophysis) was enhanced in arthritic rats. It is suggested that polyarthritis is a complex condition entailing many changes, both behavioral and endocrinological. Further, arthritic rats cannot simply be described as “hyperalgesic”: of critical importance is the nature of the nociceptive stimulus applied. The parallel alterations in spinal cord pools of DYN and kappa-receptors (see also Millan et al., 1986) and the changes in the influence on nociception of kappa-agonists and kappa-antagonists suggest an increased activity of spinal DYN. Thus, spinal kappa- receptors may play a role in the modulation of nociception under chronic pain.(ABSTRACT TRUNCATED AT 400 WORDS)

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“…Subsequent one-way ANOVA followed by Fisher's PLSD indicated that significant tolerance developed at 30 min post-injection ("morphine" < "saline"; F3,28=6.6; p<0.05) but not at later time points (p>0.05). The shorter lasting analgesia (and subsequently, tolerance) compared to Figure 1 could be due to a combination of both a lower challenge dose used in this experiment (5 mg/kg versus 7.5 mg/kg, s.c.) and cross-tolerance of stress-induced analgesia across all groups (Lewis et al 1981) because this regimen required three times as many injections and concomitant handling. Co-administration of MK-801 with morphine completely blocked the development of morphine tolerance exhibited at 30 min in the 129S6/ SvEv strain as these mice demonstrated significantly greater analgesia than morphine-tolerant mice (p<0.05) but did not differ from control mice (p>0.05) ( Figure 3A).…”

Section: Resultsmentioning

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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Opioid and non-opioid stress analgesia: assessment of tolerance and cross-tolerance with morphine

Cited by 205 publications

References 15 publications

Cross-sensitization and cross-tolerance between exogenous cannabinoid antinociception and endocannabinoid-mediated stress-induced analgesia

Cross-sensitization and cross-tolerance between exogenous cannabinoid antinociception and endocannabinoid-mediated stress-induced analgesia

A model of chronic pain in the rat: functional correlates of alterations in the activity of opioid systems

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

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