A Critical Review of Some New Methods in Animal Analgesiometry

Evans, Wayne Ο.

doi:10.1002/j.1552-4604.1964.tb00199.x

Cited by 12 publications

(4 citation statements)

References 21 publications

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“…The magnitude of the hyperalgesra induced by a test substance was calculated as the percentage decrease in pressure requrred to elicit withdrawal, relative to the base Irne. In the rat, the maximum decrease in mechanical nociceptive thresholds produced by test substances using the paw withdrawal test correlates well with the analgesic potency of intradermal injections of the same substance in humans (Evans, 1964;Ferriera, 1983). The fMLP (Sigma Chemrcal Co., St. LOUIS, MO) was initially dissolved In 10 ~1 of dimethylsulfoxide to which, then, was added Hanks' balanced salt solution (HBSS) containing 0.1% ovalbumrn and 10 mM HEPES (pH 7.4).…”

Section: Methodsmentioning

confidence: 91%

The role of the polymorphonuclear leukocyte in hyperalgesia

Levine¹,

Gooding²,

Donatoni³

et al. 1985

J. Neurosci.

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The results of recent studies of the mechanism of leukotriene B4-induced hyperalgesia suggest a dependence on polymorphonuclear leukocytes (PMNLs). In this study, we addressed the contribution of PMNLs to hyperalgesia evoked by the peptide chemotactic factors N-formyl-methionyl-leucyl-phenylalanine (fMLP) and the anaphylatoxin fragment of the fifth component of the complement pathway (C5a). Local injection of glycogen, which attracts but does not activate PMNLs, produced a marked shift to the left (toward lower concentrations) in the concentration dependence curve of fMLP-induced hyperalgesia. In addition, PMNL repletion by transfusion with syngeneic PMNLs reestablished fMLP-induced hyperalgesia in PMNL-depleted rats. Finally, supernatants from rat and human PMNLs, that had been stimulated with fMLP in vitro, produced hyperalgesia in PMNL-depleted rats. Preliminary characterization of the hyperalgesia-inducing activity released by stimulated PMNLs indicated that it is lipid in nature. The nonsteroidal anti-inflammatory indomethacin did not attenuate C5a and fMLP-induced hyperalgesia. Thus, the hyperalgesia produced by fMLP and C5a is similar to that produced by leukotriene B4 in that it is dependent on PMNLs and independent of the cyclo-oxygenation of arachidonic acid. Taken together, these data suggest that structurally diverse PMNL-chemotactic factors produce hyperalgesia by a novel mechanism, involving PMNL-derived factors.

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Section: Methodsmentioning

confidence: 91%

The role of the polymorphonuclear leukocyte in hyperalgesia

Levine¹,

Gooding²,

Donatoni³

et al. 1985

J. Neurosci.

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“…This conditioning analysis of morphine tolerance is supported by several findings: (a) It is necessary to have a consistent set of environmental cues reliably predicting the systemic effects of morphine if rapid tolerance is to be observed (Adams et al, 1969;Kay an et al, 1969; Experiment 1A of the present report); (b) experience with morphine in one environment does not facilitate the acquisition of morphine tolerance in another environment (Experiment IB); (c) the compensatory hyperalgesic CR may be directly observed in morphine-tolerant animals when they are confronted by the drug administration ritual not followed by the central effects of the drug (Experiments 2A and 2B), this hyperalgesic CR being subject to experimental extinction (Experiment 2B); and (d) mere presentation of those environmental cues previously associated with the narcotic, when presented in conjunction with a placebo, is an effective procedure for extinguishing established morphine tolerance (Experiment 3). The conclusions concerning the mechanism of morphine tolerance in the rat are, of course, limited to the relatively small dose of the drug (5 mg/kg) and to the analgesia-evaluation situation used in these experiments (although the hot plate procedure is perhaps the most commonly used of the simple assessment techniques for pharmacologically induced analgesia; see Evans, 1964).…”

Section: Discussionmentioning

confidence: 99%

Evidence from rats that morphine tolerance is a learned response.

Siegel

1975

Journal of Comparative and Physiological Psychology

653

332

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It is proposed that the direct analgesic effect of morphine becomes attenuated over the course of successive administrations of the narcotic by a conditioned, compensatory, hyperalgesic response elicited by the administration procedure, the net result being analgesic tolerance. Using the "hot plate" analgesia assessment situation with rats, this conditioning view of tolerance is supported by several findings: (a) It is necessary to have reliable environmental cues predicting the systemic effects of morphine if tolerance is to be observed, (b) a hyperalgesic conditioned response may be observed in morphine-tolerant subjects when drug administration cues are followed by a placebo, and (c) merely by repeatedly presenting environmental cues previously associated with morphine (but now presented with a placebo), morphine tolerance can be extinguished.

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“…Evidence relevant to the second interpretation is limited. The limbic system is known to influence sensory input (Ball, 1967;Cazard, 1959;Lorens & Brown, 1967;Redding, 1967;Rose & Frommer, 1969), and septal lesions have been demonstrated to decrease threshold for shock needed to elicit "jump" responses (Lints & Harvey, 1969;Rose & Frommer, 1969), a standard measure of pain reactivity (Evans, 1964). However, Blanchard and Fial (1968) failed to find a clearcut effect of hippocampal, septal, or cingulum lesions on a similar measure.…”

Section: Extinction Phasementioning

confidence: 99%

Effects of CS preexposures on avoidance learning in rats with hippocampal lesions.

Ackil¹,

Mellgren²,

Halgren³

et al. 1969

Journal of Comparative and Physiological Psychology

146

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Hooded rats with hippocampal lesions, with neocortical lesions, or with no lesions received either 0 or 30 presentations (preexposures) of a stimulus later used as CS in a two-way shuttle-avoidance task. The 30 preexposures slowed acquisition of the avoidance response and speeded its extinction in the unoperated control group and in the group with neocortical lesions, but not in the group with hippocampal lesions. The latter group did not differ on either measures from any of the subgroups that received 0 preexposures, none of which differed from each other. The results are viewed as support for models attributing an inhibitory function to the hippocampus and suggest an attentional involvement in the preexposure effect.

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A Critical Review of Some New Methods in Animal Analgesiometry

Cited by 12 publications

References 21 publications

The role of the polymorphonuclear leukocyte in hyperalgesia

The role of the polymorphonuclear leukocyte in hyperalgesia

Evidence from rats that morphine tolerance is a learned response.

Effects of CS preexposures on avoidance learning in rats with hippocampal lesions.

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