Pain modulating and reward systems: A single brain mechanism?

Magnen, J. Le; Marfaing-Jallat, P.; Miceli, D.; Devos, M.

doi:10.1016/0091-3057(80)90157-4

Cited by 145 publications

(38 citation statements)

References 36 publications

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“…In support of this suggestion, Levine et al (1982) demonstrate that the opiate antagonist naloxone blocks both feeding and analgesic responses elicited by tail-pinch, and Roane and Martin (1990) report that morphine analgesia is increased following continuous sucrose feeding. Furthermore, naloxone enhances a taste aversio~ and abolishes a taste preference (Le Magnen et al, 1980). These findings imply that pleasurable and aversive sensations may be a~~ociated with high and low opioid activity respectively.…”

Section: ------------------------------------------------------------mentioning

confidence: 72%

Effects of pedunculopontine tegmental nucleus lesions on morphine-induced conditioned place preference and analgesia in the formalin test

Olmstead

Franklin

1993

Neuroscience

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Section: ------------------------------------------------------------mentioning

confidence: 72%

Effects of pedunculopontine tegmental nucleus lesions on morphine-induced conditioned place preference and analgesia in the formalin test

Olmstead

Franklin

1993

Neuroscience

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“…Cooper and Kirkham 1993). In support of this, opioid antagonists have been found to reduce or abolish both sweet (Le Magnen et al 1980;Cooper 1983;Lynch and Libby 1983), and salt taste preferences (Cooper and Gilbert 1984), and to reduce food preference (Cooper and Turkish 1989). Conversely, opioid agonists have been reported to enhance taste acceptance and preference (Calcagnetti and Reid 1983;Bertino and Abelson 1988;Gosnell and Majchrzak 1989).…”

Section: Introductionmentioning

confidence: 93%

Evidence for early opioid modulation of licking responses to sucrose and Intralipid: a microstructural analysis in the rat

Higgs¹,

Cooper²

1998

Psychopharmacology

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The behavioural mechanisms underlying the effects of the opioid antagonist naloxone (0.3-3 mg/kg i.p.), and the opioid agonists morphine (0.3-3 mg/kg s.c.), and U-50, 488H (0.3-3 mg/kg s.c.) on ingestive behaviour were investigated using a microstructural analysis of licking patterns for sucrose solutions and Intralipid (fat emulsions) in a brief contact test. Naloxone dose-dependently decreased the total number of licks and the number of bouts for sucrose and Intralipid, but did not affect mean bout duration. Morphine dose-dependently increased the total number of licks and the number of bouts for both test fluids. For Intralipid but not for sucrose drinking, morphine actually decreased mean bout duration. U-50, 488H significantly affected total licks, although the dose-effect relationship showed an inverted U-shaped function. There was a dose-dependent increase in mean bout duration following administration of U-50, 488H and an increase in bout number, although only the lowest dose differed significantly from the control condition. The results show that microstructural analysis can distinguish between the effects of naloxone, morphine and U-50, 488H on licking behaviour and indicate that selective opioid receptor subtypes may be differentially involved in ingestive processes.

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“…However, the effects of ultra-low doses of opioid antagonists on the characteristic rewarding effects of morphine to our knowledge are not known. The overlap of the sites mediating both the supraspinal analgesic and rewarding effects of morphine (Le Magnen et al, 1980;Franklin, 1989Franklin, , 1998 suggests that their rewarding effects may also be influenced by ultra-low doses of naltrexone. Thus, using a place preference-conditioning paradigm, we examined whether ultra-low doses of naltrexone influence the rewarding effects of systemic morphine.…”

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confidence: 99%

Paradoxical Effects of the Opioid Antagonist Naltrexone on Morphine Analgesia, Tolerance, and Reward in Rats

Powell¹,

Abul‐Husn²,

Jhamandas³

et al. 2002

J Pharmacol Exp Ther

121

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Opioid agonists such as morphine have been found to exert excitatory and inhibitory receptor-mediated effects at low and high doses, respectively. Ultra-low doses of opioid antagonists (naloxone and naltrexone), which selectively inhibit the excitatory effects, have been reported to augment systemic morphine analgesia and inhibit the development of tolerance/physical dependence. This study investigated the site of action of the paradoxical effects of naltrexone and the generality of this effect. The potential of ultra-low doses of naltrexone to influence morphine-induced analgesia was investigated in tests of nociception. Administration of intrathecal (0.05 and 0.1 ng) or systemic (10 ng/kg i.p.) naltrexone augmented the antinociception produced by an acute submaximal dose of intrathecal (5 g) or systemic (7.5 mg/kg i.p.) morphine in the tail-flick test. Chronic intrathecal (0.005 and 0.05 ng) or systemic (10 ng/kg) naltrexone combined with morphine (15 g i.t.; 15 mg/kg i.p.) over a 7-day period inhibited the decline in morphine antinociception and prevented the loss of morphine potency. In animals rendered tolerant to intrathecal (15 g) or systemic (15 mg/kg) morphine, administration of naltrexone (0.05 ng i.t.; 10 and 50 ng/kg i.p.) significantly restored the antinociceptive effect and potency of morphine. Thus, in ultra-low doses, naltrexone paradoxically enhances morphine analgesia and inhibits or reverses tolerance through a spinal action. The potential of naltrexone to influence morphine-induced reward was also investigated using a place preference paradigm. Systemic administration of ultra-low doses of naltrexone (16.7, 20.0, and 25.0 ng/kg) with morphine (1.0 mg/kg) extended the duration of the morphine-induced conditioned place preference. These effects of naltrexone on morphine-induced reward may have implications for chronic treatment with agonist-antagonist combinations.Opioid drugs such as morphine are widely used in the treatment of severe pain; however, their chronic administration results in the development of tolerance to their analgesic effects, limiting their clinical usefulness in pain management. Although the mechanisms underlying the development of opioid tolerance are poorly understood, recent studies have suggested that alterations in the coupling of opioid receptors to G protein-linked effectors may play a significant role (Crain and Shen, 2000). Morphine and related agonists are recognized to produce their characteristic acute and chronic effects by activating spinal and supraspinal -, ␦-, and -opioid receptors. Classically, morphine activates G i protein-coupled -opioid receptors to inhibit adenylyl cyclase activity and decrease neuronal cAMP levels (Uhl et al., 1994). At the presynaptic level, -opioid receptor activation inhibits voltage-sensitive Ca 2ϩ channels (Tallent et al., 1994) and reduces neurotransmitter release, whereas at the postsynaptic level, it opens potassium channels and hyperpolarizes neurons (North and Williams, 1983;Ikeda et al., 1995). The net result of th...

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Pain modulating and reward systems: A single brain mechanism?

Cited by 145 publications

References 36 publications

Effects of pedunculopontine tegmental nucleus lesions on morphine-induced conditioned place preference and analgesia in the formalin test

Effects of pedunculopontine tegmental nucleus lesions on morphine-induced conditioned place preference and analgesia in the formalin test

Evidence for early opioid modulation of licking responses to sucrose and Intralipid: a microstructural analysis in the rat

Paradoxical Effects of the Opioid Antagonist Naltrexone on Morphine Analgesia, Tolerance, and Reward in Rats

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