Differential antagonism of the rate-decreasing effects of κ-opioid receptor agonists by naltrexone and norbinaltorphimine

Powell, Kelly R.; Holtzman, Stephen G.

doi:10.1016/s0014-2999(99)00394-5

Cited by 11 publications

(19 citation statements)

References 19 publications

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“…Similarly, nor-BNI did not antagonize the antinociceptive effects of enadoline in rhesus monkeys (Butelman et al, 1998), although it did attenuate the discriminative stimulus effects of enadoline in squirrel monkeys (Carey and Bergman, 2001). Consistent with the findings of Butelman et al (1998) and Powell and Holtzman (1999), our data suggest that the effects of spiradoline and enadoline may be mediated by a subpopulation of receptors that is largely insensitive to antagonism by nor-BNI.…”

Section: Discussionsupporting

confidence: 93%

“…Finally, the CRF 1 receptor antagonist CP 154,526 and the ␣ 2 -adrenoceptor agonist clonidine significantly attenuated spiradoline-induced reinstatement, suggesting a possible role for putative stress mechanisms. The differential antagonism of spiradoline and enadoline by naltrexone and nor-BNI in our study parallels the results of previous studies demonstrating differences in the abilities of naltrexone and nor-BNI to block the effects of enadoline in rhesus and squirrel monkeys (e.g., Butelman et al, 1998;Powell and Holtzman, 1999). Various studies have provided evidence for the existence of multiple receptor subtypes (Nock et al, 1988;Clark et al, 1989).…”

Section: Discussionsupporting

confidence: 91%

“…Another chemical class of agonists, the benzomorphans typified by bremazocine, exhibits putative selectivity at the 2 receptor subtype (Zukin et al, 1988). Previous studies suggested that nor-BNI may be more effective in antagonizing the effects of benzomorphans than of the arylacetamides (Butelman et al, 1998;Powell and Holtzman, 1999;but see Carey and Bergman, 2001). In the study by Powell and Holtzman (1999), for example, the response ratedecreasing effects of enadoline were significantly attenuated by naltrexone but not by nor-BNI, whereas both antagonists blocked the effects of bremazocine.…”

Section: Discussionmentioning

confidence: 99%

“…Previous studies suggested that nor-BNI may be more effective in antagonizing the effects of benzomorphans than of the arylacetamides (Butelman et al, 1998;Powell and Holtzman, 1999;but see Carey and Bergman, 2001). In the study by Powell and Holtzman (1999), for example, the response ratedecreasing effects of enadoline were significantly attenuated by naltrexone but not by nor-BNI, whereas both antagonists blocked the effects of bremazocine. Similarly, nor-BNI did not antagonize the antinociceptive effects of enadoline in rhesus monkeys (Butelman et al, 1998), although it did attenuate the discriminative stimulus effects of enadoline in squirrel monkeys (Carey and Bergman, 2001).…”

Section: Discussionmentioning

confidence: 99%

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κ Agonist-Induced Reinstatement of Cocaine Seeking in Squirrel Monkeys: A Role for Opioid and Stress-Related Mechanisms

Valdez

Platt²,

Rowlett³

et al. 2007

J Pharmacol Exp Ther

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Opioid agonists were at one time proposed as candidate pharmacotherapies for cocaine addiction, mainly because of their ability to decrease dopamine neurotransmission and attenuate the behavioral effects of cocaine in laboratory animals. Recent studies, however, suggest that agonists also may mimic and/or enhance some of the effects of cocaine through mechanisms related to stress. The current study used a reinstatement procedure to examine the ability of the agonists spiradoline and enadoline to reinstate extinguished cocaine seeking in squirrel monkeys previously trained to self-administer cocaine under a second-order schedule of i.v. drug injection. Opioid-and stress-related mechanisms were evaluated in antagonism studies with the opioid antagonists naltrexone and nor-binaltorphimine (nor-BNI), the corticotropin-releasing fac- (CP 154,526), and the ␣ 2 -adrenoceptor agonist clonidine combined with either spiradoline or enadoline. When tested alone, priming with spiradoline and enadoline induced significant reinstatement of cocaine-seeking behavior to approximately 45% of the maximum reinstatement induced by cocaine. Reinstatement of cocaine seeking induced by intermediate doses of spiradoline was greater in the presence than in the absence of responsecontingent presentations of a cocaine-paired stimulus. Spiradoline-and enadoline-induced reinstatement of drug seeking was attenuated by naltrexone but not by nor-BNI. Spiradolineinduced reinstatement of cocaine seeking was also antagonized by CP 154,526 and clonidine. The results point to interactions between a subpopulation of opioid receptors and central corticotropin-releasing factor and noradrenergic stress systems in the reinstatement of cocaine seeking induced by agonists.Opioid agonists have been proposed as potential pharmacotherapies for cocaine addiction because of their ability to decrease dopamine neurotransmission (Devine et al., 1993) and suppress certain behavioral effects of cocaine (Mello and Negus, 1998;Schenk et al., 1999;Beardsley et al., 2005). Recent evidence suggests, however, that reductions in cocaine-related behaviors induced by agonists may be secondary to a generalized response-suppressing effect of these drugs, and that the interaction between cocaine and agonists depends on the context and timing of their administration. When tested using a choice procedure of cocaine versus food reinforcement, rhesus monkeys showed an overall decrease in response rate but an increase in cocaine preference after intermittent infusions of the agonist U50,488 (Negus, 2004). McLaughlin et al. (2006a) demonstrated enhancement of cocaine-conditioned place preference when mice were given U50,488 1 h before cocaine and suppression of cocaineconditioned place preference when U50,488 was administered at a later time point.The effects of agonists on cocaine preference may partially reflect activation of physiological stress mechanisms, as opioid receptors and the endogenous opioid peptide dynorphin have been shown to regulate aspects of the stress resp...

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Section: Discussionsupporting

confidence: 93%

Section: Discussionsupporting

confidence: 91%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

See 2 more Smart Citations

κ Agonist-Induced Reinstatement of Cocaine Seeking in Squirrel Monkeys: A Role for Opioid and Stress-Related Mechanisms

Valdez

Platt²,

Rowlett³

et al. 2007

J Pharmacol Exp Ther

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show abstract

“…Bremazocine was prepared in de-ionized water, while U69,593 was dissolved in 3 parts 8.5% lactic acid and 2 parts 1.0 N sodium hydroxide. Agonist doses chosen for this study were based on previous work, demonstrating behavioral effects [3,14,34,42]. Drug doses are expressed as the free base.…”

Section: Drugsmentioning

confidence: 99%

Acute delta- and kappa-opioid agonist pretreatment potentiates opioid antagonist-induced suppression of water consumption

White

Ballard

Harmon

et al. 2008

Brain Research Bulletin

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The primary objective of this study was to determine whether pretreatment with kappa-and deltaopioid agonists potentiates naltrexone-induced suppression of water consumption following 24-hr of deprivation. This study also examined the temporal effects of agonist-induced antinociception using the tail-flick and hot plate tests. Adult male Sprague-Dawley rats were water deprived 20 hr and then given an injection (s.c. or i.c.) of an opioid agonist or saline. Drugs included the mu-opioid agonists morphine and DAMGO, the kappa-opioid agonists spiradoline, bremazocine, and U69,593, and the delta-opioid agonists BW 373U86 and DPDPE). Three hr and 45 min later, animals received a single dose of naltrexone (0.1 -30 mg/kg, s.c.) or saline. Fifteen minutes later, animals were allowed free access to water for 30 min. For the tail-flick and hot plate tests, animals were given a single injection of agonist and tested in both procedures every 30 min for up to 2 hr, then hourly up to 6 hr post-injection. Naltrexone dose-dependently suppressed fluid consumption 24 hr after deprivation. The effects of naltrexone on drinking were potentiated following pretreatment with at least one dose of the agonists tested except BW 373U86. With the exception of BW 373U86, DAMGO, and DPDPE, all of the opioid agonists produced significant antinociception in the hot plate test. Only BW 373U86 failed to have an antinociceptive effect in the tail-flick test. By 4 hr after treatment, drug-induced antinociception had largely waned, suggesting the potentiation of naltrexone-induced drinking suppression was not a result of a direct interaction with the agonists. In conclusion, kappa-opioid and delta-opioid receptors appear to contribute to the manifestation of acute opioid dependence, albeit to a lesser degree than mu-opioid receptors.

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Opioid mediation of amniotic fluid effects on chemosensory responsiveness in the neonatal rat

Méndez-Gallardo

Robinson

2010

Developmental Psychobiology

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The present study investigated if oral exposure to milk or amniotic fluid (AF) alters responsiveness to sensory stimulation in the neonatal rat, and whether these effects are mediated by the opioid system. Facial wiping evoked by intraoral lemon infusion was used as a measure of sensory responsiveness. Pups were tested in a supine posture, because they showed more paw-face strokes during facial wiping than pups tested prone (Experiment 1). Moreover, pups orally exposed to milk (Experiment 2) or AF (Experiment 3) showed a diminished wiping response to lemon compared to controls exposed to water. Blockade of opioid receptors with the non-selective antagonist naltrexone (Experiment 4) or the kappa antagonist nor-binaltorphimine (Experiment 5) reinstated higher levels of facial wiping after AF exposure. These findings confirm developmental continuity between fetal and neonatal behavioral responses to AF and the ability of AF to induce activity at kappa receptors of the endogenous opioid system.

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Differential antagonism of the rate-decreasing effects of κ-opioid receptor agonists by naltrexone and norbinaltorphimine

Cited by 11 publications

References 19 publications

κ Agonist-Induced Reinstatement of Cocaine Seeking in Squirrel Monkeys: A Role for Opioid and Stress-Related Mechanisms

κ Agonist-Induced Reinstatement of Cocaine Seeking in Squirrel Monkeys: A Role for Opioid and Stress-Related Mechanisms

Acute delta- and kappa-opioid agonist pretreatment potentiates opioid antagonist-induced suppression of water consumption

Opioid mediation of amniotic fluid effects on chemosensory responsiveness in the neonatal rat

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