Naloxone inhibits nicotine-induced receptor current and catecholamine secretion in bovine chromaffin cells

Tomé, Ângelo R.; Izaguirre, Víctor; Rosário, Luı́s M.; Ceña, Valentı́n; González-García, Cristina

doi:10.1016/s0006-8993(01)02388-5

Cited by 22 publications

(11 citation statements)

References 22 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Also, in humans, naloxone administration has been reported to induce somatic signs of nicotine withdrawal in heavy chronic smokers (Krishnan-Sarin et al, 1999). However, these effects could be a result of, at least in part, direct blockade of nAChRs, because this opioid antagonist was found to bind nAChRs (Tome et al, 2001). Besides these pharmacological data, there are molecular studies showing a possible role of the endogenous opioid system in nicotine abstinence.…”

Section: Discussionmentioning

confidence: 99%

Nicotine-Induced Antinociception, Rewarding Effects, and Physical Dependence Are Decreased in Mice Lacking the Preproenkephalin Gene

Berrendero¹,

Mendizábal²,

Robledo³

et al. 2005

J. Neurosci.

127

119

View full text Add to dashboard Cite

It has been shown previously that the endogenous opioid system may be involved in the behavioral effects of nicotine. In the present study, the participation of endogenous enkephalins on nicotine responses has been investigated by using preproenkephalin knock-out mice. Acute nicotine-induced hypolocomotion remained unaffected in these mice. In contrast, antinociception elicited in the tailimmersion and hot-plate tests by acute nicotine administration was reduced in mutant animals. The rewarding properties of nicotine were then investigated using the place-conditioning paradigm. Nicotine induced a conditioned place preference in wild-type animals, but this effect was absent in knock-out mice. Accordingly, in vivo microdialysis studies revealed that the enhancement in dopamine extracellular levels in the nucleus accumbens induced by nicotine was also reduced in preproenkephalin-deficient mice. Finally, the somatic expression of the nicotine withdrawal syndrome precipitated in nicotine-dependent mice by mecamylamine was significantly attenuated in mutant animals. In summary, the present results indicate that endogenous opioid peptides derived from preproenkephalin are involved in the antinociceptive and rewarding properties of nicotine and participate in the expression of physical nicotine dependence.

show abstract

Section: Discussionmentioning

confidence: 99%

Nicotine-Induced Antinociception, Rewarding Effects, and Physical Dependence Are Decreased in Mice Lacking the Preproenkephalin Gene

Berrendero¹,

Mendizábal²,

Robledo³

et al. 2005

J. Neurosci.

127

119

View full text Add to dashboard Cite

show abstract

“…At the receptor level, the opioid antagonists naloxone and naltrexone have been shown to block nAChRs [123][124][125][126] (Talka, unpublished results). Naloxone and naltrexone are in clinical use for opioid intoxication and alcohol dependence [127,128].…”

Section: Nicotine Interactions With Other Opioids-experimental Evidenmentioning

confidence: 99%

Methadone’s effect on nAChRs—a link between methadone use and smoking?

Talka

Tuominen

Salminen

2015

Biochemical Pharmacology

View full text Add to dashboard Cite

“…Naloxone was even more effective than the nAChR antagonist mecamylamine in precipitating the negative emotional manifestations of nicotine withdrawal measured in the place conditioning paradigm in mice (Balerio et al, 2004). However, the opioid antagonists naloxone (Tome et al, 2001) and naltrexone (Almeida et al, 2000) also show some affinity to nAChRs, which could have some influence in the behavioral effects induced by these antagonists in nicotine-dependent animals and humans. On the other hand, the administration of MOR, DOR or KOR agonists reduces the capability of mecamylamine to produce aversive manifestations of nicotine withdrawal in the place conditioning paradigm (Ise et al 2000, 2002).…”

Section: The Role Of the Endogenous Opioid System In The Developmementioning

confidence: 99%

Neurobiological mechanisms involved in nicotine dependence and reward: Participation of the endogenous opioid system

Berrendero

Robledo

Trigo

et al. 2010

Neuroscience & Biobehavioral Reviews

131

View full text Add to dashboard Cite

Nicotine is the primary component of tobacco that maintains the smoking habit and develops addiction. The adaptive changes of nicotinic acetylcholine receptors produced by repeated exposure to nicotine play a crucial role in the establishment of dependence. However, other neurochemical systems also participate in the addictive effects of nicotine including glutamate, cannabinoids, GABA and opioids. This review will cover the involvement of these neurotransmitters in nicotine addictive properties, with a special emphasis on the endogenous opioid system. Thus, endogenous enkephalins and beta-endorphins acting on mu-opioid receptors are involved in nicotine rewarding effects, whereas opioid peptides derived from prodynorphin participate in nicotine aversive responses. An upregulation of mu-opioid receptors has been reported after chronic nicotine treatment that could counteract the development of nicotine tolerance, whereas the downregulation induced on kappaopioid receptors seems to facilitate nicotine tolerance. Endogenous enkephalins acting on mu-opioid receptors also play a role in the development of physical dependence to nicotine. In agreement with these actions of the endogenous opioid system, the opioid antagonist naltrexone has shown to be effective for smoking cessation in certain subpopulations of smokers.

show abstract

Naloxone inhibits nicotine-induced receptor current and catecholamine secretion in bovine chromaffin cells

Cited by 22 publications

References 22 publications

Nicotine-Induced Antinociception, Rewarding Effects, and Physical Dependence Are Decreased in Mice Lacking the Preproenkephalin Gene

Nicotine-Induced Antinociception, Rewarding Effects, and Physical Dependence Are Decreased in Mice Lacking the Preproenkephalin Gene

Methadone’s effect on nAChRs—a link between methadone use and smoking?

Neurobiological mechanisms involved in nicotine dependence and reward: Participation of the endogenous opioid system

Contact Info

Product

Resources

About