Alteration of intravenous nicotine self-administration by opioid receptor agonist and antagonists in rats

Ismayilova, Naila; Shoaib, Mohammed

doi:10.1007/s00213-010-1845-4

Cited by 42 publications

(38 citation statements)

References 49 publications

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“…The present findings offer support for previous studies which demonstrated a specific role for the KOR system in drug seeking, particularly, nicotine seeking (Al-Hasani et al, 2013; Ismayilova and Shoaib, 2010; Jackson et al, 2010, 2013; Smith et al, 2012). We found that activation of KORs with U50,488 dose dependently reinstated nicotine seeking, an effect which was attenuated by the KOR antagonist nor-BNI.…”

Section: Discussionsupporting

confidence: 91%

Role of the kappa-opioid receptor system in stress-induced reinstatement of nicotine seeking in rats

Grella

Funk

Coen

et al. 2014

Behavioural Brain Research

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Rationale The correlation between stress and smoking is well established. The mechanisms that underlie this relationship are, however, unclear. Recent data suggest the kappa-opioid system is involved in the mediation of negative affective states associated with stress thereby promoting drug addiction and relapse. Pharmacological treatments targeting the kappa opioid system and this mechanism may prove to be useful therapeutics for nicotine addiction in the future. Objectives We sought to determine whether there was a stress-specific role of the kappa opioid system in nicotine seeking behavior. Method Groups of male Long Evans rats were trained to self-administer nicotine intravenously; their operant responding for nicotine was extinguished prior to tests of reinstatement. Pretreatment with systemic injections of the kappa opioid receptor (KOR) antagonist nor-binaltorphimine (nor-BNI) was given prior to tests of stress (systemic injections of yohimbine (YOH)) or cue-induced reinstatement of nicotine seeking. Systemic injections of the KOR agonist U50,488 were also given in a test for reinstatement of nicotine seeking. Results Nor-BNI pretreatment at 1 hr and 24 hrs prior to testing was able to block YOH-induced, but not cue-induced reinstatement of nicotine seeking. U50,488 reinstated nicotine seeking behavior in a dose-dependent manner. Conclusions These findings support the hypothesis that the kappa opioid system is involved in relapse to nicotine seeking induced by stress, but not by conditioned cues. KOR antagonists such as nor-BNI may therefore be useful novel therapeutic agents for decreasing the risk of stress-induced drug relapse.

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Section: Discussionsupporting

confidence: 91%

Role of the kappa-opioid receptor system in stress-induced reinstatement of nicotine seeking in rats

Grella

Funk

Coen

et al. 2014

Behavioural Brain Research

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“…In the hypothalamus, injection of the ENK analog [D-Ala(2),N-MePhe(4),Gly(5)-ol]-Enkephalin (DAMGO) in the PVN or of OX in the PFLH stimulates the drinking of ethanol and consumption of a high-fat diet (Clegg et al, 2002;Naleid et al, 2007;Morganstern et al, 2010a), with opposite effects produced by the receptor antagonists (Lawrence et al, 2006;Naleid et al, 2007;Moorman and Aston-Jones, 2009;, and administration of DAMGO directly in the CeA also increases consumption of a fat-rich diet ). In addition, peripheral administration of an OX receptor 1 antagonist or of opioid antagonists is found to reduce the self-administration of nicotine (Corrigall et al, 2002;Hollander et al, 2008;Ismayilova and Shoaib, 2010;LeSage et al, 2010). Although yet to be studied with nicotine self-administration, MCH when centrally injected increases the consumption of ethanol (Duncan et al, 2005;Morganstern et al, 2011) and is endogenously elevated in the PFLH of rats prone to overconsuming fat (Morganstern et al, 2010a).…”

Section: Discussionmentioning

confidence: 99%

“…Self-administration of nicotine is reduced by hypothalamic administration of an OX receptor 1 antagonist (LeSage et al, 2010) and peripheral opioid antagonist (Ismayilova and Shoaib, 2010), and although yet to be studied with nicotine, central injection of MCH increases the consumption of ethanol (Duncan et al, 2005;Morganstern et al, 2011). Conversely, administration of nicotine stimulates expression of OX in the perifornical lateral hypothalamus (PFLH) and ENK in the hypothalamic paraventricular nucleus (PVN) and central nucleus of the amygdala (CeA) (Houdi et al, 1998;Loughlin et al, 2006) and OX mRNA is increased by chronic nicotine (Houdi et al, 1998;Kane et al, 2000). If these peptides do in fact have a role in potentiating the offspring's consumption, the effect of prenatal exposure to nicotine on the in utero development of these neurochemical systems would be expected to be stimulatory, rather than suppressive, in nature.…”

Section: Introductionmentioning

confidence: 99%

Prenatal Exposure to Nicotine Stimulates Neurogenesis of Orexigenic Peptide-Expressing Neurons in Hypothalamus and Amygdala

2013

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Animal and clinical studies show that gestational exposure to nicotine increases the propensity of offspring to consume nicotine, but the precise mechanism mediating this behavioral phenomenon is unclear. The present study in Sprague Dawley rats examined the possibility that the orexigenic peptide systems, enkephalin (ENK) and orexin (OX), which are stimulated by nicotine in adult animals and promote consummatory behavior, may be similarly responsive to nicotine's stimulatory effect in utero while having long-term behavioral consequences. The results demonstrated that nicotine exposure during gestation at low doses (0.75 or 1.5 mg/kg/d) significantly increased mRNA levels and density of neurons that express ENK in the hypothalamic paraventricular nucleus and central nucleus of the amygdala, OX, and another orexigenic peptide, melanin-concentrating hormone, in the perifornical lateral hypothalamus in preweanling offspring. These effects persisted in the absence of nicotine, at least until puberty. Colabeling of the cell proliferation marker BrdU with the neuronal marker NeuN and peptides revealed a marked stimulatory effect of prenatal nicotine on neurogenesis, but not gliogenesis, and also on the number of newly generated neurons expressing ENK, OX, or melanin-concentrating hormone. During adolescence, offspring also exhibited significant behavioral changes, increased consumption of nicotine and other substances of abuse, ethanol and a fat-rich diet, with no changes in chow and water intake or body weight. These findings reveal a marked sensitivity during gestation of the orexigenic peptide neurons to low nicotine doses that may increase the offspring's propensity to overconsume substances of abuse during adolescence.

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“…Prenatal exposure to fat is found to stimulate the expression of these peptides in the hypothalamus and nucleus accumbens (Chang et al, 2008; Vucetic et al, 2010) and produce changes in the mesolimbic dopaminergic reward system (Naef et al, 2011; Ong & Muhlhausler, 2011; Vucetic et al, 2010) and in cholinergic activity in mesostriatal and hypothalamic areas (Morganstern et al, 2013). The possibility that these neurochemical changes in the offspring can, in turn, promote later consumption of nicotine is supported by pharmacological evidence in rats, showing that nicotine self-administration is reduced by hypothalamic administration of an OX receptor 1 antagonist or peripheral administration of an opioid antagonist (Ismayilova & Shoaib, 2010; LeSage, Perry, Kotz, Shelley, & Corrigall, 2010), by dopaminergic blockade through peripheral injection of receptor antagonists or lesions in the mesolimbic dopaminergic system (Corrigall & Coen, 1991; Corrigall, Franklin, Coen, & Clarke, 1992; Kutlu et al, 2013), and by systemic injection of a specific α7 nAChR antagonist, methyllycaconitine (Markou & Paterson, 2001). With additional evidence showing that nicotine injection can stimulate these orexigenic peptides and the dopaminergic and cholinergic systems (Houdi, Dasgupta, & Kindy, 1998; Loughlin et al, 2006; Rada, Jensen, & Hoebel, 2001), it is likely that nicotine self-administration and these neurochemicals function within a positive feedback loop.…”

Section: Discussionmentioning

confidence: 99%

Nicotine and ethanol co-use in Long-Evans rats: Stimulatory effects of perinatal exposure to a fat-rich diet

Karatayev

Lukatskaya

Moon

et al. 2015

Alcohol

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Clinical studies demonstrate frequent co-existence of nicotine and alcohol abuse and suggest that this may result, in part, from the ready access to and intake of fat-rich diets. Whereas animal studies show that high-fat diet intake in adults can enhance the consumption of either nicotine or ethanol and that maternal consumption of a fat-rich diet during pregnancy increases operant responding for nicotine in offspring, little is known about the impact of dietary fat on the co-abuse of these two drugs. The goal of this study was to test in Long-Evans rats the effects of perinatal exposure to fat on the co-use of nicotine and ethanol, using a novel paradigm that involves simultaneous intravenous (IV) self-administration of these two drugs. Fat- vs. chow-exposed offspring were characterized and compared, first in terms of their nicotine self-administration behavior, then in terms of their nicotine/ethanol self-administration behavior, and lastly in terms of their self-administration of ethanol in the absence of nicotine. The results demonstrate that maternal consumption of fat compared to low-fat chow during gestation and lactation significantly stimulates nicotine self-administration during fixed-ratio testing. It also increases nicotine/ethanol self-administration during fixed-ratio and dose-response testing, with BEC elevated to 120 mg/dL, and causes an increase in breakpoint during progressive ratio testing. Of particular note is the finding that rats perinatally exposed to fat self-administer significantly more of the nicotine/ethanol mixture as compared to nicotine alone, an effect not evident in the chow-control rats. After removal of nicotine from the nicotine/ethanol mixture, this difference between the fat- and chow-exposed rats was lost, with both groups failing to acquire the self-administration of ethanol alone. Together, these findings suggest that perinatal exposure to a fat-rich diet, in addition to stimulating self-administration of nicotine, causes an even greater vulnerability to the excessive co-use of nicotine and ethanol.

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Alteration of intravenous nicotine self-administration by opioid receptor agonist and antagonists in rats

Cited by 42 publications

References 49 publications

Role of the kappa-opioid receptor system in stress-induced reinstatement of nicotine seeking in rats

Role of the kappa-opioid receptor system in stress-induced reinstatement of nicotine seeking in rats

Prenatal Exposure to Nicotine Stimulates Neurogenesis of Orexigenic Peptide-Expressing Neurons in Hypothalamus and Amygdala

Nicotine and ethanol co-use in Long-Evans rats: Stimulatory effects of perinatal exposure to a fat-rich diet

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