Interactive effects of ethanol and nicotine on learning in C57BL/6J mice depend on both dose and duration of treatment

Gulick, Danielle; Gould, Thomas J.

doi:10.1007/s00213-007-0982-x

Cited by 50 publications

(55 citation statements)

References 55 publications

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“…Some studies have shown that foreground conditioning results in stronger conditioning [62,77], while other studies have not found this effect [15,5,43,51,60,61]. Although no differences in freezing to the context were found between background and foreground conditioning in the current study, previous work in our lab has demonstrated that there are differences in the effects of foreground and background conditioning that are visible at one week, but not at 24 hours, post-training [32]. This and other evidence suggests that differences do exist in the neural mechanisms that underlie foreground and background contextual fear conditioning.…”

Section: Discussioncontrasting

confidence: 75%

“…Although animal models have been used to examine the somatic and affective symptoms of nicotine withdrawal, less research has focused on the effects of nicotine withdrawal on learning and memory. One behavioral paradigm that has been used to examine the effects of nicotine on learning and memory is contextual fear conditioning [see 31 for review], and studies have consistently shown that acute nicotine enhances contextual conditioning, chronic nicotine does not alter contextual conditioning and nicotine withdrawal disrupts contextual conditioning [16,13,15,32,64,65].…”

Section: Introductionmentioning

confidence: 99%

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Nicotine withdrawal disrupts both foreground and background contextual fear conditioning but not pre-pulse inhibition of the acoustic startle response in C57BL/6 mice

André

Gulick

Portugal

et al. 2008

Behavioural Brain Research

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Nicotine withdrawal is associated with multiple symptoms such as anxiety, increased appetite, and disrupted cognition in humans. Although animal models have provided insights into the somatic and affective symptoms of nicotine withdrawal, less research has focused on the effects of nicotine withdrawal on cognition. Therefore, in this study, C57BL/6 mice were used to test the effects of withdrawal from chronic nicotine on foreground and background contextual fear conditioning, which present the context as a primary or secondary stimulus, respectively. Mice withdrawn from 12 days of chronic nicotine (6.3 mg/kg/day) or saline were trained and tested in either foreground or background contextual fear conditioning; nicotine withdrawal-associated deficits in contextual fear conditioning were observed in both conditions. Mice were also tested for the effects of withdrawal on pre-pulse inhibition of the acoustic startle reflex (PPI), a measure of sensory gating, and on the acoustic startle reflex. Mice withdrawn from 12 days of chronic nicotine (6.3 or 12.6 mg/kg/day) or saline underwent one 30-minute PPI and startle session; no effect of withdrawal from chronic nicotine on PPI or startle was observed for either dose at 24 hours after nicotine removal. Therefore, mice were tested at different time points following withdrawal from 12.6 mg/kg/day chronic nicotine (8, 24, and 48 hours after nicotine removal). No effect of withdrawal from chronic nicotine was observed at any time point for PPI. Overall, these results demonstrate that nicotine withdrawal disrupts two methods of contextual learning but not sensory gating in C57BL/6 mice.

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Section: Discussioncontrasting

confidence: 75%

Section: Introductionmentioning

confidence: 99%

Nicotine withdrawal disrupts both foreground and background contextual fear conditioning but not pre-pulse inhibition of the acoustic startle response in C57BL/6 mice

André

Gulick

Portugal

et al. 2008

Behavioural Brain Research

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“…Nicotine-induced sensitization is a mechanism that is thought to underlie craving and risk for relapse to smoking [27]. Interestingly, exposure to alcohol attenuated the nicotine withdrawal signs, similar to reports by Gulick and Gould, who found that ethanol reversed nicotine withdrawal symptoms [56]. Thus, alcohol might have a protective effect against nicotine withdrawal.…”

Section: Effect Of Nt69l On Nicotine Withdrawalsupporting

confidence: 73%

Novel Therapy for Nicotine Addiction in Alcohol Dependent Rats

Boules¹,

Stennett²,

Muhktar³

et al. 2013

J Addict Res Ther

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IntroductionNicotine and alcohol addiction are frequently co-morbid problems [1]. The co-dependence of nicotine and alcohol addiction complicates treatment and is often associated with significant morbidity and mortality. Prevalence of smoking in alcoholics is as high as 90% compared to 30% for the general population [2] and alcohol consumption is associated with high nicotine use [3,4]. Co-morbid cigarette smoking and alcoholism has been associated with higher rates of depression in comparison with non-alcoholic smokers [5] and increased cravings for nicotine in comparison with non alcohol dependent smokers [6]. Additionally, smoker alcoholics are more likely to die from smoking related diseases rather than directly from an alcohol related medical condition [7]. Pharmacotherapeutic options for the treatment of alcohol and tobacco co-dependence are limited. Thus, there is a critical need for the development of novel drugs implementing new therapeutic targets.Neurotensin (NT) is a neuropeptide that is closely associated with, and modulates dopamine (DA) [8], acetylcholine (ACh), glutamate, and γ-aminobutyric acid (GABA) neurotransmission, all of which are involved in addiction and reward pathways. Local administration of NT in the prefrontal cortex (PFC) increases extracellular levels of ACh and GABA [9]. Similar data were obtained with the extracranial injection of the NT agonist NT69L [10], a compound that was developed in our laboratory. NT also enhances GABAergic activity in rat hippocampus [11] and reduces glutamatergic neurotransmission in dorsolateral striatum [12]. However, NT must be administered centrally to have an effect because it is easily degraded by peptidases. Our laboratory has developed many NT agonists that can be administered extracranially and mimic the central effects of NT. The most studied of these agonists is NT69L, which binds with equal affinity to the two well-characterized NT receptors, subtype 1 (NTS1) and subtype 2 (NTS2). Our work with NT69L shows that it blocks nicotine-induced sensitization and nicotine self-administration [13][14][15].In addition to its role in animal models for nicotine addiction, the NT system has been strongly implicated in the neurochemical and behavioral effects of alcohol use [16,17]. Chronic administration of NT69L reduces alcohol preference and consumption in mice through modulation of the NTS1 [18]. Biochemically, NT69L normalizes the nicotine-induced changes in DA [19], the neurotransmitter that promotes the motivational process for both nicotine and alcohol, and the alcohol-induced increase in DA and glutamate in the striatum [20]. Additionally, NT modulates other neurotransmitters implicated in alcohol use disorder (AUD). It causes neurochemical changes similar to acamprosate (the calcium salt of acetylhomotaurine), which is one of three FDA-approved drugs to treat AUD. Administration of acamprosate or NT69L increases extracellular concentration of DA in striatum [10,11] and both acamprosate and NT69L modulate glutamate [21,22].Considering the behav...

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“…A considerable body of evidence suggests a solid interaction between ethanol and nicotine in the central nervous system (Collins et al 1993(Collins et al , 1996Smith et al 1999;Lê et al 2003) in which the nicotinic acetylcholine receptors seem to have an important role for such interrelation (3,15,16).Former reports have indicated that the combination of alcohol and nicotine may produce state-dependent learning in humans (17). In addition, according to some later studies, the administration of nicotinic receptor agonists reversed the ethanol-induced amnesia in laboratory animals (7,(18)(19)(20).While nicotine may reverse the ethanol-induced amnesia (similar to pre-test ethanol), the drugs have some opposite effects on other cognitive functions (6,8,21). Where nicotine enhances learning either through a direct effect on attention or affecting the pre-synaptic nicotinic acetylcholine receptors, ethanol may potentially impair learning (4)(5)(6).…”

Section: Introductionmentioning

confidence: 95%

Activation of the Nitric-Oxide System in Nucleus Accumbens Inhibits the Nicotine Reversal Effects upon Ethanol-Induced Amnesia

Raoufi¹,

Moshfegh²,

Piri³

et al. 2016

Journal of Advanced Medical Sciences and Applied Technologies

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The present study investigated the possible involvement of the nucleus accumbens' (NAc) nitric oxide system in nicotine's reversal effect upon ethanol-induced amnesia. The hypothesis was tested through ethanol state-dependent memory assessment in adult male Wistar rats. Bilateral chronic cannulae were implanted in the NAc and the animals were trained in a step-through type inhibitory avoidance memory task. The step-through latency was examined 24 h after animals' training. The pre-training or pre-test intraperitoneal (i.p.) injection of ethanol (0.9 g/kg) decreased the step-through latency, indicating an amnesic effect of the drug. Meanwhile, the pre-test administration of ethanol (0.6 and 0.9 g/kg) could reverse the pre-training ethanol (0.9 g/kg)-induced amnesia, suggesting a state-dependent effect. Similar to ethanol, the pre-test intra-NAc microinjection of nicotine (0.25 and 0.5 µg/rat) alone or nicotine (0.1, 0.25 and 0.5 µg/mouse, intra-NAc) in combination with an ineffective dose of ethanol (0.3 g/kg) could significantly reverse the (pre-training) ethanol-induced memory impairment. The ethanol (0.9 g/kg)-induced amnesia was similarly prevented following the pre-test intra-NAc administration of a nitric oxide synthase (NOS) inhibitor, L-NAME (0.4 and 0.8 µg/rat). Of note, the co-administration of L-NAME (0.04 and 0.08 µg/rat, intra-NAc) with an ineffective dose of nicotine (0.1 µg/rat, intra-NAc) could significantly potentiate the memoryimproving effect of nicotine on ethanol-induced amnesia and resembled the effects of pretest administration of a higher dose of nicotine. Furthermore, while the pre-test intra-NAc injection of L-NAME impaired the memory retrieval by itself, the pre-test intra-NAc administration of L-arginine, a nitric oxide precursor (0.3 and 0.6 µg/rat, intra-NAc), did not exert any effect either alone or in combination with an effective dose of nicotine (0.5 µg/rat, intra-NAc) on pre-training ethanol-induced memory impairment. Our findings indicated a possible role of the nucleus accumbens' nitric oxide system in the improving effects of nicotine on ethanol-induced amnesia and the related state-dependent learning.

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Interactive effects of ethanol and nicotine on learning in C57BL/6J mice depend on both dose and duration of treatment

Cited by 50 publications

References 55 publications

Nicotine withdrawal disrupts both foreground and background contextual fear conditioning but not pre-pulse inhibition of the acoustic startle response in C57BL/6 mice

Nicotine withdrawal disrupts both foreground and background contextual fear conditioning but not pre-pulse inhibition of the acoustic startle response in C57BL/6 mice

Novel Therapy for Nicotine Addiction in Alcohol Dependent Rats

Activation of the Nitric-Oxide System in Nucleus Accumbens Inhibits the Nicotine Reversal Effects upon Ethanol-Induced Amnesia

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