Nicotine dependence in rats

Carroll, Marilyn E.; Sylvie, T.; Asencio, Marisel; Keenan, Robert M.

doi:10.1016/0024-3205(89)90025-8

Cited by 35 publications

(17 citation statements)

References 34 publications

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“…Nicotine-exposed rats were faster in responding than saline-exposed rats, and there was a trend for this effect to be larger during the first two days of exposure to nicotine. Finally, consistent with previous reports, chronic nicotine administration suppressed body weight gain compared to the weight gain of saline-exposed animals (Carroll et al 1989;Grunberg et al 1986;Levin et al 1987).…”

Section: Discussionsupporting

confidence: 92%

Fluoxetine Combined with a Serotonin-1A Receptor Antagonist Reversed Reward Deficits Observed during Nicotine and Amphetamine Withdrawal in Rats

Harrison

Liem

Markou

2001

Neuropsychopharmacology

158

126

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Cessation of chronic nicotine or amphetamine administration precipitates withdrawal syndromes characterized by affective symptoms, including "diminished interest or pleasure" in rewarding stimuli (i.e., anhedonia) (American Psychiatric Association 1994;Covey et al. 1998;Glassman 1993;Hughes 1992). Interestingly, the symptom of "diminished interest or pleasure" is not only a symptom of drug withdrawal, but also a core symptom of depression and a negative symptom of schizophrenia (American Psychiatric Association 1994;Markou et al. 1998). Brain reward threshold elevation is an operational measure of this symptom because it reflects diminished sensitivity to rewarding electrical stimuli. In rats, withdrawal from drugs of abuse belonging to diverse pharmacological classes, such as nicotine (Epping-Jordan et al. 1998 Watkins et al. 2000b), amphetamine Zacharko 1980a, 1980b;Kokkinidis et al. 1980Kokkinidis et al. , 1986 Barrett 1976, 1980;Lin et al. 1999Lin et al. , 2000Paterson et al. 2000;Wise and Munn 1995), cocaine (Baldo et al. 1999;Kokkinidis and McCarter 1990; Koob 1991, 1992a;Markou et al. 1992) morphine (Schulteis et al. 1994) and ethanol (Schulteis et al. 1995) elevated brain stimulation reward thresholds.In addition to the affective aspects of drug withdrawal reflected in threshold elevations, nicotine, opiate, or ethanol withdrawal also lead to alterations in a set of behaviors termed somatic signs. In the case of nicotine, these somatic signs are primarily gasps, writhes, eye blinks, and ptosis (Epping-Jordan et al. 1998;Hildebrand et al. 1997Hildebrand et al. , 1999Malin et al. 1992). It is unlikely that these somatic signs in the rat reflect the affective component of drug withdrawal. Nevertheless, the study of both threshold elevations and somatic signs permits the investigation of the effects of manipulations on the various aspects of withdrawal.Based on evidence demonstrating the efficacy of serotonergic antidepressant treatments, reduced cerebrospinal fluid levels of serotonin metabolites, endocrine measures reflecting reduced serotonergic neurotransmission and the exacerbation of depressive symptomatology seen after serotonin (5-HT) depletion in depressed individuals, it is hypothesized that reduced serotonergic neurotransmission underlies at least some aspects or some subtypes of non-drug-induced depressions (for reviews, see Caldecott-Hazard et al. 1991; CaldecottHazard and Schneider 1992;Heninger et al. 1996;Markou et al. 1998;Meltzer and Lowy 1988;Willner 1985). The purpose of the present study was to test the hypothesis that reduced serotonergic neurotransmission mediates some of the affective aspects, not only of non-drug-induced depressions, but also of druginduced depressions. Thus, the present study tested the hypothesis that enhancement of serotonergic neurotransmission through acute administration of the selective serotonin reuptake inhibitor (SSRI) fluoxetine (Wong et al. 1995) in combination with a relatively selective 5-HT 1A receptor antagonist would alleviate the symptom of "dimin...

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Section: Discussionsupporting

confidence: 92%

Fluoxetine Combined with a Serotonin-1A Receptor Antagonist Reversed Reward Deficits Observed during Nicotine and Amphetamine Withdrawal in Rats

Harrison

Liem

Markou

2001

Neuropsychopharmacology

158

126

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“…These results appear fairly consistent with human research showing no acute effects of tobacco or nicotine on perception or liking of sweet taste (Redington 1984;Mela t989;Perkins et al 1990b) and on reducing intake of sweet foods . Interestingly, several recent studies of rats have found increased intake of sucrose (Jias and Ellison 1990) or glucose/saccharin (Carroll et al 1989) solutions during nicotine treatment. However, other animal research has reported specific declines in sweet food intake during nicotine treatment (Grunberg et al 1985).…”

Section: Discussionmentioning

confidence: 97%

Effects of nicotine on hunger and eating in male and female smokers

et al. 1992

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We tested whether the inverse relationship between smoking and body weight may be due in part to nicotine's acute effects on reducing hunger and eating. On four mornings, male and female smokers (n = 10 each), abstinent overnight from smoking and food, received one of three nicotine doses (7.5, 15, and 30 micrograms/kg) or placebo (0) via nasal spray every 30 min for 2 h. Self-reported hunger and satiety ("fullness") and craving for cigarettes were obtained after each dose presentation. Subjects subsequently ate ad lib from a large array of food items varying in sweet taste and fat content. For both males and females, nicotine had no effect on self-reported hunger, but cigarette craving was decreased. Rather than being decreased, caloric intake during the meal was unexpectedly increased following nicotine compared with placebo. Cigarette craving increased after the meal, and this increase was unaffected by nicotine dose. There were virtually no differences between males and females in any effects of nicotine. These results indicate that nicotine may not acutely suppress appetite in fasting smokers and suggest that other actions of nicotine or smoking may account for the lower body weights of smokers.

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“…This withdrawal syndrome is considered one of the major causes of the high relapse rate among people undergoing smoking cessation. The evaluation of nicotine withdrawal has been attempted using various models, such as operant schedules of reinforcement (Carroll et al, 1989;Corrigall et al, 1989), place preference (Costall et al, 1990;Suzuki et al, 1996), brain-stimulation reward threshold (Epping-Jordan et al, 1998), and auditory startle (Helton et al, 1993;Acri, 1994). Moreover, several groups reported that rats that have been chronically treated with nicotine for 7 days or more showed several withdrawal somatic signs after mecamylamine or dihydro-␤-erythroidine injections such as shakes, tremors, wet dog shakes, teeth chatters, eye blinks, and abdominal constrictions (Malin et al, 1992;Hildebrand et al, 1997;Epping-Jordan et al, 1998;Bancroft and Levin, 2000) (however, also see Stolerman et al, 1973;Corrigall et al, 1989;Helton et al, 1993;Suzuki et al, 1996).…”

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confidence: 99%

Characterization of Spontaneous and Precipitated Nicotine Withdrawal in the Mouse

Damaj¹,

Kao²,

Martin³

2003

J Pharmacol Exp Ther

205

252

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The nicotine withdrawal syndrome was validated and characterized in the mouse using both somatic and affective measures after infusion with nicotine daily via subcutaneous minipumps. The influence of dose, duration of infusion, and repeated withdrawal as well as the contribution of genetic factors were investigated. We then characterized the contribution of nicotinic receptor and site mechanisms to withdrawal signs using various nicotinic antagonists. Our results showed that spontaneous nicotine withdrawal increased the number of somatic signs, decreased the time spent in open arms of the plus-maze test, and induced hyperalgesia. The effect was dose-dependent in all measures with no significant changes at the lowest dose of nicotine (6 mg/kg/day). Withdrawal signs were prominent shortly after pump removal and remained prominent through day 3 or 4. The results with the different antagonists (mecamylamine, dihydro-␤-erythroidine, and methyllycaconitine) suggest the involvement of several nicotinic subtypes such as ␣3␤4*, ␣4␤2*, and ␣7 in nicotine withdrawal. Increasing the duration of nicotine exposure (from 7 to 60 days) and the total nicotine exposure (increasing doses of infusing) augmented the severity of nicotine withdrawal signs. The withdrawal severity of nicotine differs between C57/BL and 129/SvEv inbred mice with nicotine withdrawal in C57 being more severe than in the 129 strain. In summary, our present results suggest that withdrawal from nicotine can be modulated by genetic factors, daily nicotine intake, duration of nicotine exposure, and withdrawal history. The present study demonstrates that our mouse nicotine withdrawal model will be useful for studying the pharmacological, biochemical, and genetic mechanisms involved in nicotine dependence.

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Nicotine dependence in rats

Cited by 35 publications

References 34 publications

Fluoxetine Combined with a Serotonin-1A Receptor Antagonist Reversed Reward Deficits Observed during Nicotine and Amphetamine Withdrawal in Rats

Fluoxetine Combined with a Serotonin-1A Receptor Antagonist Reversed Reward Deficits Observed during Nicotine and Amphetamine Withdrawal in Rats

Effects of nicotine on hunger and eating in male and female smokers

Characterization of Spontaneous and Precipitated Nicotine Withdrawal in the Mouse

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