Rat strain differences in nicotine self-administration using an unlimited access paradigm

Brower, Victoria G.; Fu, Yongjian; Matta, Shannon G.; Sharp, Burt M.

doi:10.1016/s0006-8993(01)03375-3

Cited by 79 publications

(82 citation statements)

References 25 publications

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“…As reported previously (Brower et al, 2002;Parker et al, 2004;Valentine et al, 1997), SD and Lewis rats acquired nicotine (0.03 mg/kg) SA without prior training, priming or food deprivation when the drug was available 23 h/day. Similar levels of nicotine SA were achieved by the rats used throughout these experiments.…”

Section: Nicotine Samentioning

confidence: 83%

“…dose. SA was performed according to our previously published protocol with some modifications (Brower et al, 2002;Valentine et al, 1997). Briefly, rats received jugular and femoral cannulae and were then housed individually in operant chambers (Coulbourn Instruments, Allentown, PA).…”

Section: Nicotine Samentioning

confidence: 99%

“…Therefore, based on the foregoing data obtained in SD rats, selective comparisons were made to inbred Lewis rats, known for their atypical HPA responsiveness (Kosten and Ambrosio, 2002) and sensitivity to nicotine SA (Brower et al, 2002). HPA responses to nicotine SA on the first and third day of access to nicotine and to mild foot shock were evaluated.…”

Section: Effects Of Nicotine Sa On Hpa Responses In Lewis Ratsmentioning

confidence: 99%

“…Since stress responsiveness is known to vary between rat strains, we evaluated Sprague-Dawley (SD) rats comprehensively and then made selective comparisons to Lewis rats. The inbred Lewis strain has atypical HPA responsiveness (Kosten and Ambrosio, 2002), and is vulnerable to the SA of nicotine and other abused substances (Brower et al, 2002).…”

Section: Introductionmentioning

confidence: 99%

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Chronic Nicotine Self-Administration Augments Hypothalamic–Pituitary–Adrenal Responses to Mild Acute Stress

Chen

Sharp

2007

Neuropsychopharmacol

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We investigated the effect of chronic nicotine self-administration (SA) on hypothalamic-pituitary-adrenal (HPA) hormonal responses to acute stressors. Adult male Sprague-Dawley rats were given access to nicotine (0.03 mg/kg) for 23 h per day for 20 days. On day 1 of acquisition of nicotine SA, plasma levels of both adrenocorticotropin and corticosterone were significantly increased 15-30 min after the first dose of nicotine. These hormonal changes were no longer significant on day 3, when adrenocorticotropin levels were o60 pg/ml and corticosterone levels were o110 ng/ml during the hour after the first dose of nicotine. Chronic nicotine SA (20 days) significantly augmented (2-3-fold) both hormonal responses to mild foot shock stress (0.6 mA, 0.5 s per shock, 5 shocks per 5 min), but did not affect hormonal responses to moderate shock (1.2 mA, 0.5 s per shock, 5 shocks per 5 min), lipopolysaccharide or immobilization. Similar data were obtained in Lewis rats. These results provide further support for the concept that chronic nicotine SA is a stressor. In alignment with the effects of other stressors, nicotine activated the HPA axis on the first day of SA, but desensitization occurred with repeated exposure. Furthermore, chronic nicotine SA selectively cross-sensitized the HPA response to a novel stressor. These observations suggest that nicotine may selectively increase the HPA response to stressors in human smokers.

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Section: Nicotine Samentioning

confidence: 83%

Section: Nicotine Samentioning

confidence: 99%

Section: Effects Of Nicotine Sa On Hpa Responses In Lewis Ratsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Chronic Nicotine Self-Administration Augments Hypothalamic–Pituitary–Adrenal Responses to Mild Acute Stress

Chen

Sharp

2007

Neuropsychopharmacol

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“…For instance, several differences in the rewarding properties of nicotine have been characterized in the Lewis and Fischer 344 inbred rat strains. Lewis rats can learn to self-administer nicotine in an unlimited access procedure but not when there is limited access to nicotine, whereas Fischer 344 rats do not self-administer nicotine in either procedure [12,151]. Furthermore, Lewis rats can rapidly learn nicotine CPP when lower doses of nicotine are used, whereas Fischer 344 rats require more trials to acquire nicotine CPP at lower doses and can only learn the procedure rapidly when a high dose of nicotine is used [69,128].…”

Section: The Effects Of Nicotine In Inbred Rodent Strainsmentioning

confidence: 99%

Genetic variability in nicotinic acetylcholine receptors and nicotine addiction: Converging evidence from human and animal research

Portugal

Gould

2008

Behavioural Brain Research

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Tobacco smoking is a leading preventable cause of death in the United States and produces a major health and economic burden. Although the majority of smokers want to quit, few are successful. These data highlight the need for additional research into the neurobiology of tobacco dependence. Addiction to nicotine, the main psychoactive component of tobacco, is influenced by multiple factors that include individual differences in genetic makeup. Twin studies have demonstrated that genetic factors can influence vulnerability to nicotine addiction, and subsequent research has identified genes that may alter sensitivity to nicotine. In humans, genome-wide and candidate gene association studies have demonstrated that genes encoding nicotinic acetylcholine receptor (nAChR) proteins are associated with multiple smoking phenotypes. Similarly, research in mice has provided evidence that naturally occurring variability in nAChR genes is associated with changes in nicotine sensitivity. Furthermore, the use of genetic knockout mice has allowed researchers to determine the nAChR genes that mediate the effects of nicotine, whereas research with knockin mice has demonstrated that changes to nAChR genes can dramatically alter nicotine sensitivity. This review will examine the genetic factors that alter susceptibility to nicotine addiction, with an emphasis on the genes that encode nAChR proteins.

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Nicotine Self-Administration

Sorge

Clarke

2010

Animal Models of Drug Addiction

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Rat strain differences in nicotine self-administration using an unlimited access paradigm

Cited by 79 publications

References 25 publications

Chronic Nicotine Self-Administration Augments Hypothalamic–Pituitary–Adrenal Responses to Mild Acute Stress

Chronic Nicotine Self-Administration Augments Hypothalamic–Pituitary–Adrenal Responses to Mild Acute Stress

Genetic variability in nicotinic acetylcholine receptors and nicotine addiction: Converging evidence from human and animal research

Nicotine Self-Administration

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