Periadolescent nicotine exposure produces sensitization to reinforcement by diazepam in the rat

James-Walke, Nissa L.; Williams, Helen L.; Taylor, David A.; McMillen, Brian A.

doi:10.1016/j.ntt.2006.09.022

Cited by 11 publications

(6 citation statements)

References 22 publications

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“…Adolescent females are more likely to initiate smoking and are less likely to quit than adolescent males (Anderson and Burns, 2000; James-Walke et al, 2007; Perkins, 2001). External factors also appear to contribute to nicotine use in adolescent females, including appetite suppression and a desire to project a more appealing self-image (Seguire and Chalmers, 2000).…”

Section: Clinical Researchmentioning

confidence: 99%

A mechanistic hypothesis of the factors that enhance vulnerability to nicotine use in females

O’Dell

Torres

2014

Neuropharmacology

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Women are particularly more vulnerable to tobacco use than men. This review proposes a unifying hypothesis that females experience greater rewarding effects of nicotine and more intense stress produced by withdrawal than males. We also provide a neural framework whereby estrogen promotes greater rewarding effects of nicotine in females via enhanced dopamine release in the nucleus accumbens (NAcc). During withdrawal, we suggest that corticotropin-releasing factor (CRF) stress systems are sensitized and promote a greater suppression of dopamine release in the NAcc of females versus males. Taken together, females display enhanced nicotine reward via estrogen and amplified effects of withdrawal via stress systems. Although this framework focuses on sex differences in adult rats, it is also applied to adolescent females who display enhanced rewarding effects of nicotine, but reduced effects of withdrawal from this drug. Since females experience strong rewarding effects of nicotine, a clinical implication of our hypothesis is that specific strategies to prevent smoking initiation among females are critical. Also, anxiolytic medications may be more effective in females that experience intense stress during withdrawal. Furthermore, medications that target withdrawal should not be applied in a unilateral manner across age and sex, given that nicotine withdrawal is lower during adolescence. This review highlights key factors that promote nicotine use in females, and future studies on sex-dependent interactions of stress and reward systems are needed to test our mechanistic hypotheses. Future studies in this area will have important translational value toward reducing health disparities produced by nicotine use in females.

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Section: Clinical Researchmentioning

confidence: 99%

A mechanistic hypothesis of the factors that enhance vulnerability to nicotine use in females

O’Dell

Torres

2014

Neuropharmacology

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“…Injections were given daily for 10 consecutive days from PND34 to PND43. This time period is considered mid to late adolescence (Spear, 2000), and the specific time period, dose and route of administration were selected based on prior assessments of nicotine preexposure during periadolescence (specifically, Adriani et al , 2006, James-Walke et al, 2007, Shram et al , 2006). Subsequent to the nicotine preexposure, animals remained on ad libitum food and water and were handled daily for weighing, but were otherwise left undisturbed to mature until PND60, at which point they were individually housed in hanging wire mesh cages for the remainder of the study.…”

Section: Experiments 1: Adolescent Nicotine Preexposurementioning

confidence: 99%

“…Additionally, early onset of nicotine use usually precedes the use of other drugs of abuse, particularly alcohol (Nelson et al , 1995), and is seen as a risk factor for and strong predictor of the development of alcohol use and abuse and dependence disorders later in life (DiFranza and Guerrera, 1990, Grant, 1998, Grucza and Bierut, 2006, Hanna and Grant, 1999, USDHHS, 1994). Nicotine preexposure during periadolescence has also been shown to enhance the reinforcing and rewarding effects of other drugs of abuse, such as cocaine (McMillen et al , 2005, McQuown et al , 2007) and diazepam (James-Walke et al , 2007). …”

Section: Introductionmentioning

confidence: 99%

Exposure to nicotine during periadolescence or early adulthood alters aversive and physiological effects induced by ethanol

Rinker

Hutchison

Chen

et al. 2011

Pharmacology Biochemistry and Behavior

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The majority of smokers begin their habit during adolescence, which often precedes experimentation with alcohol. Interestingly, very little preclinical work has been done examining how exposure to nicotine during periadolescence impacts the affective properties of alcohol in adulthood. Understanding how periadolescent nicotine exposure influences the aversive effects of alcohol might help to explain why it becomes more acceptable to this preexposed population. Thus, Experiment 1 exposed male Sprague Dawley rats to either saline or nicotine (0.4 mg/kg, IP) from postnatal day 34 to 43 (periadolescence) and then examined changes in the aversive effects of alcohol (0, 0.56, 1.0 and 1.8 g/kg, IP) in adulthood using the conditioned taste aversion (CTA) design. Changes in blood alcohol concentration (BAC) as well as alcohol-induced hypothermia and locomotor suppression were also assessed. To determine if changes seen were specific to nicotine exposure during periadolescence, the procedures were replicated in adults (Experiment 2). Preexposure to nicotine during periadolescence attenuated the acquisition of the alcohol-induced CTAs (at 1.0 g/kg) and the hypothermic effects of alcohol (1.0 g/kg). Adult nicotine preexposure produced similar attenuation in alcohol's aversive (at 1.8 g/kg) and hypothermic (1.8 g/kg) effects. Neither adolescent nor adult nicotine preexposure altered BACs or alcohol-induced locomotor suppression. These results suggest that nicotine can alter the aversive and physiological effects of alcohol, regardless of the age at which exposure occurs, possibly increasing its overall reinforcing value and making it more likely to be consumed.

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“…These changes support prior results implicating involvement of nucleus accumbens in behavioral changes related to drug abuse and, for the first time, identify nicotine-induced altered gene expression in the granule cell layer of hippocampal dentate gyrus, a brain region involved in learning and memory. Because patterns of persistently induced FosB expression were similar after both peri-and post-adolescent nicotine treatments, increased expression of this transcription factor cannot be directly responsible for the behavioral differences observed after the respective treatment periods, and additional studies are required to establish the physiological basis for the distinct effects of peri-vs post-adolescent nicotine treatments (Adriani et al 2003;James-Walke et al 2007;McMillen et al 2005).…”

Section: Discussionmentioning

confidence: 99%

“…To determine if nicotine-induced changes in FosB expression may be restricted to peri-and not post-adolescent treatment, and thus potentially directly involved in behavioral effects produced only during periadolescence (Adriani et al 2003;James-Walke et al 2007), we also investigated effects of post-adolescent nicotine administration and have compared them to the earlier treatment period.…”

Section: Introductionmentioning

confidence: 99%

Nicotine increases FosB expression within a subset of reward- and memory-related brain regions during both peri- and post-adolescence

et al. 2007

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Periadolescent nicotine exposure produces sensitization to reinforcement by diazepam in the rat

Cited by 11 publications

References 22 publications

A mechanistic hypothesis of the factors that enhance vulnerability to nicotine use in females

A mechanistic hypothesis of the factors that enhance vulnerability to nicotine use in females

Exposure to nicotine during periadolescence or early adulthood alters aversive and physiological effects induced by ethanol

Nicotine increases FosB expression within a subset of reward- and memory-related brain regions during both peri- and post-adolescence

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