Age, sex and early environment contribute to individual differences in nicotine/acetaldehyde-induced behavioral and endocrine responses in rats

Park, Minjung K.; Belluzzi, James D.; Han, Sang Hoon; Cao, Jun; Leslie, Frances M.

doi:10.1016/j.pbb.2006.10.002

Cited by 26 publications

(21 citation statements)

References 60 publications

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“…This finding of early adolescence as a critical period of vulnerability to the effects of nicotine is consistent with other recent animal studies that have shown unique effects of nicotine at this age (Azam et al, 2007;Adriani et al, 2003;Belluzzi et al, 2004;Park et al, 2007;Kota et al, 2007). Furthermore, the actively maturing PFC-NAc-BLA triadic circuit appears to be highly sensitive to the effects of early adolescent nicotine exposure.…”

Section: Adolescent Maturation Of the Mesocorticolimbic Systemsupporting

confidence: 90%

Nicotine Alters Limbic Function in Adolescent Rat by a 5-HT1A Receptor Mechanism

Dao

McQuown

Loughlin

et al. 2011

Neuropsychopharmacol

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Epidemiological studies have shown that adolescent smoking is associated with health risk behaviors, including high-risk sexual activity and illicit drug use. Using rat as an animal model, we evaluated the behavioral and biochemical effects of a 4-day, low-dose nicotine pretreatment (60 mg/kg; intravenous) during adolescence and adulthood. Nicotine pretreatment significantly increased initial acquisition of cocaine self-administration, quinpirole-induced locomotor activity, and penile erection in adolescent rats, aged postnatal day (P)32. These effects were long lasting, remaining evident 10 days after the last nicotine treatment, and were observed when nicotine pretreatment was administered during early adolescence (P28-31), but not late adolescence (P38-41) or adulthood (P86-89). Neurochemical analyses of c-fos mRNA expression, and of monoamine transmitter and transporter levels, showed that forebrain limbic systems are continuing to develop during early adolescence, and that this maturation is critically altered by brief nicotine exposure. Nicotine selectively increased c-fos mRNA expression in the nucleus accumbens shell and basolateral amygdala in adolescent, but not adult animals, and altered serotonin markers in these regions as well as the prefrontal cortex. Nicotine enhancement of cocaine self-administration and quinpirole-induced locomotor activity was blocked by co-administration of WAY 100 635 (N-{2-[4-(2-methoxyphenyl)-1-piperazinyl] ethyl}-N-(2-pyridinyl)cyclohexanecarboxamide), a selective serotonin 1A (5-HT1A) receptor antagonist. Early adolescent pretreatment with the mixed autoreceptor/heteroceptor 5-HT1A receptor agonist, 8-OH-DPAT, but not the autoreceptor-selective agonist, S-15535, also enhanced quinpirole-induced locomotor activation. Nicotine enhancement of quinpirole-induced penile erection was not blocked by WAY 100 635 nor mimicked by 8-OH-DPAT. These findings indicate that early adolescent nicotine exposure uniquely alters limbic function by both 5-HT1A and non-5-HT1A receptor mechanisms.

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Section: Adolescent Maturation Of the Mesocorticolimbic Systemsupporting

confidence: 90%

Nicotine Alters Limbic Function in Adolescent Rat by a 5-HT1A Receptor Mechanism

Dao

McQuown

Loughlin

et al. 2011

Neuropsychopharmacol

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“…administration under small FR or PR schedules or oral self-administration models (Donny et al, 2000; Klein et al, 2004; Chaudhri et al, 2005; Park et al, 2007; Lynch, 2009; Li et al, 2012), but is inconsistent with some other studies showing no sex difference or higher nicotine intake in males (Chen et al, 2007; Nesil et al, 2011; Feltenstein et al, 2012; Johnson et al, 2012; Li et al, 2012). It is unclear what accounts for these discrepancies, as numerous methodological factors vary across studies; including the unit dose, strain, age, session duration, and maintenance schedule.…”

Section: Discussionmentioning

confidence: 58%

Sex differences in nicotine self-administration in rats during progressive unit dose reduction: Implications for nicotine regulation policy

Grebenstein

Burroughs

Zhang

et al. 2013

Pharmacology Biochemistry and Behavior

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Reducing the nicotine content in tobacco products is being considered by the FDA as a policy to reduce the addictiveness of tobacco products. Understanding individual differences in response to nicotine reduction will be critical to developing safe and effective policy. Animal and human research demonstrating sex differences in the reinforcing effects of nicotine suggests that males and females may respond differently to nicotine-reduction policies. However, no studies have directly examined sex differences in the effects of nicotine unit-dose reduction on nicotine self-administration (NSA) in animals. The purpose of the present study was to examine this issue in a rodent self-administration model. Male and female rats were trained to self-administer nicotine (0.06 mg/kg) under an FR 3 schedule during daily 23 h sessions. Rats were then exposed to saline extinction and reacquisition of NSA, followed by weekly reductions in the unit dose (0.03 to 0.00025 mg/kg) until extinction levels of responding were achieved. Males and females were compared with respect to baseline levels of intake, resistance to extinction, degree of compensatory increases in responding during dose reduction, and the threshold reinforcing unit dose of nicotine. Exponential demand-curve analysis was also conducted to compare the sensitivity of males and females to increases in the unit price (FR/unit dose) of nicotine (i.e., elasticity of demand or reinforcing efficacy). Females exhibited significantly higher baseline intake and less compensation than males. However, there were no sex differences in the reinforcement threshold or elasticity of demand. Dose–response relationships were very well described by the exponential demand function (r2 values > 0.96 for individual subjects). These findings suggest that females may exhibit less compensatory smoking in response to nicotine reduction policies, even though their nicotine reinforcement threshold and elasticity of demand may not differ from males.

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“…In addition, concurrent acetaldehyde, the primary metabolite of ethanol, increases initial acquisition of nicotine self-administration in adolescent male rats (142). Whereas males exhibited a decrease in responding to nicotine-acetaldehyde combinations with age, females did not (143). More recent work demonstrates that adolescent males find concurrent intravenous nicotine and alcohol significantly more reinforcing than either drug alone.…”

Section: Concurrent Use Of Nicotine and Alcoholmentioning

confidence: 99%

Mechanisms and genetic factors underlying co-use of nicotine and alcohol or other drugs of abuse

Cross

Lotfipour

Leslie

2016

The American Journal of Drug and Alcohol Abuse

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Concurrent use of tobacco and alcohol or psychostimulants represents a major public health concern, with use of one substance influencing consumption of the other. Co-abuse of these drugs leads to substantial negative health outcomes, reduced cessation, and high economic costs, but the underlying mechanisms are poorly understood. Epidemiological data suggest that tobacco use during adolescence plays a particularly significant role. Adolescence is a sensitive period of development marked by major neurobiological maturation of brain regions critical for reward processing, learning and memory, and executive function. Nicotine exposure during this time produces a unique and long-lasting vulnerability to subsequent substance use, likely via actions at cholinergic, dopaminergic, and serotonergic systems. In this review, we discuss recent clinical and preclinical data examining the genetic factors and mechanisms underlying co-use of nicotine and alcohol or cocaine and amphetamines. We evaluate the critical role of nicotinic acetylcholine receptors throughout, and emphasize the dearth of preclinical studies assessing concurrent drug exposure. We stress important age and sex differences in drug responses, and highlight a brief, low-dose nicotine exposure paradigm that may better model early use of tobacco products. The escalating use of e-cigarettes among youth necessitates a closer look at the consequences of early adolescent nicotine exposure on subsequent alcohol and drug abuse.

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Age, sex and early environment contribute to individual differences in nicotine/acetaldehyde-induced behavioral and endocrine responses in rats

Cited by 26 publications

References 60 publications

Nicotine Alters Limbic Function in Adolescent Rat by a 5-HT1A Receptor Mechanism

Nicotine Alters Limbic Function in Adolescent Rat by a 5-HT1A Receptor Mechanism

Sex differences in nicotine self-administration in rats during progressive unit dose reduction: Implications for nicotine regulation policy

Mechanisms and genetic factors underlying co-use of nicotine and alcohol or other drugs of abuse

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