Enhanced nicotine reward in adulthood after exposure to nicotine during early adolescence in mice

Kota, Dena; Robinson, Susan E.; Damaj, M. Imad

doi:10.1016/j.bcp.2009.06.099

Cited by 53 publications

(59 citation statements)

References 26 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Alcohol-induced dopamine release was decreased by nicotine administration [106], although the effects on dopamine release in the nucleus accumben of alcohol and nicotine are additive [116]. As mentioned, prenatal drug influences are beyond the scope of this review, but it is of interest that prenatal exposure of both alcohol and nicotine decreased ethanol preference and consumption in males during adolescence in females during adulthood [117], nicotine exposure in early adolescence, but not later increased nicotine preference [105]. Some effects of alcohol differ from nicotine-induced effect so nicotine addition may alter some alcohol effects.…”

Section: Interactionsmentioning

confidence: 94%

“…Nicotine pretreatment also increases nicotine preference. Animals given nicotine in early adolescence (but not at late adolescence or adulthood) show increased nicotine conditioned place preference when tested as adults [105]. Pre-treatment with nicotine (also with a cannabinoid agonist) decreased alcohol-induced dopamine release in the nucleus accumbens shell [106].…”

Section: Interactionsmentioning

confidence: 98%

“…Some of the differences in the effects of nicotine versus alcohol are summarized in Table 4. Receptor systems [85,89,106,112,117,118] Transmitter changes [64,107,108,116] Effects of antagonists [140,[143][144][145][146] Other interaction effects [96, 98-106, 109, 112, 115] Changes in development [105,113,114,117] Effect on peptides [129] Other drug interactions [108,110,111] Choline acetyltransferase, choline esterase [89,[118][119][120][121][122] Nicotine binding [102] Opioid peptide formation [129] Endocannabinoid content of some areas [64] Glutamate transporter expression [107] Locomotor activity, transcription factors [115] Cross tolerance [102,103] Neurochem Res (2010) 35:1248-1258 1253…”

Section: Antagonism Of the Effectsmentioning

confidence: 99%

See 2 more Smart Citations

Nicotine: Alcohol Reward Interactions

Lajtha

Sershen

2010

Neurochem Res

View full text Add to dashboard Cite

It is well established that the continued intake of drugs of abuse is reinforcing-that is repeated consumption increases preference. This has been shown in some studies to extend to other drugs of abuse; use of one increases preference for another. In particular, the present review deals with the interaction of nicotine and alcohol as it has been shown that smoking is a risk factor for alcoholism and alcohol use is a risk factor to become a smoker. The review discusses changes in the brain caused by chronic nicotine and chronic alcohol intake to approach the possible mechanisms by which one drug increases the preference for another. Chronic nicotine administration was shown to affect nicotine receptors in the brain, affecting not only receptor levels and distribution, but also receptor subunit composition, thus affecting affinity to nicotine. Other receptor systems are also affected among others catecholamine, glutamate, GABA levels and opiate and cannabinoid receptors. In addition to receptor systems and transmitters, there are endocrine, metabolic and neuropeptide changes as well induced by nicotine. Similarly chronic alcohol intake results in changes in the brain, in multiple receptors, transmitters and peptides as discussed in this overview and also illustrated in the tables. The changes are sex and age-dependent-some changes in males are different from those in females and in general adolescents are more sensitive to drug effects than adults. Although nicotine and alcohol interact-not all the changes induced by the combined intake of both are additive-some are opposing. These opposing effects include those on locomotion, acetylcholine metabolism, nicotine binding, opiate peptides, glutamate transporters and endocannabinoid content among others. The two compounds lower the negative withdrawal symptoms of each other which may contribute to the increase in preference, but the mechanism by which preference increases-most likely consists of multiple components that are not clear at the present time. As the details of induced changes of nicotine and alcohol differ, it is likely that the mechanisms of increasing nicotine preference may not be identical to that of increasing alcohol preference. Stimulation of preference of yet other drugs may again be different -representing one aspect of drug specificity of reward mechanisms.

show abstract

Section: Interactionsmentioning

confidence: 94%

Section: Interactionsmentioning

confidence: 98%

Section: Antagonism Of the Effectsmentioning

confidence: 99%

See 1 more Smart Citation

Nicotine: Alcohol Reward Interactions

Lajtha

Sershen

2010

Neurochem Res

View full text Add to dashboard Cite

show abstract

“…Moreover, smoking is a prospective risk factor for impaired cognitive function in later life (Cervilla et al, 2000;Richards et al, 2003), and adolescent tobacco use is associated with increased risk of developing mental and behavioral problems, including abuse of other drugs, later in life (Brown et al, 1996;Johnson et al, 2000;McGee et al, 2000;Ellickson et al, 2001;Brook et al, 2004). In rodents, adolescent animals are more susceptible to nicotine-induced CPP than adults (Vastola et al, 2002;Belluzzi et al, 2004;Shram et al, 2006;Kota et al, 2009;Shram and Le, 2010;Brielmaier et al, 2012;Ahsan et al, 2014). Moreover, nicotine administration during, but not after adolescence, has long-lasting effects on cognitive, emotional, and addiction-related behaviors (Adriani et al, 2003(Adriani et al, , 2004Counotte et al, 2009Counotte et al, , 2011Iniguez et al, 2009).…”

Section: Nicotinementioning

confidence: 99%