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

Dao, Jasmin M.; McQuown, Susan C.; Loughlin, Sandra E.; Belluzzi, James D.; Leslie, Frances M.

doi:10.1038/npp.2011.8

Cited by 76 publications

(120 citation statements)

References 81 publications

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“…Korpi and colleagues have elegantly discussed the effects of nicotine use on brain development, including during adolescence, in a recent review paper (Korpi et al, 2015). For example, it has been shown that adolescent but not adult exposure to nicotine alters serotonin receptors in the cerebral cortex (Slotkin and Seidler, 2009), decreases striatal serotonin activity and content (Slotkin and Seidler, 2007) increases dopamine transporter densities and decreases serotonin transporter densities in the striatum (Collins et al, 2004b), and can lead to increased dopamine D2 receptor function (Dao et al, 2011; McQuown et al, 2007). Nicotine-induced increases in dopaminergic function and decreases in serotonergic function all can contribute to increased rewarding properties of cocaine.…”

Section: Discussionmentioning

confidence: 99%

Nicotine produces long-term increases in cocaine reinforcement in adolescent but not adult rats

Reed

Izenwasser

2017

Brain Research

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Studies have shown that many smokers begin using nicotine during adolescence, yet the influence of early nicotine use on the response to other drugs of abuse in adulthood is not fully understood. In the current study, nicotine was administered to adolescent and adult rats for seven days. Thirty days later, cocaine-induced locomotor activity and cocaine self-administration were examined when the rats pretreated as adolescents were adults. Rats exposed to nicotine during early adolescence were sensitized thirty days later to the locomotor-activating effects of cocaine and self-administered a greater number of cocaine infusions than adolescent rats pretreated with vehicle. As a result of this increased intake, the cocaine self-administration dose-response curve was shifted upward indicating an increase in cocaine reinforcement. Rats pretreated with nicotine as adults, however, did not show a difference in locomotor activity or cocaine self-administration thirty days later compared to adult rats pretreated with vehicle. These findings suggest that early exposure to nicotine has long-term consequences on cocaine use. These data further suggest that nicotine use may carry a greater risk during adolescence than adulthood and adolescents who smoke may be particularly vulnerable to stimulant use.

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Section: Discussionmentioning

confidence: 99%

Nicotine produces long-term increases in cocaine reinforcement in adolescent but not adult rats

Reed

Izenwasser

2017

Brain Research

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“…Rats exposed to experimenter-administered nicotine during early adolescence (P28-31) were found to subsequently exhibit increased cocaine self-administration, an effect not evident with exposure later in adolescence (P38-41) or in adulthood (P86-89)(Dao et al, 2011). In contrast, adolescent-onset nicotine self-administration was not observed to alter later cocaine self-administration, although females allowed to self-administer nicotine from 4-8 weeks of age self-administered more nicotine after a week of abstinence than females given the opportunity to self-administer nicotine from 8-12 weeks of age; this effect was not evident in males (Levin et al, 2011).…”

Section: Animal Studiesmentioning

confidence: 99%

Adolescent alcohol exposure: Are there separable vulnerable periods within adolescence?

Spear

2015

Physiology & Behavior

224

189

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There are two key alcohol use patterns among human adolescents that confer increased vulnerability for later alcohol abuse/dependence, along with neurocognitive alterations: (a) early initiation of use during adolescence, and (b) high rates of binge drinking that are particularly prevalent late in adolescence. The central thesis of this review is that lasting neurobehavioral outcomes of these two adolescent exposure patterns may differ. Although it is difficult to disentangle consequences of early use from later binge drinking in human studies given the substantial overlap between groups, these two types of problematic adolescent use are differentially heritable and hence separable to some extent. Although few studies using animal models have manipulated alcohol exposure age, those studies that have have typically observed timing-specific exposure effects, with more marked (or at least different patterns of) lasting consequences evident after exposures during early-mid adolescence than late-adolescence/emerging adulthood, and effects often restricted to male rats in those few instances where sex differences have been explored. As one example, adult male rats exposed to ethanol during early-mid adolescence (postnatal days [P] 25-45) were found to be socially anxious and to retain adolescent-typical ethanol-induced social facilitation into adulthood, effects that were not evident after exposure during late-adolescence/emerging adulthood (P45-65); exposure at the later interval, however, induced lasting tolerance to ethanol's social inhibitory effects that was not evident after exposure early in adolescence. Females, in contrast, were little influenced by ethanol exposure at either interval. Exposure timing effects have likewise been reported following social isolation as well as after repeated exposure to other drugs such as nicotine (and cannabinoids), with effects often, although not always, more pronounced in males where studied. Consistent with these timing-specific exposure effects, notable maturational changes in brain have been observed from early to late adolescence that could provide differential neural substrates for exposure timing-related consequences, with for instance exposure during early adolescence perhaps more likely to impact later self-administration and social/affective behaviors, whereas exposures later in adolescence may be more likely to influence cognitive tasks whose neural substrates (such as the prefrontal cortex [PFC]) are still undergoing maturation at that time. Substantial more work is needed, however to characterize timing-specific effects of adolescent ethanol exposures and their sex dependency, determine their neural substrates, and assess their comparability to and interactions with adolescent exposure to other drugs and stressors. Such information could prove critical for informing intervention/prevention strategies regarding the potential efficacy of efforts directed toward delaying onset of alcohol use versus toward reducing high levels of use and risks associated with that u...

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“…Generally speaking, decreases in drug reward sensitivity are often associated with compensatory increases in drug self-administration under relatively low levels of response effort (see Koob & LeMoal, 2006). Indeed, age-specific enhancement of self-administration of nicotine (Adriani et al, 2003, 2006) and cocaine (McQuown et al, 2007; Dao et al, 2011) has sometimes (albeit not always – see Weaver et al, 2012; Levin et al, 2011) been reported after adolescent exposure to nicotine, with these effects generally restricted to exposures during early-mid adolescence, and not late adolescence or adulthood. This enhanced self-administration does not extend to all types of rewards given that similar effects were not evident when animals were given the opportunity to self-administer sucrose pellets (McQuown et al, 2007).…”

Section: Nicotinementioning

confidence: 99%

Consequences of adolescent use of alcohol and other drugs: Studies using rodent models

Spear

2016

Neuroscience & Biobehavioral Reviews

140

112

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Studies using animal models of adolescent exposure to alcohol, nicotine, cannabinoids, and the stimulants cocaine, 3,4-Methylenedioxymethampethamine and methamphetamine have revealed a variety of persisting neural and behavioral consequences. Affected brain regions often include mesolimbic and prefrontal regions undergoing notable ontogenetic change during adolescence, although it is unclear whether this represents areas of specific vulnerability or particular scrutiny to date. Persisting alterations in forebrain systems critical for modulating reward, socioemotional processing and cognition have emerged, including apparent induction of a hyper-dopaminergic state with some drugs and/or attenuations in neurons expressing cholinergic markers. Disruptions in cognitive functions such as working memory, alterations in affect including increases in social anxiety, and mixed evidence for increases in later drug self-administration have also been reported. When consequences of adolescent and adult exposure were compared, adolescents were generally found to be more vulnerable to alcohol, nicotine, and cannabinoids, but generally not to stimulants. More work is needed to determine how adolescent drug exposure influences sculpting of the adolescent brain, and provide approaches to prevent/reverse these effects.

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

Cited by 76 publications

References 81 publications

Nicotine produces long-term increases in cocaine reinforcement in adolescent but not adult rats

Nicotine produces long-term increases in cocaine reinforcement in adolescent but not adult rats

Adolescent alcohol exposure: Are there separable vulnerable periods within adolescence?

Consequences of adolescent use of alcohol and other drugs: Studies using rodent models

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