Nicotine alters limbic function in adolescent rat by a 5-HT1A receptor mechanism
Open accessAbstract
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 μg/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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In Dao et al. (2011), c-fos mRNA expression in PFC and DS showed no age differences.
“fos in PFC and DS no age differences.”
From Age-dependent Effects of Tobacco Smoke and Nicotine on Cognition and the Brain: A Systematic Review of the Human and Animal Literature Comparing Adolescents and Adults. (2023) · cites this paper as Dao et al. (2011)
The ‘Acute and Subchronic Nicotine Treatment Induces Age-dependent Neural Activation’ section reports significant age differences in basal c-fos expression in both PFC and DS. It says acute nicotine had no significant effect in those regions, which is different from saying there were no age differences. (LLM, conf=0.92)
Checked by a reasoning model — may be wrong.
Experimental — accuracy not yet measured5-HT levels in the BLA were increased in adolescent-exposed rats compared to adult-exposed rats and age-matched controls, while no age differences were found in the PFC, DS or NAc.
“5-HT levels in the BLA were increased in adolescent-exposed rats compared to adult-exposed rats and age-matched controls, whilst no age differences were found in the PFC, DS or NAc.”
From Age-dependent Effects of Tobacco Smoke and Nicotine on Cognition and the Brain: A Systematic Review of the Human and Animal Literature Comparing Adolescents and Adults. (2023) · cites this paper as Dao et al., 2011
In “Adolescent Nicotine Pretreatment Alters Monoamines in Mesolimbic Reward Circuitry” (page unavailable), the paper reports significant age differences in 5-HT content in the PFC and NAc, contrary to the claim. It reports an age-by-pretreatment interaction in the BLA, but does not state that adolescent nicotine-exposed rats had higher BLA 5-HT than both adult-exposed rats and age-matched controls. (LLM, conf=0.88)
Checked by a reasoning model — may be wrong.
Experimental — accuracy not yet measuredNo age differences in c-fos expression in the PFC or basolateral amygdala were found.
“No age differences in c-fos expression in the PFC or basolateral amygdala were found.”
From Age-dependent Effects of Tobacco Smoke and Nicotine on Cognition and the Brain: A Systematic Review of the Human and Animal Literature Comparing Adolescents and Adults. (2023) · cites this paper as Dao et al., 2011
The “Acute and Subchronic Nicotine Treatment Induces Age-dependent Neural Activation” section reports significant age differences in basal c-fos expression in the PFC and an age-dependent increase after acute nicotine in the basolateral amygdala. Although the paper reports no age difference in the basolateral amygdala response after subchronic treatment, the unqualified claim that neither region showed age differences is contrary to its findings. Page numbers were not provided in our copy. (LLM, conf=0.90)
Checked by a reasoning model — may be wrong.
Experimental — accuracy not yet measuredRepeated nicotine treatment induces elevated mesocortical dopamine release in adolescents but not adults.
“However, repeated nicotine treatment has been shown to induce elevated mesocortical dopamine release in adolescents but not adults (Counotte et al. 2009; Dao et al. 2011).”
From <scp>N</scp> icotine and the adolescent brain (2015) · cites this paper as Dao et al. 2011
In “Adolescent Nicotine Pretreatment Alters Monoamines in Mesolimbic Reward Circuitry” (page unavailable), the paper reports increased dopamine levels after nicotine pretreatment in the nucleus accumbens, but explicitly says the effect was not age specific. It reports lower prefrontal-cortex dopamine content in adolescent controls, not nicotine-induced mesocortical dopamine release in adolescents alone. (LLM, conf=0.83)
Checked by a reasoning model — may be wrong.
Experimental — accuracy not yet measuredIn Dao et al. (2011), c-fos mRNA expression in NAc shell was increased in adolescents versus adults and age-matched controls.
“c-fos in NAc shell: Adolescents ↑ vs adults and age-matched controls.”
From Age-dependent Effects of Tobacco Smoke and Nicotine on Cognition and the Brain: A Systematic Review of the Human and Animal Literature Comparing Adolescents and Adults. (2023) · cites this paper as Dao et al. (2011)
The ‘Acute and Subchronic Nicotine Treatment Induces Age-dependent Neural Activation’ section reports increased NAc-shell c-fos mRNA after nicotine treatment in adolescents, but not adults, with a significant age-by-nicotine interaction. The citing sentence omits the nicotine-treatment condition, so it could be read as claiming a general adolescent increase rather than a nicotine-induced one. Page numbers are not available in the supplied passages. (LLM, conf=0.84)
Experimental — accuracy not yet measured
Nicotine enhanced DA levels in the NAc, but this effect was not age-dependent, and no age-related differences were found in the PFC, BLA or DS.
“Nicotine enhanced DA levels in the NAc, although this effect was not age-dependent and no age-related differences were found in the PFC, BLA or DS.”
From Age-dependent Effects of Tobacco Smoke and Nicotine on Cognition and the Brain: A Systematic Review of the Human and Animal Literature Comparing Adolescents and Adults. (2023) · cites this paper as Dao et al., 2011
In “Adolescent Nicotine Pretreatment Alters Monoamines in Mesolimbic Reward Circuitry,” the paper says nicotine pretreatment increased NAc DA levels and that this effect was not age-specific. It also reports age differences in the other regions: adolescents had lower DA content in the PFC and DS and lower DAT density in the BLA. The claim’s statement that no age-related differences were found there is therefore not supported. (LLM, conf=0.90)
Experimental — accuracy not yet measuredIncreased regional SERT binding in the PFC, BLA and DS was observed in adolescent-exposed rats compared to adult-exposed and age-matched controls, but not within the NAc.
“Increased regional serotonin transporter (SERT) bind ing in the PFC, BLA and DS was also observed in adolescent-exposed rats compared to adult-exposed and age-matched controls, but not within the NAc.”
From Age-dependent Effects of Tobacco Smoke and Nicotine on Cognition and the Brain: A Systematic Review of the Human and Animal Literature Comparing Adolescents and Adults. (2023) · cites this paper as Dao et al., 2011
The Results section ('Adolescent Nicotine Pretreatment Alters Monoamines in Mesolimbic Reward Circuitry'; page unavailable) reports significant nicotine-induced SERT increases in adolescent rats in the PFC and BLA, but not in the DS on post hoc testing. Figure 6 specifies comparison with age-matched saline controls; the copy does not establish that adolescent-exposed rats had higher binding than adult-exposed rats across the claimed regions. It reports no corresponding nicotine-induced SERT increase in the NAc. (LLM, conf=0.88)
Experimental — accuracy not yet measuredNicotine exposure increased c-fos expression in the basolateral amygdala of both age groups compared to age-matched controls.
“However, nicotine expo sure did increase c-fos expression in the basolateral amygdala of both age groups compared to age-matched controls.”
From Age-dependent Effects of Tobacco Smoke and Nicotine on Cognition and the Brain: A Systematic Review of the Human and Animal Literature Comparing Adolescents and Adults. (2023) · cites this paper as Dao et al., 2011
The section “Acute and Subchronic Nicotine Treatment Induces Age-dependent Neural Activation” reports increased BLA c-fos mRNA in both adolescent and adult rats after four days of nicotine treatment. The claim omits that condition: after acute treatment, the increase was observed in adolescents but not adults. No page number is available in the supplied passages. (LLM, conf=0.86)
Experimental — accuracy not yet measuredAcross two studies, chronic nicotine exposure during early adolescence (PND28<) resulted in elevated c-fos and deltafos-B expression in the NAc when tested 24 h after last dosing.
“Across two studies, chronic nicotine exposure during early adolescence (PND28 < ) resulted in elevated c-fos (Dao et al., 2011) and deltafos-B (Alajaji et al., 2016) expression in the NAc when tested 24 h after last dosing.”
From Age-dependent Effects of Tobacco Smoke and Nicotine on Cognition and the Brain: A Systematic Review of the Human and Animal Literature Comparing Adolescents and Adults. (2023) · cites this paper as Dao et al., 2011
The ‘Acute and Subchronic Nicotine Treatment’ section reports increased c-fos mRNA in the NAc shell of adolescent rats on the fourth treatment day. But ‘In situ Hybridization’ says the animals were examined 30 minutes after the last injection, not 24 hours later. Dao et al. is cited for c-fos, not deltafos-B, in the citing sentence. (LLM, conf=0.93)
Experimental — accuracy not yet measuredVarious neurobiological changes (region-dependent changes in 5-HT levels in the BLA, increased SERT binding in the BLA, PFC and DS, greater plasticity of pyramidal neurons in the prelimbic cortex and medium spiny neurons in the NAc, greater c-fos and deltaFosB expression in the thalamus and NAc, and increases in nAChRs in the midbrain, striatum and mPFC) have previously been found to mediate the奖励
“Additionally, the region-dependent changes in 5-HT levels in the BLA (Dao et al., 2011), increased SERT binding in the BLA, PFC and DS (Dao et al., 2011), greater plasticity of pyramidal neurons in the pre limbic cortex and medium spiny neurons in the NAc (Bergstrom et al., 2008; McDonald et al., 2007), greater c-fos and deltaFosB expression in the thalamus and NAc and increases in nAChRs in the”
From Age-dependent Effects of Tobacco Smoke and Nicotine on Cognition and the Brain: A Systematic Review of the Human and Animal Literature Comparing Adolescents and Adults. (2023) · cites this paper as Dao et al., 2011
The Results section, “Adolescent Nicotine Pretreatment Alters Monoamines in Mesolimbic Reward Circuitry” (page not available), reports an age-by-pretreatment interaction for BLA 5-HT and significant nicotine-induced increases in SERT binding in adolescent rats’ BLA and PFC. The corresponding increase in the dorsal striatum (DS) was not significant in post hoc comparisons, so the claim overstates that part. The other changes in the citing sentence are attached to other citations, not Dao et al. (LLM, conf=0.91)
Experimental — accuracy not yet measuredIn adolescent-exposed rodents, changes in DA and serotonin functioning within mesolimbic brain regions were altered to a larger extent than in adults.
“For example, changes in DA and serotonin functioning within mesolimbic brain regions, known to play a role in craving, were altered to a larger extent in adolescent exposed rodents (Dao et al., 2011).”
From Age-dependent Effects of Tobacco Smoke and Nicotine on Cognition and the Brain: A Systematic Review of the Human and Animal Literature Comparing Adolescents and Adults. (2023) · cites this paper as Dao et al., 2011
The sections on monoamines in mesolimbic reward circuitry and adolescent maturation report adolescent-specific nicotine effects on serotonin markers and altered D2-like receptor responses after adolescent exposure (page numbers unavailable). But the paper says nicotine increased dopamine levels in the nucleus accumbens without an age-dependent effect, so it does not support the broad claim that both dopamine and serotonin changes in these regions were greater in adolescents than adults. (LLM, conf=0.84)
Experimental — accuracy not yet measuredNicotine-induced neuronal activation, measured by immediate early gene expression, is enhanced during adolescence in several limbic regions, including nucleus accumbens shell, basolateral amygdala, VTA, and medial prefrontal cortex.
“Nicotine-induced neuronal activation, as measured by immediate early gene expression, is also enhanced during adolescence in several limbic regions, including nucleus accumbens shell, basolateral amygdala, VTA and medial prefrontal cortex (Schochet et al., 2005; Shram et al., 2007; Dao et al., 2011).”
From Unique, long-term effects of nicotine on adolescent brain. (2020) · cites this paper as Dao et al., 2011
The ‘Acute and Subchronic Nicotine Treatment Induces Age-dependent Neural Activation’ section reports greater nicotine-induced c-fos expression in adolescent rats’ nucleus accumbens shell and basolateral amygdala. It reports no significant acute nicotine effect in the prefrontal cortex, and the supplied passages do not establish comparable immediate-early-gene activation in the VTA. Those regions may be covered by the sentence’s other citations, but Dao et al. supports only part of the list. (LLM, conf=0.90)
Experimental — accuracy not yet measuredThe long-lasting enhancement of cocaine intake after adolescent nicotine can be blocked by co-administering a serotonin 5HT1A or dopamine D2 receptor antagonist during nicotine pretreatment.
“The long-lasting enhancement of cocaine intake can be blocked by co-administration of a serotonin 5HT1A or dopamine D2 receptor antagonist during nicotine pretreatment”
From Unique, long-term effects of nicotine on adolescent brain. (2020) · cites this paper as Dao et al., 2011
The section on 5-HT1A receptors reports that an antagonist co-administered during adolescent nicotine pretreatment blocked enhanced cocaine self-administration at the initial test. The cocaine self-administration section separately shows that nicotine’s effect persisted for at least 10 days, but does not show antagonist blockade at that later time. The paper discusses a dopamine D2-like agonist, not blockade of cocaine intake by a D2 antagonist. (LLM, conf=0.88)
Experimental — accuracy not yet measuredIn Sprague Dawley rats, once-daily low-dose nicotine (0.06 mg/kg, i.v.) for four days, intended to mimic early teen smoking, enhances subsequent reinforcing effects of cocaine, methamphetamine, and alcohol in adolescents but not adults of both sexes.
“we have used a paradigm in which Sprague Dawley rats are treated once daily for four days with a low dose of nicotine (0.06 mg/kg, i.v.), intended to mimic the early phase of teen smoking, and have shown this enhances subsequent reinforcing effects of cocaine, methamphetamine and alcohol”
From Unique, long-term effects of nicotine on adolescent brain. (2020) · cites this paper as Dao et al., 2011
Split into 2 atoms — 1 confirmed, 1 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
Experimental — accuracy not yet measuredBrief pretreatment of early adolescent rats (P28-31) with a low dose of nicotine that models smoking initiation significantly increases self-administration of cocaine, ethanol, fentanyl, and methamphetamine when compared to adults.
“Brief pretreatment of early adolescent rats (postnatal days (P) 28–31) with a low dose of nicotine that models smoking initiation significantly increases self-administration of cocaine, ethanol, fentanyl, and methamphetamine when compared to adults [146–151].”
From Nicotine on the developing brain. (2023) · cites this paper as [146]
The Results section ('Nicotine Pretreatment Enhances Adolescent Acquisition of Cocaine Self-administration'; page unavailable) reports significantly increased cocaine responding after nicotine pretreatment at P28–31, but not in adults, and reports similar enhancement for methamphetamine and ethanol. The Intravenous Self-administration methods list those three drugs, not fentanyl; our copy does not support the fentanyl part of the claim. (LLM, conf=0.90)
Experimental — accuracy not yet measuredNicotine pretreatment induces serotonin release and 5HT1A receptor activation, leading to enhanced D2 receptor function in adolescents but not adults.
“This nicotine pretreatment also induces serotonin release and 5HT1A receptor activation that leads to enhanced D2 receptor function in adolescents but not adults (Dao et al. 2011).”
From <scp>N</scp> icotine and the adolescent brain (2015) · cites this paper as Dao et al. 2011
The Discussion reports that nicotine pretreatment enhanced responses to the D2-like agonist quinpirole after early-adolescent, but not adult, treatment. The Receptor Mechanisms section suggests that serotonin release and 5-HT1A receptor activation mediate the enhanced quinpirole-induced locomotion. It does not establish the full causal chain as fact or attribute the enhanced erectile response to that same 5-HT1A mechanism. (LLM, conf=0.84)
Experimental — accuracy not yet measuredBrief treatment of adolescent rats with a low dose of nicotine enhances sexual arousal.
“However, brief treatment of adolescent rats with a low dose of nicotine, equivalent to one to two cigarettes per day for 4 days, enhances acquisition of self-administration for cocaine, methamphetamine and alcohol, induces cocaine locomotor sensitization, and enhances sexual arousal (McQuown et al. 2007; McQuown et al. 2009; Dao et al. 2011; Figs 5 and 6).”
From <scp>N</scp> icotine and the adolescent brain (2015) · cites this paper as Dao et al. 2011
The Results section, “Involvement of 5-HT1A Receptors in Nicotine-Enhanced Behaviors” (page unavailable), reports that brief nicotine pretreatment enhanced quinpirole-induced penile erection in early-adolescent rats. That supports an enhanced erectile response under a specific drug challenge, but not the broader claim that nicotine enhances sexual arousal generally. (LLM, conf=0.86)
Experimental — accuracy not yet measuredIn Dao et al. (2011), c-fos mRNA expression in BLA was increased in adolescents versus age-matched controls.
“c-fos in BLA: Adolescents ↑ vs age-matched controls.”
From Age-dependent Effects of Tobacco Smoke and Nicotine on Cognition and the Brain: A Systematic Review of the Human and Animal Literature Comparing Adolescents and Adults. (2023) · cites this paper as Dao et al. (2011)
Testing 30 min after the last dosage of a four day exposure paradigm, adolescent rats showed elevated levels of c-fos expression in the NAc shell compared to adult counterparts and age-matched controls.
“Testing 30 min after the last dosage of a four day exposure paradigm, adolescent rats did show elevated levels of c-fos expression in the NAc shell compared to their adult counterparts and relative to age-matched controls (Dao et al., 2011).”
From Age-dependent Effects of Tobacco Smoke and Nicotine on Cognition and the Brain: A Systematic Review of the Human and Animal Literature Comparing Adolescents and Adults. (2023) · cites this paper as Dao et al., 2011
Nicotine exposure increased c-fos expression in the amygdala in both age groups, whilst no effects of nicotine were found on fosB expression in both age groups.
“Nicotine exposure increased c-fos expression in the amyg dala in both age groups (Dao et al., 2011; Cao et al., 2007), whilst no effects of nicotine were found on fosB expression in both age groups (Funk et al., 2016).”
From Age-dependent Effects of Tobacco Smoke and Nicotine on Cognition and the Brain: A Systematic Review of the Human and Animal Literature Comparing Adolescents and Adults. (2023) · cites this paper as Dao et al., 2011
Experimental — accuracy not yet measuredNicotine increases DA levels in the NAc regardless of age.
“Nicotine was found to increase DA levels in the NAc regardless of age (Dao et al., 2011), whilst region-dependent changes in 5-HT levels were only found after adolescent-exposure (Dao et al., 2011).”
From Age-dependent Effects of Tobacco Smoke and Nicotine on Cognition and the Brain: A Systematic Review of the Human and Animal Literature Comparing Adolescents and Adults. (2023) · cites this paper as Dao et al., 2011
Region-dependent changes in 5-HT levels were only found after adolescent exposure to nicotine.
“Nicotine was found to increase DA levels in the NAc regardless of age (Dao et al., 2011), whilst region-dependent changes in 5-HT levels were only found after adolescent-exposure (Dao et al., 2011).”
From Age-dependent Effects of Tobacco Smoke and Nicotine on Cognition and the Brain: A Systematic Review of the Human and Animal Literature Comparing Adolescents and Adults. (2023) · cites this paper as Dao et al., 2011
Serotonin systems are uniquely sensitive to nicotine during adolescence.
“Serotonin systems are also uniquely sensitive to nicotine during adolescence (Slotkin & Seidler, 2009; Bang & Commons, 2011; Dao et al., 2011).”
From Unique, long-term effects of nicotine on adolescent brain. (2020) · cites this paper as Dao et al., 2011
Experimental — accuracy not yet measuredBrief low-dose nicotine treatment during early adolescence (P28-31), but not adulthood, increases presynaptic markers of serotonin function in the forebrain.
“Brief treatment with low-dose nicotine during early adolescence (postnatal days (P) 28–31) but not adulthood, also increases presynaptic markers of serotonin function in the forebrain (Dao et al., 2011).”
From Unique, long-term effects of nicotine on adolescent brain. (2020) · cites this paper as Dao et al., 2011
Nicotine pretreatment of adolescents, but not adults, increases the subsequent reinforcing effects of cocaine.
“nicotine pretreatment of adolescents, but not adults, increases the subsequent reinforcing effects of cocaine”
From Unique, long-term effects of nicotine on adolescent brain. (2020) · cites this paper as Dao et al., 2011
Adolescent nicotine treatment also increases methamphetamine and ethanol intake.
“A similar increase in methamphetamine and ethanol intake following adolescent nicotine treatment has also been seen”
From Unique, long-term effects of nicotine on adolescent brain. (2020) · cites this paper as Dao et al., 2011
These lasting age-specific alterations result in increased quinpirole-induced locomotion and acquisition of cocaine self-administration.
“These lasting age-specific alterations result in increased quinpirole-induced locomotion and acquisition of cocaine self-administration (McQuown et al. 2007; Dao et al. 2011).”
From <scp>N</scp> icotine and the adolescent brain (2015) · cites this paper as Dao et al. 2011
Very few age differences have been reported in the effect of chronic nicotine on presynaptic markers of dopaminergic function.
“Although striatal dopamine transporters have been reported to be upregulated by nicotine in adolescents but not adults, very few age differences have been reported in the effect of chronic nicotine on presynaptic markers of dopaminergic function (Collins et al. 2004; Dao et al. 2011).”
From <scp>N</scp> icotine and the adolescent brain (2015) · cites this paper as Dao et al. 2011
Current data indicate that nicotine disrupts normative limbic development and primes behavioral susceptibility to drugs of abuse.
“Current data indicate that nicotine disrupts normative limbic development and primes behavioral susceptibility to drugs of abuse (McQuown et al. 2009; Dao et al. 2011).”
From <scp>N</scp> icotine and the adolescent brain (2015) · cites this paper as Dao et al. 2011
Brief treatment of adolescent rats with a low dose of nicotine induces cocaine locomotor sensitization.
“However, brief treatment of adolescent rats with a low dose of nicotine, equivalent to one to two cigarettes per day for 4 days, enhances acquisition of self-administration for cocaine, methamphetamine and alcohol, induces cocaine locomotor sensitization, and enhances sexual arousal (McQuown et al. 2007; McQuown et al. 2009; Dao et al. 2011; Figs 5 and 6).”
From <scp>N</scp> icotine and the adolescent brain (2015) · cites this paper as Dao et al. 2011
Brief treatment of adolescent rats with a low dose of nicotine, equivalent to one to two cigarettes per day for 4 days, enhances acquisition of self-administration for cocaine.
“However, brief treatment of adolescent rats with a low dose of nicotine, equivalent to one to two cigarettes per day for 4 days, enhances acquisition of self-administration for cocaine, methamphetamine and alcohol, induces cocaine locomotor sensitization, and enhances sexual arousal (McQuown et al. 2007; McQuown et al. 2009; Dao et al. 2011; Figs 5 and 6).”
From <scp>N</scp> icotine and the adolescent brain (2015) · cites this paper as Dao et al. 2011
Brief treatment of adolescent rats with a low dose of nicotine enhances acquisition of self-administration for alcohol.
“However, brief treatment of adolescent rats with a low dose of nicotine, equivalent to one to two cigarettes per day for 4 days, enhances acquisition of self-administration for cocaine, methamphetamine and alcohol, induces cocaine locomotor sensitization, and enhances sexual arousal (McQuown et al. 2007; McQuown et al. 2009; Dao et al. 2011; Figs 5 and 6).”
From <scp>N</scp> icotine and the adolescent brain (2015) · cites this paper as Dao et al. 2011
The early adolescent period is uniquely sensitive to the effects of nicotine as compared to late adolescence and adulthood.
“Another key feature of the adolescent effects of nicotine, as seen in animal studies, is the unique sensitivity of the early adolescent period as compared to late adolescence and adulthood (Laviola et al. 2001; Cao et al. 2010; Dao et al. 2011; Kawai et al. 2011).”
From <scp>N</scp> icotine and the adolescent brain (2015) · cites this paper as Dao et al. 2011
Brief treatment of adolescent rats with a low dose of nicotine enhances acquisition of self-administration for methamphetamine.
“However, brief treatment of adolescent rats with a low dose of nicotine, equivalent to one to two cigarettes per day for 4 days, enhances acquisition of self-administration for cocaine, methamphetamine and alcohol, induces cocaine locomotor sensitization, and enhances sexual arousal (McQuown et al. 2007; McQuown et al. 2009; Dao et al. 2011; Figs 5 and 6).”
From <scp>N</scp> icotine and the adolescent brain (2015) · cites this paper as Dao et al. 2011
Animal studies point to the unique sensitivity of the adolescent serotonin system to regulation by nicotine.
“Although dopamine is clearly involved, animal studies also point to the unique sensitivity of the adolescent serotonin system to regulation by nicotine (Shearman et al. 2008; Bang & Commons, 2011; Dao et al. 2011).”
From <scp>N</scp> icotine and the adolescent brain (2015) · cites this paper as Dao et al. 2011
Striatal dopamine transporters are upregulated by nicotine in adolescents but not adults.
“Although striatal dopamine transporters have been reported to be upregulated by nicotine in adolescents but not adults, very few age differences have been reported in the effect of chronic nicotine on presynaptic markers of dopaminergic function (Collins et al. 2004; Dao et al. 2011).”
From <scp>N</scp> icotine and the adolescent brain (2015) · cites this paper as Dao et al. 2011
The section “Adolescent Nicotine Pretreatment Alters Monoamines in Mesolimbic Reward Circuitry” (page unavailable) reports lower baseline DAT density in the basolateral amygdala of adolescents and a nicotine-induced increase in nucleus accumbens dopamine that was not age-specific. It does not report nicotine upregulating striatal DAT in adolescents but not adults. I searched for age-specific nicotine effects on DAT binding in the dorsal striatum and nucleus accumbens. (LLM, conf=0.73)
Experimental — accuracy not yet measured
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<scp>N</scp> icotine and the adolescent brain
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Self-citationUnique, long-term effects of nicotine on adolescent brain.
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“), intended to mimic the early phase of teen smoking, and have shown this enhances subsequent reinforcing effects of cocaine, methamphetamine and alcohol (McQown et al., 2007; Dao et al., 2011) in adolescents but not adults of both sexes.”
BackgroundResultInfluentialSelf-citationNicotine Gateway Effects on Adolescent Substance Use
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Nicotine on the developing brain.
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Self-citationAdolescent neurodevelopment and substance use: receptor expression and behavioral consequences
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Microglial activation increases cocaine self-administration following adolescent nicotine exposure
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Unique effects of nicotine across the lifespan
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Self-citationEarly adolescent nicotine exposure affects later-life cocaine reward in mice
Alajaji, M., Lazenka, M. F., Kota, D., Wise, L. E., Younis, R. M., Carroll, F. I., Levine, A., Selley, D. E., Sim-Selley, L. J., & Damaj, M. I. (2016) · Neuropharmacology · doi:10.1016/j.neuropharm.2016.01.032 · Cited by 39 · see citing works
Nicotine increases alcohol intake in adolescent male rats
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Age-dependent alterations in reward-seeking behavior after brief nicotine exposure
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Cadoni, C., De Felice, M., Corongiu, S., Dessì, C., Espa, E., Melis, M., & Fenu, S. (2020) · Addiction Biology · doi:10.1111/adb.12803 · Cited by 10 · see citing works
- Authors
- Dao, J. M., McQuown, S. C., Loughlin, S. E., Belluzzi, J. D., & Leslie, F. M.
- Affiliations
- University of California, Irvine (US)
- Corresponding author
- Dao, Jasmin M
- ORCID
- Leslie, Frances M
- Venue
- Neuropsychopharmacology
- Published
- 2011-03-16
- Volume
- 36
- Issue
- 7
- Pages
- 1319-1331
- ISSN
- 0893-133X (ISSN-L)
- 1740-634X
- PMC
- PMC3096821
- OpenAlex
- W2015725514
- Cited by
- 79
- References
- 87
- Citations by year
- 2026: 2 · 2025: 4 · 2024: 8 · 2023: 6 · 2022: 2 · 2021: 3 · 2020: 12 · 2019: 7 · 2018: 2 · 2017: 3 · 2016: 7 · 2015: 6 · 2014: 5 · 2013: 6 · 2012: 4
- FWCI
- 3.71
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Neuropsychopharmacology (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute on Drug Abuse (DA 19138, R01DA019138)
- Topics
- Health Sciences › Medicine › Physiology › Smoking Behavior and Cessation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Nicotinic Acetylcholine Receptors Study
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Keywords
- adolescent nicotine exposure, 5-HT1A receptor, cocaine self-administration, penile erection, nucleus accumbens shell, basolateral amygdala, prefrontal cortex, Fos expression, serotonin, WAY-100635, 8-OH-DPAT, adolescent smoking, adolescent rats
- MeSH terms
- Age Factors, Analysis of Variance, Animals, Animals, Newborn, Autoradiography, Catecholamines, Drug Administration Schedule, Drug Interactions, Gene Expression Regulation, Limbic System, Locomotion, Male, Nicotine, Piperazines, Protein Binding, Reward, RNA, Messenger, Self Administration, Time Factors, 3,4-Dihydroxyphenylacetic Acid, Rats, Sprague-Dawley, Serotonin Receptor Agonists, 8-Hydroxy-2-(di-n-propylamino)tetralin, Dopamine Agonists, Nicotinic Agonists, Quinpirole, Receptor, Serotonin, 5-HT1A, Serotonin Plasma Membrane Transport Proteins, Rats
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