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Nicotine exposure during adolescence induces a depression-like state in adulthood.

Iñiguez SD, Warren BL, Parise EM, Alcantara LF, Schuh B, Maffeo ML, Manojlovic Z, Bolaños-Guzmán CA - Neuropsychopharmacology (2008)

Bottom Line: It has been suggested that afflicted individuals smoke to manage mood, however, there is evidence indicating that tobacco consumption can induce negative mood.We further demonstrate that these deficits can be normalized by subsequent nicotine (0.32 mg/kg) or antidepressant (ie fluoxetine or bupropion; 10 mg/kg) treatment in adulthood.These data suggest that adolescent exposure to nicotine results in a negative emotional state rendering the organism significantly more vulnerable to the adverse effects of stress.

View Article: PubMed Central - PubMed

Affiliation: Program in Neuroscience, Department of Psychology, Florida State University, Tallahassee, FL 32306-4301, USA.

ABSTRACT
There is a strong link between tobacco consumption and mood disorders. It has been suggested that afflicted individuals smoke to manage mood, however, there is evidence indicating that tobacco consumption can induce negative mood. This study was designed to investigate whether nicotine exposure during adolescence influences emotionality/behavioral functioning later in life. Adolescent (postnatal days, PD 30-44) male rats were treated with twice-daily injections of nicotine (0, 0.16, 0.32, or 0.64 mg/kg) for 15 consecutive days, and their behavioral reactivity to various behavioral paradigms (the elevated plus maze (EPM), sucrose preference, locomotor activity in the open field, and forced swim test (FST) was assessed 24 h (short term) or 1-month (long term) after exposure. Separate groups of adult rats received nicotine (0.32 mg/kg) to control for age-dependent effects. We report that nicotine exposure during adolescence-but not adulthood-leads to a depression-like state manifested in decreased sensitivity to natural reward (sucrose), and enhanced sensitivity to stress- (FST) and anxiety-eliciting situations (EPM) later in life. Our data show that behavioral dysregulation can emerge 1 week after drug cessation, and that a single day of nicotine exposure during adolescence can be sufficient to precipitate a depression-like state in adulthood. We further demonstrate that these deficits can be normalized by subsequent nicotine (0.32 mg/kg) or antidepressant (ie fluoxetine or bupropion; 10 mg/kg) treatment in adulthood. These data suggest that adolescent exposure to nicotine results in a negative emotional state rendering the organism significantly more vulnerable to the adverse effects of stress. Within this context, our findings, together with others indicating that nicotine exposure during adolescence enhances risk for addiction later in life, could serve as a potential model of comorbidity.

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Effects of NIC on weight gain (A–B). (A) Adolescents (n = 32): body weight increased across days regardless of condition, and NIC treatment resulted in significantly lower weight gain when compared to control rats. *Significantly different from NIC-treated rats (p < 0.05). (B) Adults (n = 14): no difference in body weight after NIC (0.32 mg/kg) was apparent. Data are presented average weight gain across days and drug treatment (mean ± SEM, in g).
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Figure 1: Effects of NIC on weight gain (A–B). (A) Adolescents (n = 32): body weight increased across days regardless of condition, and NIC treatment resulted in significantly lower weight gain when compared to control rats. *Significantly different from NIC-treated rats (p < 0.05). (B) Adults (n = 14): no difference in body weight after NIC (0.32 mg/kg) was apparent. Data are presented average weight gain across days and drug treatment (mean ± SEM, in g).

Mentions: Figure 1A shows the effects of chronic VEH or NIC (0.16, 0.32, 0.64 mg/kg) treatment on weight-gain in adolescent rats. Repeated measures ANOVA (for day of injection) revealed that NIC treatment significantly influenced body weight across days (within subject main effect: F(14,420) = 258.03, p < 0.0001) and drug treatment (between subject main effect: F(3,420)= 50.47, p < 0.001). Although body-weight increased with age across all groups, NIC rats displayed significantly lower weights when compared to controls (p < 0.05) as of the fourth day of treatment (n = 8 per group). Overall, body weight between VEH- and NIC-treated groups did not differ at the time of behavioral testing in adulthood. Data presented in the inset of figure 1A are representative of rats treated with 0.32 mg/kg NIC during adolescence, and tested for sucrose preference in adulthood. As can be seen in figure 1B, NIC (0.32 mg/kg) or VEH treatment did not affect weight-gain in adult rats (n = 7 per condition).


Nicotine exposure during adolescence induces a depression-like state in adulthood.

Iñiguez SD, Warren BL, Parise EM, Alcantara LF, Schuh B, Maffeo ML, Manojlovic Z, Bolaños-Guzmán CA - Neuropsychopharmacology (2008)

Effects of NIC on weight gain (A–B). (A) Adolescents (n = 32): body weight increased across days regardless of condition, and NIC treatment resulted in significantly lower weight gain when compared to control rats. *Significantly different from NIC-treated rats (p < 0.05). (B) Adults (n = 14): no difference in body weight after NIC (0.32 mg/kg) was apparent. Data are presented average weight gain across days and drug treatment (mean ± SEM, in g).
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2692426&req=5

Figure 1: Effects of NIC on weight gain (A–B). (A) Adolescents (n = 32): body weight increased across days regardless of condition, and NIC treatment resulted in significantly lower weight gain when compared to control rats. *Significantly different from NIC-treated rats (p < 0.05). (B) Adults (n = 14): no difference in body weight after NIC (0.32 mg/kg) was apparent. Data are presented average weight gain across days and drug treatment (mean ± SEM, in g).
Mentions: Figure 1A shows the effects of chronic VEH or NIC (0.16, 0.32, 0.64 mg/kg) treatment on weight-gain in adolescent rats. Repeated measures ANOVA (for day of injection) revealed that NIC treatment significantly influenced body weight across days (within subject main effect: F(14,420) = 258.03, p < 0.0001) and drug treatment (between subject main effect: F(3,420)= 50.47, p < 0.001). Although body-weight increased with age across all groups, NIC rats displayed significantly lower weights when compared to controls (p < 0.05) as of the fourth day of treatment (n = 8 per group). Overall, body weight between VEH- and NIC-treated groups did not differ at the time of behavioral testing in adulthood. Data presented in the inset of figure 1A are representative of rats treated with 0.32 mg/kg NIC during adolescence, and tested for sucrose preference in adulthood. As can be seen in figure 1B, NIC (0.32 mg/kg) or VEH treatment did not affect weight-gain in adult rats (n = 7 per condition).

Bottom Line: It has been suggested that afflicted individuals smoke to manage mood, however, there is evidence indicating that tobacco consumption can induce negative mood.We further demonstrate that these deficits can be normalized by subsequent nicotine (0.32 mg/kg) or antidepressant (ie fluoxetine or bupropion; 10 mg/kg) treatment in adulthood.These data suggest that adolescent exposure to nicotine results in a negative emotional state rendering the organism significantly more vulnerable to the adverse effects of stress.

View Article: PubMed Central - PubMed

Affiliation: Program in Neuroscience, Department of Psychology, Florida State University, Tallahassee, FL 32306-4301, USA.

ABSTRACT
There is a strong link between tobacco consumption and mood disorders. It has been suggested that afflicted individuals smoke to manage mood, however, there is evidence indicating that tobacco consumption can induce negative mood. This study was designed to investigate whether nicotine exposure during adolescence influences emotionality/behavioral functioning later in life. Adolescent (postnatal days, PD 30-44) male rats were treated with twice-daily injections of nicotine (0, 0.16, 0.32, or 0.64 mg/kg) for 15 consecutive days, and their behavioral reactivity to various behavioral paradigms (the elevated plus maze (EPM), sucrose preference, locomotor activity in the open field, and forced swim test (FST) was assessed 24 h (short term) or 1-month (long term) after exposure. Separate groups of adult rats received nicotine (0.32 mg/kg) to control for age-dependent effects. We report that nicotine exposure during adolescence-but not adulthood-leads to a depression-like state manifested in decreased sensitivity to natural reward (sucrose), and enhanced sensitivity to stress- (FST) and anxiety-eliciting situations (EPM) later in life. Our data show that behavioral dysregulation can emerge 1 week after drug cessation, and that a single day of nicotine exposure during adolescence can be sufficient to precipitate a depression-like state in adulthood. We further demonstrate that these deficits can be normalized by subsequent nicotine (0.32 mg/kg) or antidepressant (ie fluoxetine or bupropion; 10 mg/kg) treatment in adulthood. These data suggest that adolescent exposure to nicotine results in a negative emotional state rendering the organism significantly more vulnerable to the adverse effects of stress. Within this context, our findings, together with others indicating that nicotine exposure during adolescence enhances risk for addiction later in life, could serve as a potential model of comorbidity.

Show MeSH
Related in: MedlinePlus