The effects of chronic ethanol consumption during gestation on the development of layer V pyramidal cells was studied quantitatively in the somatosensory cerebral cortex of the newborn guinea-pig. The spread of the basilar dendritic arborizations and counts of dendritic spines on the apical dendrite of neurons that had been processed with the rapid Golgi method were compared with those found in age-matched controls receiving an isocaloric diet without alcohol. There were significant differences in the number of primary basilar dendrites (P less than 0.05) and dendritic ramifications at a distance of 25 micron from the soma (P less than 0.01) between the alcohol-exposed and control animals. There also were significant differences in the number of dendritic spines on the apical dendrite (P less than 0.001). This experimental model further illustrates developmental anomalies in the cerebral cortex following prenatal ethanol exposure.
Introduction Traditional cigarette use influences cost-benefit decision making by promoting impulsive choice. However, the impact of exposure via electronic nicotine delivery systems on impulsive choice remains unclear. Hence, the present study examined the short- and long-term effects of nicotine vapor on impulsive choice. Methods Twenty-four adult male rats were trained in the delay discounting task, to choose between small, immediate food rewards or large, delayed food rewards. After 24 days of training in the task, rats were exposed to vapor containing either 0, 12, or 24 mg/mL of nicotine, for ten days. To validate inhalation of nicotine vapor, serum cotinine levels were analyzed on exposure days 1, 5, and 10 using enzyme-linked immunosorbent assay (ELISA). Following vapor exposure, rats were retrained in the discounting task until rats displayed stable responding, and the effects of nicotine vapor on choice preference were assessed. Results Rats exposed to 12 and 24 mg/mL nicotine vapor displayed higher serum cotinine levels than control rats exposed to 0 mg/mL vapor. There were no differences in impulsive choice between any vapor exposure groups when tested 15 days after exposure, across 6 days of stable responding, suggesting that nicotine vapor does not have long lasting effects on impulsive choice. Interestingly, a subsequent nicotine vapor challenge revealed short-term increases in impulsive choice immediately following a single exposure to 24 mg/mL nicotine vapor, relative to choice preference immediately following exposure to 0 mg/mL vapor. Conclusions These results suggest that exposure to nicotine vapor causes immediate, short-term increases in impulsive choice. Implications E-cigarette use is increasing at an alarming rate, particularly among adolescents and young adults. This is concerning given the lack of research into the effects of nicotine vapor exposure on the brain and behavior. The present study describes a viable rodent model of human e-cigarette use and suggest that exposure to nicotine vapor produces short-term increases in impulsive choice.
While the cognitive enhancing effects of nicotine use have been well documented, it has also been shown to impair decision making. The goal of this study was to determine if exposure to nicotine vapor increases risky decision making. The study also aims to investigate possible long-term effects of nicotine vapor exposure on the expression of genes coding for cholinergic and dopaminergic receptors in brain. Thirty-two adult male Sprague Dawley rats were exposed to 24 mg/mL nicotine vapor or vehicle control, immediately followed by testing in the probability discounting task for 10 consecutive days. Fifty-four days after the 10-day vapor exposure, animals were sacrificed and expression of genes coding for the α4 and β2 cholinergic receptor subunits, and dopamine D1 and D2 receptors, were analyzed using RT-PCR. Exposure to nicotine vapor caused an immediate and transient increase in risky choice. Analyses of gene expression identified significant reductions in CHRNB2 and DRD1 in the nucleus accumbens core and CHRNB2 and DRD2 in the medial prefrontal cortex of rats previously exposed to nicotine vapor, relative to vehicle controls. Results provide data on the negative cognitive effects of nicotine vapor exposure and identify cholinergic and dopaminergic mechanisms that may affected with repeated use.
The goal of our laboratory is to study the mechanisms that promote nicotine use, particularly in vulnerable populations. To more closely mimic human use patterns, the present study employed nicotine vapor methods involving passive exposure for 14 days in adolescent and adult female and male rats. Age and sex differences in approach behavior (nosepokes) were assessed in a port that delivered nicotine plumes on Day 1 and 14 of our exposure regimen. Controls received ambient air in exposure chambers. After the final session, rats received a nicotinic receptor antagonist to precipitate withdrawal. Then, physical signs, anxiety‐like behavior, and plasma levels of cotinine (a nicotine metabolite) were assessed. Over time, females displayed a larger increase in approach behavior to the nicotine port than males, an effect that was larger in adolescents. Nosepoke responses in adolescent females were correlated with anxiety‐like behavior, but not physical signs of withdrawal. Adolescents gained more weight than adults regardless of treatment, and the weight gain was larger in male adolescents. Female adolescents also displayed the highest levels of cotinine than all other groups. These findings suggest that nicotine vapor produces greater motivational effects in adolescent females as compared to their adult and male counterparts.
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