Hartless, Christopher B. The Effects of Dual Ethanol and Nicotine Exposure on Hippocampal Neurogenesis. 2015. Radford University, Thesis. Radford University Scholars' Repository.
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Abstract
Binge alcohol consumption is one of the most prevalent, yet problematic, patterns of substance abuse behavior in this country. Further, individuals who binge drink account for about half of all tobacco consumption in the United States. Both ethanol and nicotine have been shown to impair adult hippocampal integrity; however, little is known about the combined influence this may have over hippocampal neurogenesis. The aim of the current study was to confirm the impairing effects nicotine and ethanol have been shown to have on hippocampal cell proliferation in adolescent and adult rats, and to further extend previous findings by identifying the interactive effects nicotine and ethanol may have on proliferation within the dentate gyrus. Adolescent (N = 42) and adult (N = 37) male Sprague-Dawley rats were administered nicotine (0.3 mg/kg in 0.9% saline, subcutaneously) or saline alone every 8 hours for 10 days. On the last 4 days of nicotine exposure, an ethanol (25% w/v in Vanilla Ensure® Plus, adult: 9.25 and adolescent: 11.87 g/kg/day, oral gavage) or isocaloric dextrose diet was administered following a modified Majchrowicz procedure. Animals were euthanized following the last dose in the treatment schedule. Brains were extracted, and coronal tissue sections were obtained. Ki67 immunohistochemistry was used to quantify cell proliferation in the sub-granular zone of the dentate gyrus within the hippocampus. As hypothesized, individual exposure to chronic nicotine and binge levels of ethanol produced deficits in cell proliferation for both adolescent and adult treatment groups. Further, an additive effect was observed in the adult subjects following combined alcohol and nicotine treatment. However, this effect was not observed in adolescent subjects. When comparing adolescents to adults and adults exposed to ethanol or nicotine alone, adolescent proliferation appears more impaired than in their adult counterparts. Lastly, non-injected controls provided evidence to suggest that the method of administration of ethanol may also impair cell proliferation. In conclusion, there is sufficient evidence to suggest that nicotine and ethanol both produce impairments in hippocampal proliferation. Future research should focus on eliminating a potential confound produced by the route of administration. Once addressing this issue, further focus can be employed to understand better the relationship between ethanol- and nicotine-induced impairments in cell proliferation and how these affects may promote memory alterations as shown in the Morris water maze and radial arm maze paradigms.
| Item Type: | Thesis |
|---|---|
| Uncontrolled Keywords: | Ethanol, nicotine, adolescence, hippocampus, coabuse |
| Subjects: | B Philosophy. Psychology. Religion > BF Psychology Q Science > Q Science (General) Q Science > QM Human anatomy |
| Divisions: | Radford University > College of Humanities and Behavioral Sciences > Department of Psychology |
| Date Deposited: | 09 May 2016 12:47 |
| Last Modified: | 20 Apr 2023 18:10 |
| URI: | http://wagner.radford.edu/id/eprint/222 |
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