Undergraduate Honors Theses

Thesis Defended

Spring 2018

Document Type


Type of Thesis

Departmental Honors


Integrative Physiology

First Advisor

Jerry Stitzel, Ph.D.

Second Advisor

Hunter Mathews, Predoctoral Trainee

Creative Commons License

Creative Commons Attribution 4.0 License
This work is licensed under a Creative Commons Attribution 4.0 License.


NREM and REM sleep have shown an exceptional importance in controlling various cognitive functions (Brown et al, 2012), and disruption of such sleep states can cause mental and physical impairments (Christie et al, 2008). Disruptions in sleep stages (Wakefulness, REM, NREM) can be identified via EEG recordings in mice without much interference (Mckenna et al, 2008). Circadian Rhythm, hormonal markers, and stress all affect the duration, intensity and timing of these sleep stages (Brown et al, 2004; Veasey et al 2004; Christie et al, 2008). One cohort of mice (n=7) underwent a baseline condition (BL), a nicotine administration condition (Nicotine day 8 or N8), and a withdrawal condition (Withdrawal day one, or WD1) to see nicotine/withdrawals effect on sleep. Data was collected through EEG recordings of both muscle tone and brain activity. A Corticosterone immunoassay with a separate cohort was used to assess levels of corticosterone stress response to nicotine/withdrawal. Results: Nicotine withdrawal increased sleep latency related to baseline. Wake percentage as well as Wake Bout Duration (average length of Wake stages) were increased in withdrawal condition, and overall sleep percentage went down in withdrawal, driven by a decrease in NREM percentage. Total Stage Shifts as well as Sleep Stage Shifts decreased in withdrawal condition. REM Bout Duration also decreased during withdrawal condition. We also found that corticosterone levels did not alter significantly in either the withdrawal or nicotine condition. Mice showed no difference in any measured sleep variables in the nicotine condition compared to baseline.