Undergraduate Honors Theses

Thesis Defended

Spring 2011

Document Type

Thesis

First Advisor

Jerry Stitzel

Abstract

Nicotine is a widely popular addictive drug that alters neural circuits in the brain. The resulting neuronal plasticity is varied by the inherent circadian rhythm. During the circadian rhythm, high levels of melatonin are present in the dark phase and low levels in the light phase. Two immediate early genes, Activity-regulated cytoskeleton (Arc) and Early growth response 1 (Egr1), were used as markers to analyze the effects of nicotine-induced plasticity in the light and dark phases. The results showed lower levels of nicotine-induced neuronal plasticity (both Arc and Egr1 present in lower levels) in dark nicotine groups than in light nicotine groups. This is because nicotine-induced Arc and Egr1 levels are suppressed in the presence of melatonin. Melatonin inhibits long term potentiation (LTP), which is an essential mechanism for neuronal plasticity (Wang et al, 2005). Hence the circadian rhythm does affect nicotine-induced neuronal plasticity by suppressing the effects of nicotine in the dark.

Share

COinS