Testing a Gateway to Addiction: Behavioral and Neurophysiological Effects of Early Exposure to Saccharin, Caffeine, and Nicotine in Adolescent Mice

Open Access
Latten, Bethany J
Area of Honors:
Biobehavioral Health
Bachelor of Science
Document Type:
Thesis Supervisors:
  • David John Vandenbergh, Thesis Supervisor
  • Joseph Peter Gyekis, Faculty Reader
  • David John Vandenbergh, Honors Advisor
  • Addiction
  • Nicotine
  • Adolescence
  • Mice
For my honors thesis research project, I tested one facet of the gateway hypothesis of addiction to explore how nicotine consumption is altered in adolescent mice after exposure to more commonly available appetitive substances. The gateway hypothesis has been the subject of much criticism since it first became popularized several decades ago. While it was once thought that marijuana was the crucial gateway substance that compelled marijuana users to use other illicit drugs, now researchers have turned their attention to its legal yet significantly more addictive predecessor in the gateway pathway, nicotine. The idea for studying the gateway hypothesis originated from considering how humans often progress from licit to illicit substance use. Children are continuously exposed to various substances that they learn to associate with reward. For example, sugar and caffeine containing foods and beverages lead to a pleasurable, rewarding taste (Temple, 2009). Although children are often exposed to low levels of nicotine through second-hand smoke, either in their homes or on city streets, it is unclear if this level of exposure is associated with behavioral changes. As described in this chapter, I used an animal model to study whether exposure to appetitive substances and low levels of nicotine in young mice increased nicotine consumption later in life. While the results I obtained did not demonstrate a significant association between exposure to low levels of nicotine during early adolescence and greater nicotine consumption later in life, the results do suggest that further studies should be performed to examine whether the effects of exposure to low levels of nicotine is associated with greater nicotine consumption when studied over a longer period of time. The second component of my thesis consisted of molecular analysis of gene expression in a representative sample of the mice’s brains. Addiction has long been implicated as a form of learning (Wikler, 1961), and recent work by Cao et al. has associated early exposure to nicotine in rodents with myelin-related gene expression changes, one of many findings that suggest the presence of a molecular component in the addiction-learning process (2013). Real-Time PCR was performed to determine if the gateway pathway described above affected expression of Mobp: Myelin-associated oligodendrocyte basic protein. While the expected trend of Mobp upregulation was observed, the results failed to reach significance. Moreover, the amount of nicotine consumed during the exposure experiment was not correlated with the amount of Mobp upregulation.