Rachel Klausner

 Rachel Klausner
Mentor: Dr. Adriaan Bruijnzeel
College of Medicine
 
"Working in Dr. Bruijnzeel’s lab has given me opportunity to investigate the biochemical pathways of nicotine addiction and withdrawal from many different angles, and be involved in a project long term. Becoming involved in research has opened up many opportunities, not only the University Scholars Program but also presenting at the Florida Undergraduate Research Conference and getting to work with new technology such as the 11T MRI. I hope to continue learning about neuroscience and addiction medicine by working in Dr. Bruijnzeel’s lab, specifically as it applies to the potential clinical application of drug treatments for nicotine addiction."
 

Major

Biochemistry and Nutrition

Minor

N/A

Research Interests

  • Neuroscience
  • Biochemistry
  • Addiction Medicine

Academic Awards

  • CLAS Dean's Office Anderson Scholarship
  • Anderson Scholar with Highest Distinction
  • Thomas J. Watson Memorial Scholarship
  • AT&T Foundation Scholarship

Organizations

  • Global Medical Training
  • OHLPA P3 Pre-Health Peer Mentoring Program
  • UF Chemistry Club

Volunteer

  • Shands Hospital
  • Tampa General Hospital
  • UF Chemistry Club Outreach Program

Hobbies and Interests

  • Reading
  • Volleyball
  • Exercising

Research Description

Effect of AAV2 shRNA-Mediated Knockdown of the CRF1 receptor in the Central Nucleus of the Amygdala on Nicotine Withdrawal-induced Negative Mood States
Extensive evidence indicates that brain corticotropin releasing factor (CRF) plays a critical role in depression, anxiety, and drug addiction. The preliminary work in our lab has demonstrated that overexpression of CRF in the central nucleus of the amygdale (CeA), an important brain area involved in mood modulation, decreased the negative mood state associated with nicotine withdrawal by desensitizing its receptors. Based on these results, we hypothesize that the knockdown of the CRF1 receptor (CRF1R) in the CeA will have a similar effect. Thus, the present study will investigate the effect of knockdown of the CRF1R in the CeA on the dysphoria associated with nicotine withdrawal via injection of the AAV2-shRNA vector, which specifically targets the CRF1R. The effects of the CRF1R knockdown on negative mood state will be evaluated through intracranial self-stimulation (ICSS) procedure. The proposed experiment will further the understanding of which brain areas, neuropeptides and receptors are responsible for the negative mood state associated with nicotine withdrawal. Ultimately, this could lead to new targets for the development of treatments for tobacco addiction, by reducing the negative mood states associated with tobacco smoking cessation.