Steven Youngentob, PhD

Senior Vice Chancellor of Research

Professor
Department of Anatomy and Neurobiology
The University of Tennessee
Health Science Center 

The University of Tennessee Health Science Center
Office of Research
910 Madison, Suite 608
Memphis, TN 38163
Phone: (901) 448-1278
Fax: (901) 448-7133
Email: Steven L. Youngentob

Education

  • PhD Institution: State of New York, Upstate Medical Center, Department of Physiology

Research Interests

In Utero Alcohol Exposure, Chemosensory Fetal Programming and Adolescent Drug Preference

Human clinical studies demonstrate a highly predictive relationship between alcohol exposure during fetal development and the probability of later alcohol abuse during the already “at risk” age of adolescence.  There is also an inverse association between the age at which an individual first experiences alcohol and the likelihood of continued abuse.  Yet, the mechanism(s) underlying this progressive pattern of alcohol use and abuse are poorly understood.  How does fetal exposure alter adolescent alcohol acceptability?  How does re-exposure to the drug during adolescence increase adult acceptance?  The senses of smell, taste and oral irritation, which integrate to give us our perception of flavor, are highly plastic throughout the lifespan, including fetal development.  Further, prenatal and postnatal experiences with salient chemosensory stimuli can alter subsequent behavioral responses to the exposure stimulus.  Why is this important? - Because the flavor attributes of alcohol are known to be important determinants of acceptance and intake behavior.

 As a consequence, work in the lab focuses on the hypothesis that fetal alcohol exposure induces developmental changes in the neural systems involved in the preference for alcohol odor and the acceptability of alcohol’s flavor.  This, in turn, contributes to the risk of initial ingestion and continued adolescent abuse.  Further, adolescent experience with the drug augments the fetal effect and perpetuates the alcohol-induced changes into adulthood.  To date, our behavioral studies using a rodent model have shown that fetal exposure increases adolescent alcohol avidity by, in part, making it taste and smell better (that is, a decreased aversion to alcohol’s bitter and oral irritation qualities, as well as its odor).  In addition, alcohol re-exposure during adolescence augments the fetal effect and is critical for perpetuating it into adulthood.

 Applying behavioral, genomic, proteomic and neurophysiologic methods, the current objectives of the lab are to understand the mechanisms by which maternal alcohol use can be transferred to offspring, and via which, the adolescent system is primed to have the effects of fetal exposure augmented and preserved into adulthood.  Toward this end, recent new data has from the lab has shown that the expression of olfactory bulb genes involved in, for example, synaptic transmission and odor-mediated plasticity are altered in adolescent animals exposed to fetal alcohol.  Further, in accordance with our published taste-mediated behavioral findings, fetal alcohol exposure decreases the expression of bitter and oral irritation receptor genes fundamental to alcohol flavor perception in adolescent rats.

Representative Publications