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Metin Akay

The Effects of Nicotine Exposure on the Complexity and the Genetic Patterns of Dopamine Neurons in VTA
 
Metin Akay
 
Founding Chair, John S Dunn Endowed Chair Professor, Department of Biomedical Engineering, Cullen College of Engineering, University of Houston, Houston, TX, USA

Abstract

Nicotine, the biologically active substance of tobacco, has been shown to increase the ventral tegmental area (VTA) dopaminergic (DA) neuron firing rate, bursting, and enhancement of dopamine release. The previous studies have shown that most of the VTA DA neurons recorded responded to acute nicotine injection immediately. Both firing rate and bursting were increased in these neurons. However, because of the complex neuronal networks in the VTA, the mechanism by which nicotine affects VTA DA neurons firing is still not clearly understood. We believe that the further studies at both the molecular and cellular levels with multi-scale modeling approach are necessary to shed lights on the nicotine addiction.
Our results have shown that the local field potentials corresponding to the neurons located in the PIF region of the VTA have ApEn values significantly higher (p = 2x10-4) in the maternal nicotine cases when compared to the saline. Therefore, we speculate that the dopamine neurons located in the PIF sub-region of the VAT are very likely involved with the nicotine addiction.
In our recent study, we attempted to explore the effects of cigarette smoking on the genetic patterns in the substantia nigra (SN) and the VTA. A few significant differentially expressed genes between the SN and the VTA from nicotine treated Sprague - Dawley (SD) male rats within three different age groups (3 months, 12 months, and 24 months) were analyzed with quantitative real-time polymerase chain reactions. Our data indicated that in both areas, nicotine promotes the expression of the PACAP gene in 3 month old rats. The lipoprotein lipase is up-regulated in the VTA, whereas it exhibits down-regulation in the SN upon nicotine treatment in 3 months old rats, but, nicotine up-regulated the GRP1 expression in both the SN and VTA in 24 months old rats. We speculated that PACAP and GRP1 gene up-regulations by nicotine in the SN may be responsible for reducing the risk of PD.
We are currently exploring the effect of maternal smoking during pregnancy by analyzing the mRNA expressions of a single cell analysis of the infant rats' dopamine neurons using patch-clamp electrophysiology and DNA microarrays. We are trying to identify nicotine-responsive mRNAs and nicotine-induced changes in gene expressions at the single cell level. By using microarray data, we will be able to construct a network of the significant genes to identify functional significance with respect to gene ontology, molecular networks, and canonical pathways.

BIOGRAPHICAL SKETCH

Prof. Akay, received his B.S. and M.S. in Electrical Engineering from Bogazici University, Istanbul Turkey in 1981 and 1984, respectively and a Ph.D. degree from Rutgers University in 1990. He has played a key role in promoting the biomedical education in the world by writing several prestigious books and editing the Biomedical Engineering Book Series published by the Wiley and IEEE press. Prof. Akay is a recipient of the IEE EMBS Service Award, a IEEE Third Millennium Medal and the IEEE Engineering in Medicine and Biology Society Early Career Achievement Award in 1997, the Young Investigator Award of Sigma Xi Society, Northeast Region in 1998 and 2000, is a fellow of Institute of Physics and IEEE and serves on numerous editorial and advisory boards of several international journals.