Summary: A new study reports chronic nicotine exposure during pregnancy alters the genetics and dopamine neurons of newborns. The findings could help researchers develop a possible cure for nicotine addiction.
Source: University of Houston.
The Akay Lab biomedical research team at the University of Houston is reporting in the journal Nature Scientific Reports that a possible cure for addiction may be found by following the pathways of significantly altered dopamine neurons in newborns who were chronically exposed to nicotine in utero. The findings of the altered neurons come from recordings of dopamine and non-dopamine neurons in the brain’s addiction center, called the ventral tegmental area (VTA), following chronic nicotine exposure during pregnancy.
Metin Akay, John S. Dunn Endowed Chair Professor of Biomedical Engineering and department chair, and his research team noted that the dopamine neurons, in response to nicotine exposure during pregnancy, were significantly activated, allowing the release of unusually high levels of dopamine in the prefrontal cortex.
Active dopamine, known as the “feel good” hormone, might seem a good thing at first glance. It’s a neurotransmitter that carries information between neurons and regulates emotional responses. It allows us to see rewards and encourages action that will lead to reward, but since it contributes to those feelings of pleasure and reward, it also plays a part in addiction.
“The impacted dopamine can result in babies being born addicted to nicotine, but once we understand which genes are altered, which gene regulator networks are altered and which gene pathways are altered, we can develop targeted medication that could eliminate addiction in offspring,” said Akay.
Exposure to nicotine during pregnancy through maternal smoking or nicotine replacement therapy is associated with adverse birth outcomes as well as several cognitive and neurobehavioral deficits.
The Akay lab previously published work indicating that dopamine neurons in the VTA are very likely involved in nicotine addiction. Their current work speaks to the very nature of health itself, exploring how the dopamine of nicotine-exposed offspring alters gene expression, a fundamental building block of health. Many diseases are caused by a change in the DNA of a single gene.
Akay’s team includes Renee F. Keller, Tina Kazemi, Andrei Dragomir and Yasemin M. Akay, assistant professor of biomedical engineering.
Source: Laurie Fickman – University of Houston
Publisher: Organized by NeuroscienceNews.com.
Image Source: NeuroscienceNews.com image is in the public domain.
Original Research: Open access research for “Comparison between dopaminergic and non-dopaminergic neurons in the VTA following chronic nicotine exposure during pregnancy” by Renee F. Keller, Tina Kazemi, Andrei Dragomir, Yasemin M. Akay & Metin Akay in Scientific Reports. Published January 24 2019.
[cbtabs][cbtab title=”MLA”]University of Houston”Nicotine Exposure During Pregnancy Alters Dopamine Neurons and Genes in Newborns.” NeuroscienceNews. NeuroscienceNews, 6 February 2019.
<https://neurosciencenews.com/genetics-nicotine-dopamine-10699/>.[/cbtab][cbtab title=”APA”]University of Houston(2019, February 6). Nicotine Exposure During Pregnancy Alters Dopamine Neurons and Genes in Newborns. NeuroscienceNews. Retrieved February 6, 2019 from https://neurosciencenews.com/genetics-nicotine-dopamine-10699/[/cbtab][cbtab title=”Chicago”]University of Houston”Nicotine Exposure During Pregnancy Alters Dopamine Neurons and Genes in Newborns.” https://neurosciencenews.com/genetics-nicotine-dopamine-10699/ (accessed February 6, 2019).[/cbtab][/cbtabs]
Comparison between dopaminergic and non-dopaminergic neurons in the VTA following chronic nicotine exposure during pregnancy
Exposure to nicotine during pregnancy through maternal smoking or nicotine replacement therapy is associated with adverse birth outcomes as well as several cognitive and neurobehavioral deficits. Several studies have shown that nicotine produces long-lasting effects on gene expression within many brain regions, including the ventral tegmental area (VTA), which is the origin of dopaminergic neurons and the dopamine reward pathway. Using a well-established rat model for perinatal nicotine exposure, we sought to investigate altered biological pathways using mRNA and miRNA expression profiles of dopaminergic (DA) and non-dopaminergic (non-DA) neurons in this highly-valuable area. Putative miRNA-gene target interactions were assessed as well as miRNA-pathway interactions. Our results indicate that extracellular matrix (ECM) receptor interactions were significantly altered in DA and non-DA neurons due to chronic nicotine exposure during pregnancy. They also show that the PI3K/AKT signaling pathway was enriched in DA neurons with multiple significant miRNA-gene targets, but the same changes were not seen in non-DA neurons. We speculate that nicotine exposure during pregnancy could differentially affect the gene expression of DA and non-DA neurons in the VTA.