Prenatal Exposure to Nicotine May Increase Risk of Nicotine Susceptibility Later in Life

MedicalResearch.com Interview with:

Davide Dulcis, PhDAssociate ProfessorDepartment of Psychiatry, UCSD School of MedicineUniversity of California, San DiegoLa Jolla, CA 92093-0603

Dr. Dulcis

Davide Dulcis, PhD
Associate Professor
Department of Psychiatry, UCSD School of Medicine
University of California, San Diego
La Jolla, CA 92093-0603

MedicalResearch.com: What is the background for this study? What are the main findings? 

Response: Previous studies in humans have shown that pre-natal and early life exposure to nicotine can lead to altered children behavior and propensity for drug abuse, but the precise mechanisms involved are still unclear.

In this pre-clinical study we showed how nicotine “primes” neurons of the mouse brain’s reward center for a fate they normally would not have taken, making them more susceptible to the effects of nicotine when the animals are again exposed to nicotine later in life, said Dr. Benedetto Romoli, first author of the research article.  

MedicalResearch.com: What should readers take away from your report?

Response: Our study is a very important reminder of how plastic and malleable the brain is in the earliest phases of life, and how long-lasting the effects of any external manipulation could be, even if they might not be immediately detectable. These neurons acquired a ‘molecular memory’ of the neonatal nicotine exposure.  In addition, the study might also be useful for tobacco control programs. The effects we observed were induced indirectly through maternal lactation, and current state and local policies do not regulate this particular type of nicotine intake that can occur via nicotine patches or electronic cigarettes. 

MedicalResearch.com: What recommendations do you have for future research as a result of this work?

Response: For a long time, neuroscientists believed that after the initial specification neurotransmitter (the language that neurons in the brain use to communicate one another) was fixed and immutable throughout life. In recent years, studies from our and other labs have shown that this is not true. This novel kind “neurotransmitter plasticity” should be incorporated into studies involving chronic exposures to psychostimulants and substances of abuse as well as altered photoperiod and other social stressors.

MedicalResearch.com: Is there anything else you would like to add?

Response: Our plan is to investigate whether early exposure to other commonly used drugs, such as alcohol, marijuana or opioids, can induce similar adaptations of the reward center that affects drug preferences in adulthood. We are also curious to investigate whether this form of neurotransmitter plasticity is inducible or reversible at different stages of life when the brain is still extremely plastic and prone to drug addiction, like in adolescence, said Dr. Dulcis. Finally, since these neurons acquire a dopaminergic phenotype, we are also investigating applications aimed at improving the behavioral performance of animal models for diseases associated with a loss of dopaminergic neurons, such as Parkinson’s disease.

No disclosures. 

Citation:

Benedetto Romoli, Adrian F. Lozada, Ivette M. Sandoval, Fredric P. Manfredsson, Thomas S. Hnasko, Darwin K. Berg, Davide Dulcis. Neonatal nicotine exposure primes midbrain neurons to a dopaminergic phenotype and increases adult drug consumption. Biological Psychiatry, 2019; DOI: 10.1016/j.biopsych.2019.04.019

May 25, 2019 @ 12:07 am

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