Theodore Slotkin, Ph.D.

Theodore Slotkin, Ph.D. Professor of Pharmacology and Cancer Biology
Professor in Psychiatry and Behavioral Sciences
Professor in Neurobiology

Duke University School of Medicine
Box 3813
Durham, NC 27710

Phone: 919-681-8015

Research Interests

Research in this laboratory is aimed toward understanding the cellular and molecular mechanisms that control neuronal development in the fetus, newborn and adolescent, especially the adverse effects of drugs of abuse and environmental contaminants. Ongoing projects comprise three areas:

(1) Mechanisms regulating development of synapses: ontogeny of neurotransmitter receptors and intracellular signaling cascades; endocrine and trophic factors.

(2) Adverse effects of exogenous agents on development: drugs of abuse (especially nicotine), hormonal imbalances, environmental contaminants (pesticides), drug therapies for preterm labor.

(3) Unique biological properties of the adolescent brain: their role in addiction and neural injury by environmental toxicants.

Representative Publications

Slotkin TA, Card J and Seidler FJ (2014) Prenatal dexamethasone, as used in preterm labor, worsens the impact of postnatal chlorpyrifos exposure on serotonergic pathways. Brain Res. Bull. 100:44-54.

Slotkin TA, Card J and Seidler FJ (2014) Nicotine administration in adolescence reprograms the subsequent response to nicotine treatment and withdrawal in adulthood:  sex-selective effects on cerebrocortical serotonergic function. Brain Res. Bull. 102:1-8.

Slotkin TA, Skavicus S, Card J, Levin ED and Seidler FJ (2015) Amelioration strategies fail to prevent tobacco smoke effects on neurodifferentiation:  nicotinic receptor blockade, antioxidants, methyl donors. Toxicology 333:63-75. 

Slotkin TA, Skavicus S, Card J, Stadler A, Levin ED and Seidler FJ (2015) Developmental neurotoxicity of tobacco smoke directed toward cholinergic and serotonergic systems:  more than just nicotine. Toxicol. Sci. 147:178-189. 

Slotkin TA, Skavicus S and Seidler FJ (2015) Prenatal drug exposures sensitize noradrenergic circuits to subsequent disruption by chlorpyrifos. Toxicology 338:8-16.