How do addictive substances alter the brain? How do they create addictive behaviors? All drugs of abuse (opioids, cocaine, methamphetamines, nicotine, etc) alter dopamine release in the brain. In the case of nicotine, the primary addictive component of tobacco products, dopamine neurons are altered so that more dopamine is released during their highly excitable (phasic) periods of activation. 

The Neuropharmacology of Nicotine Addiction

Currently, our lab is studying how specific populations of neurons in the midbrain (dopaminergic, GABAergic, and glutamatergic) are altered by nicotine (the primary addictive compound in tobacco products) and how this changes dopamine signaling in the brain. To do this, the Henderson lab uses techniques in the fields of electrophysiology, microscopy, pharmacology, and neuroscience to understand how nicotinic acetylcholine receptors (the molecular target of nicotine) play a role in the addiction to nicotine.

With the advent of electronic cigarettes, additional flavors that have been banned in traditional cigarettes, are now available for smokers of all ages. Therefore, we also study how these flavors may alter the addiction to nicotine. 

The Neuropharmacology of Opioid Addiction and the Co-Use of Tobacco with Opioids

Almost all opioid addicts (85 - 95%) exhibit high smoking rates. Opioid addicts undergoing treatment for addiction report significantly higher rates of cessation if they are non-smokers or if they choose to abstain from smoking during their treatment. Thus, there is an urgent need to understand how nicotine and opioids act synergistically in the brain.  Our lab is beginning to examine the synergistic nature of nicotine and opioids by first examining reward-related behavior. Both opioids and nicotine, independently alter dopamine neurons in the ventral tegmental area (VTA) to provide rewarding and reinforcing properties. Therefore, our primary focus is the study of how nicotine, opioids, and both alter VTA dopamine neurons.


Parkinson's disease is a form of neurodegeneration that results from the selective degeneration of dopamine neurons in the nigrostriatal pathway (that is, the projection of dopamine neurons from the substantia nigra pars compacta to the dorsal striatum). In recent years it has been made known that smokers exhibit a significantly reduced rate of developing Parkinson's disease. In addition to studying how nicotine mediates addiction, the Henderson lab is also interested in understanding how nicotine and nicotinic drugs play a role in neuroprotection against Parkinson's disease. This work is largely done in collaboration with the Henry Lester lab at Caltech.