The potent nervous system effects of nicotine are clearly evidenced by the widespread use of tobacco products. In addition to reinforcing smoking behavior, nicotine is also reported to have analgesic, anxiolytic and memory-enhancing properties. An interesting, but confounding problem in the field is that although nAChRs are expressed throughout the brain and spinal cord, there is very little direct evidence that they mediate synaptic transmission. Rather, a major role of these receptors is the modulation of neurotransmitter release via their expression on presynaptic terminals.
We are investigating the cellular mechanisms underlying nicotine's rewarding and antinociceptive effects. All drugs of abuse are known to enhance dopamine release from midbrain reward centers and this is a crucial step in the reinforcement of drug-taking behavior. We are investigating the cellular mechanisms that contribute to this change in dopamine output. Most addictive drugs display significant analgesic profiles and our studies are also exploring the influence of nAChRs in pain control circuitry.
I am interested in the physiological actions of drugs such as nicotine and alcohol, both of which are widely abused and co-abused. My current project focuses on the role of brainstem α7-nicotonic receptors in the effects of alcohol on motor co-ordination. Other projects are looking at the effects of alcohol on nicotinic receptors in the brain's reward center. This may lead to an explanation as to how alcohol enhances the rewarding effects of tobacco smoking thus leading to alcohol and nicotine co-abuse.
My current research is focused on understanding alcohol modulation of specific subtypes of nicotinic acetylcholine receptors (nAChRs). Alcohol positively modulates nAChRs in brain regions that play a role in reward including the VTA and LDTg, this positive modulation may enhance nicotine reward and thus facilitate alcohol and nicotine co-abuse.
Synaptic plasticity is believed to underlie a number of behavioral adaptations, including addiction to drugs such as nicotine. The ventral striatum has been identified as being important for mediating the rewarding effects of drugs. Cholinergic interneurons have been demonstrated to innervate many cells in the striatum and to modulate dopamine release. My research focuses on changes in cholinergic interneuron activity following drug exposure, and the subsequent downstream consequences of modifications to cholinergic signaling.
Nicotine is the addictive component of tobacco, and smoking is one of the nation’s leading health problems. The transition from nicotine use to nicotine addiction or dependence is of great interest. Acute exposure to nicotine can have both rewarding and aversive effects, and the balance between these effects is thought to contribute to the development of addiction. Using electrophysiological and behavioral assays, my research aims to explain how the neural circuitry mediating reward and aversion influences nicotine-related behaviors and to determine how the function and dysfunction of these pathways relate to nicotine addiction.
Migraines are severe headaches that affect a substantial amount of individuals in the United States. In addition to pain, migraine sufferers display other symptoms, including nausea and blurred vision. Although the field has largely focused on vascular contribution to migraine pathophysiology, recent literature has suggested that dysfunction in descending pain modulation pathways could also play an important role in onset of migraines. My research is focused on neurons in the ventrolateral periaqueductal gray (vlPAG), a descending pain center that is located in the midbrain. I am investigating the role that cholinergic drive plays in vlPAG excitability. Furthermore, I plan to study the potential effects of vlPAG excitability on trigeminocervical complex neurons, which are downstream neurons that have been associated with migraine onset.
I manage the lab's day-to-day needs and assist in active projects. In particular, I aid in investigating the role of ventrolateral periaqueductal grey (vlPAG) alpha 7 nicotinic acetylcholine receptors (nAChRs) in descending pain pathways.