Raj S. – BASIS Chandler

BASIS Chandler Senior Raj S.

Determining the Dependence of Nicotinic Acetylcholine Receptor Expression on Opioid Receptors

Project/blog link: Determining the Dependence of Nicotinic Acetylcholine Receptor Expression on Opioid Receptors
BASIS Advisor: Mr. Matthew Cole
Internship location: Barrow Neurological Institute
Onsite Mentor: Dr. Yongchang Chang, Associate Professor, Division of Neurobiology

Project Abstract

Although the α6β2β3 nAChR subtype might seem an obscure topic, it is actually critical in rewarding nicotine addiction. When the genes for this specific receptor subtype are inactivated, mice have been shown to stop self-administering nicotine because they consequently lack the receptors necessary to release dopamine (the “feel-good” neurotransmitter behind many addictions) upon nicotine administration. Similarly disabling these receptors in humans could have a remarkable impact on smoking cessation. Unfortunately, we are not yet certain because these receptors are extremely difficult to recreate in frog oocytes (egg cells), which are typically used to study receptor function due to their manipulability. Researchers hypothesize that in order to successfully express the genes for these receptors in frog oocytes, they must be inserted alongside genes coding for opioid receptors. This lab is testing this hypothesis by injecting the oocytes with both types of DNA, then using a voltage clamp to survey any electrical responses indicating successful expression. If this hypothesis proves correct, further research can determine the function of these apparently critical receptors and how to utilize them to combat nicotine addiction.

Determining the Dependence of Nicotinic Acetylcholine Receptor Expression on Opioid Receptors