A headshot photo of Vincent S. Setola.

Vincent S. Setola, PhD

Associate Professor, PI/Director - Laboratory of Neuroscience and Genetics of Substance Abuse

Contact Information

PO Box 9303
Morgantown, WV 26506


  • Department of Neuroscience
  • Department of Behavioral Medicine & Psychiatry
  • Department of Physiology and Pharmacology
  • Rockefeller Neurosciences Institute

Graduate Training

  • MSc, Sorbonne Université (Paris VI)
  • PhD, Case Western Reserve University School of Medicine


  • Plasmalemmal monoamine transporter-G protein-coupled receptor interactions, Sorbonne Université (Paris VI)

Research Interests

1) Many drugs of abuse (e.g. amphetamine, cocaine, MDMA) and psychiatric medications (e.g., Prozac, Trintellix) exert their actions through monoamine neurotransmitter transporters, such as the dopamine transporter (DAT), the serotonin transporter (SERT), and the norepinephrine transporter (NET). Our group has discovered that mice lacking the protein RGS12 exhibit blunted responses to psychostimulants that target the aforementioned neurotransmitter transporters. For instance, wild-type mice treated with amphetamine exhibit a marked hyperlocomotor response. Mice lacking RGS12 treated with amphetamine exhibit a markedly reduced (compared with wild-type mice) response to amphetamine. The same is true for cocaine. These observations led us to discover that RGS12 is a previously unknown regulator of neurotransmitter transporter function. We are currently conducting studies to elucidate why the absence of RGS12 affects neurotransmitter transporters.

2) Prescription opioid painkillers (morphine, oxycodone, hydrocodone) are among the best treatments for severe pain; however, their addiction liability renders them very high-risk prescription drugs. We have devised an approach that increases the antinociceptive properties of opioid painkillers and decreases (if not eliminates) their rewarding properties in mice. This approach, if translatable to humans, would allow for the use of lower doses of opioid painkillers and the reduction/elimination of their euphoric properties. While our previous studies have focused on an adjuvant called nalfurafine, which is a kappa opioid receptor (KOR)-selective agonist, we are currently exploring adjuvants targeting other receptors.

3) Humans with schizophrenia (SCZ) often develop substance use disorder (SUD). We have mutant mice that are a novel model for features of human SCZ. Specifically, our mutant mice exhibit positive symptoms (e.g., sensorimotor gating deficits), negative symptoms (e.g., reduced social interaction), and cognitive symptoms (e.g., impaired novel object recognition memory) of SCZ. We are studying whether these SCZ-like phenotypes of our mutant mice are “cured” by different classes of antipsychotic medications, as well as potentially novel antipsychotics. We are also trying to understand the molecular mechanisms underlying the SCZ-like phenotypes of these mutant mice. Further, we are assessing whether (and why), like humans with SCZ, our mutant mice are susceptible to the development of SUD.