Kevin D. Wickman, PhD

Professor and Vice Head, Department of Pharmacology

Kevin D. Wickman

Contact Info

Office Phone 612-624-5966

Office Address:
NHH 3-118

Professor and Vice Head, Department of Pharmacology

Distinguished University Teaching Professor

Distinguished McKnight University Professor

PhD, Mayo Foundation for Biomedical Research


Kevin Wickman is a professor and Vice Head in the Department of Pharmacology. His research program seeks to elucidate inhibitory signaling pathways that regulate the excitability of neurons in the reward circuitry. His team's recent efforts have shown that inhibitory G protein-dependent signaling pathways in the ventral tegmental area and prefrontal cortex normally serve to limit addiction-related behaviors evoked by administration of opioids and psychostimulants, but that the influence of these pathways is diminished with repeated drug exposure. They employ intracranial viral genetic and pharmacologic approaches, together with electrophysiological and behavioral analyses, to understand the molecular and cellular mechanisms underlying the reciprocal relationship between inhibitory signaling pathways in the reward circuitry and drugs of abuse. The premise behind their efforts is that if endogenous inhibitory signaling pathways can be strengthened to prevent their suppression by drugs of abuse, then the risk of addiction in susceptible individuals and/or relapse in recovering addicts might be reduced or prevented.


Research Summary/Interests

My lab studies mechanisms controlling the excitability of cells in the brain and heart. Dysregulation of cell excitability contributes to many debilitating and/or life-threatening medical conditions, including cardiac arrhythmias, epilepsy, anxiety, depression, schizophrenia, Down Syndrome, addiction, and pain. We seek to better understand mechanisms that control cell excitability, so that safer and more effective strategies can be developed to treat these afflictions.

Research projects in my lab use state-of-the-art techniques and approaches including slice electrophysiology, traditional and conditional gene knockout/knockdown, chemogenetics (DREADDs), intracranial manipulations, and electrocardiogram telemetry, as well as behavioral assessments of reward, mood, cognition, and nociception. While these approaches can be flexibly adapted to investigate the contribution any molecular target to organ function or behavior, our recent work has focused on the G protein-gated inwardly-rectifying potassium channel, or GIRK channel.

GIRK channels mediate the impact of the parasympathetic nervous system on heart rate and arrhythmogenesis. They also play key roles in pain perception, addiction, cognition, and mood. Our ongoing funded projects are directed at identifying molecules and mechanisms that modulate GIRK channel activity in neurons and cardiac myocytes, elucidating roles for GIRK channels in mood-related behavior and cognition, understanding experience- and drug-induced plasticity of GIRK-dependent signaling in the context of addiction, and evaluating the efficacy of novel small-molecular modulators of GIRK channels in preclinical studies of mood, pain, and cognitive dysfunction.