Stanley A. Thayer, PhD

Professor, Department of Pharmacology

Stanley A. Thayer

Contact Info

Office Phone 612-626-7049

Office Address:
3-116 Nils Hasselmo Hall
312 Church St SE
Minneapolis, MN 55455

Lab Address:
2-244 Nils Hasselmo Hall
312 Church St SE
Minneapolis, MN 55455

Postdoctoral Fellow, University of Chicago

PhD, University of California - Irvine, Pharmacology

BS, University of California - Irvine, Chemistry and Biology


Dr. Thayer is a professor of pharmacology. He received BS degrees in Biology and Chemistry and a PhD in Pharmacology from the University of California at Irvine. After completing postdoctoral training at the University of Chicago in 1989, Dr. Thayer joined the faculty at the University of Minnesota.


Neuropharmacology, Neurotoxicity, Synaptic Transmission, Signal Transduction, Neuroinflammation

Awards & Recognition

2004-2014 NIH MERIT Award

1991-1993 McKnight-Land Grant Professor

Professional Associations

American Society for Pharmacology and Experimental Therapeutics

Society for Neuroscience

Society on NeuroImmune Pharmacology


Research Summary/Interests

Dr. Thayer's laboratory studies neurodegenerative processes. His group uses electrophysiological and optical techniques to measure ion currents, to image synaptic proteins and to record changes in intracellular calcium within single neurons. Current research efforts focus on three principal areas.

1.Synapse loss occurs early in neurodegenerative disease and correlates with cognitive decline in patients with HIV-associated neurocognitive disorder and Alzheimer’s disease. Recent studies indicate that loss of synapses is not a symptom of the cell’s demise but instead, is a coping mechanism to reduce excess excitotoxic input. Current studies evaluate pharmacological strategies to prevent loss or induce recovery of synapses during neurotoxic processes.

2.Calcium is an essential second messenger involved in neurotransmitter release, gene regulation, and synaptic plasticity. Inappropriate elevation of the intracellular calcium concentration contributes to the neurodegeneration associated with AIDS, ischemia, epilepsy and head trauma. Thus, neurons have developed a complex system to maintain calcium homeostasis. Current studies focus on the modulation of processes that remove calcium from the cytoplasm by drugs and second messengers.

3.Cannabinoids, analogs of the psychoactive ingredient in marijuana, act on receptors that are part of an endogenous signaling system. Endocannabinoid signaling serves as an on-demand neuroprotective mechanism. Currents studies examine the role of the endocannabinoid system in regulating synaptic transmission and neurotoxicity.

Drugs to slow the progression of neurodegenerative disease are lacking. Agents that modulate calcium signals, possibly via the endocannabinoid system, may protect synapses and cells from neurotoxic insult.