Stanley A. Thayer, PhD

Professor, Department of Pharmacology

Stanley A. Thayer

Contact Info

sathayer@umn.edu

Office Phone 612-626-7049

Office Address:
NHH 3-116

PhD, University of California - Irvine

Research

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 grown in tissue culture. Current research efforts focus on three principal areas.

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

Publications