John T. Williams, Ph.D.
- Professor, Vollum Institute
- Senior Scientist, Vollum Institute
- Neuroscience Graduate Program, School of Medicine
- Program in Molecular and Cellular Biosciences, School of Medicine
Biography
After earning his Ph.D. in Pharmacology from Loyola University in 1979, John Williams worked as a research scientist at the Max-Planck Institute in Munich and at Loyola University School of Medicine. He then spent five years as a research scientist in Biological Sciences at the Massachusetts Institute of Technology. In 1987, he became an assistant scientist at the Vollum Institute and rose to the position of senior scientist in 1996. He holds a concurrent appointment in the Department of Physiology and Pharmacology in the School of Medicine.
Williams and colleagues investigate the early events that lead to the development of tolerance to opioids. Opioids such as morphine are important therapeutic compounds used for the management of pain, but the primary problem with their use is the development of tolerance, where higher doses are required to achieve the same effect. By focusing on the long-term effects of morphine and cocaine on synaptic transmission in the reward centers of the brain—dopamine cells of the ventral tegmental area and GABA cells of the nucleus accumbens—the lab hopes to identify the cellular basis for drug addiction.
Education and training
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Degrees
- B.S., 1972, St. Lawrence University
- M.A., 1975, State University of New York, Potsdam
- Ph.D., 1979, Loyola University
Areas of interest
- opiate desensitization and tolerance
- receptor trafficking
- dendrodendritic transmission
Additional information
Publications
Publications
Improved green and red GRAB sensors for monitoring dopaminergic activity in vivo
Nature MethodsSynaptotagmin-7 Counteracts Short-Term Depression during Phasic Dopamine Release
eNeuroGait Abnormalities and Aberrant D2 Receptor Expression and Signaling in Mice Carrying the Human Pathogenic Mutation DRD2I212F
Molecular pharmacologySynaptotagmin-1 is a Ca2+ sensor for somatodendritic dopamine release
Cell ReportsAgonist-Specific Regulation of G Protein-Coupled Receptors after Chronic Opioid Treatment
Molecular pharmacologyCo-activation of GPCRs facilitate GIRK-dependent current
Journal of PhysiologySubcellular localization of D2 receptors in the murine substantia nigra
Brain Structure and FunctionA Gain-of-Function Variant in Dopamine D2 Receptor and Progressive Chorea and Dystonia Phenotype
Movement DisordersSignaling-Biased and Constitutively Active Dopamine D2 Receptor Variant
ACS Chemical NeuroscienceThe residence of synaptically released dopamine on D2 autoreceptors
Cell ReportsChronic treatment with morphine disrupts acute kinase-dependent desensitization of GPCRs
Molecular pharmacologyPhotoactivatable Dopamine and Sulpiride to Explore the Function of Dopaminergic Neurons and Circuits
ACS Chemical NeuroscienceImaging neuromodulators with high spatiotemporal resolution using genetically encoded indicators
Nature protocolsPhosphorylation-deficient G-protein-biased μ-opioid receptors improve analgesia and diminish tolerance but worsen opioid side effects
Nature communicationsRIM is essential for stimulated but not spontaneous somatodendritic dopamine release in the midbrain
eLifeSeparation of acute desensitization and long-term tolerance of m-opioid receptors is determined by the degree of C-terminal phosphorylation
Molecular pharmacologyVisualizing endogenous opioid receptors in living neurons using ligand-directed chemistry
eLifeCellular tolerance at the µ-opioid receptor is phosphorylation dependent
eLifeDesensitization and tolerance of Mu opioid receptors on pontine kölliker-fuse neurons
Molecular pharmacologyUltrafast neuronal imaging of dopamine dynamics with designed genetically encoded sensors
ScienceCholinergic interneurons underlie spontaneous dopamine release in nucleus accumbens
Journal of NeuroscienceCocaine-induced adaptation of dopamine D2S, but not D2L autoreceptors
eLifeDesensitized D2 autoreceptors are resistant to trafficking
Scientific ReportsPresynaptic gain control by endogenous cotransmission of dopamine and GABA in the olfactory bulb
Journal of neurophysiologyTwo-color, one-photon uncaging of glutamate and GABA
PloS oneCalcium Release from Stores Inhibits GIRK
Cell ReportsAgonist binding and desensitization of the μ-opioid receptor is modulated by phosphorylation of the C-terminal tail domain
Molecular pharmacology