Three faculty scientists in the Department of Neurology - each of them also a leader in UCSF's Ernest Gallo Clinic and Research Center (EGCRC) -- have been honored with prestigious new UCSF appointments.
Last summer, Raymond L. White, PhD, director of the Gallo Center, was appointed to the Rudi Schmid Distinguished Professorship in Neurology; and Robert O. Messing, MD, was appointed to the Endowed Chair in Neurology in Honor of the Gallo Family. This spring, Howard L. Fields, MD, was appointed to the Endowed Chair in Pharmacology of Addiction in Neurology.
"Understanding the biologic basis of alcoholism and other addictions is now within reach," said Stephen Hauser, MD, professor and chair of neurology at UCSF. "The discovery of pathways, molecules and genes that produce addictive behaviors will lead to new approaches for prevention, treatment and cure of these difficult medical and societal problems. These new endowed chairs will permit UCSF to expand our community of addiction scientists by providing funds for recruitment of talented new investigators."
A nationwide search is underway to fill two more endowed chairs in the department - in the areas of cell biology of addiction and genetics of addiction. All five endowments support the study of alcohol addiction.
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Raymond White
White is an internationally known geneticist and a member of the National Academy of Sciences. He is recognized for conceiving the use of natural genetic variations, or polymorphisms, to map disease genes and for demonstrating that tumors can form as a result of a two-step process: inheriting a defective copy of gene and losing the normal copy. White was a key organizer of the human genome project.
Since 2002, he has directed the EGCRC, one of the premier centers for genetic, molecular, cellular and behavioral neuroscience research focusing on the effects of alcohol on the brain. The center is affiliated with part of the UCSF Department of Neurology.
Robert Messing
Messing, associate director of the Gallo Center, studies specific signaling proteins - active in fruit flies, mice and humans - that are important in acute and chronic responses to alcohol and other drugs of abuse. His lab generates mice deficient in these proteins to understand their role in behavior, and determine if they are promising targets for drugs to treat addiction. Messing's lab has found that mice lacking one key enzyme show reduced alcohol consumption, decreased anxiety, and reduced inflammatory pain. These results suggest that a drug that inhibits the enzyme, known as protein kinase C epsilon, might decrease drinking, anxiety, and pain.
Last year, Messing's lab determined that mice deficient in a gene called ENT1 are much less intoxicated when given alcohol. The mice drink more alcohol than normal mice and have impaired signaling by the neurotransmitter adenosine. The finding points to the potential of an adenosine-like drug that might reduce alcohol drinking.
Howard Fields
Fields is a principal investigator at the EGCRC and also director of the Wheeler Center for the Neurobiology of Addiction at UCSF. He holds faculty appointments in neurology, as well as physiology and psychiatry. Fields is highly regarded for his research on brain mechanisms of pain and pain modulation. His research focuses on the function of endogenous pain-relieving opioids (endorphins) and their receptors. Opioids are of great clinical importance for their analgesic effect and because they mediate the rewarding effects of heroin, alcohol and rich foods. Fields' goal is to determine how each of the body's own opioids and their receptors contribute to pain modulation and addictive behavior.
His laboratory uses animal models and human functional imaging to identify the brain regions involved in pain and addiction. His group records from neurons in these areas to determine how opioids act on those neurons and how the activity of those neurons contributes to behavior. The laboratory has identified specific populations of neurons that are affected by opioids in both reward and pain-relief neuronal circuits.
Source: Wallace Ravven
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