Biography
Daniel Savage received his Ph.D. in Pharmacology from the University of Pennsylvania. After his postdoctoral training at Duke University, he joined the Department of Pharmacology at UNM School of Medicine in 1983. He was the Founding Chair of the UNM’s Department of Neurosciences in 1997 and served as its Chair until 2019. He is also the Director of the New Mexico Alcohol Research Center, a NIAAA-designated Specialized Alcohol Research Center, whose focus is on Fetal Alcohol Spectrum Disorder.
Areas of Specialty
Neurotransmitter Receptor Pharmacology
Hippocampal Synaptic Plasticity
Behavioral Pharmacology
Fetal Alcohol Spectrum Disorder
Education
Post-Doc, Behavioral Neuroscience (1982):
Duke University
Durham, NC
Phd, Pharmacology (1980):
University of Pennsylvania
Philadelphia, PA
BS, Biology (1973):
University of Richmond
Richmond, VA
Achievements & Awards
Distinguished Professor Award, UNM School of Medicine - 2015
Henry Rosett Award for Excellence in Fetal Alcohol Spectrum Disorders Research - 2011
A. Earl Walker Award for Excellence in Neuroscience Research at UNM - 2007
“Teacher of the Year†Award, Phase I Undergraduate Medical Curriculum - 1999
Regents’ Professorship Award, UNM Board of Regents - 1996
“An Apple for the Teacher†Award for Excellence in Medical School Teaching - 1994"
An Apple for the Teacher" Award for Excellence in Biomedical Graduate Teaching - 1993
Dean's Fellowship Award for Biomedical Research, UNM School of Medicine - 1991
Gender
Male
Courses Taught
Medical Neuropharmacology
Principles of Medical Pharmacology
Principles of Neurobiology
Developmental Neurotoxicology
Neurochemistry & Neuropharmacology
Principles of Neuropharmacology
Research and Scholarship
Our research examines whether the consumption of moderate amounts of ethanol during pregnancy results in long-lasting damage in brain function in ethanol-exposed offspring. Using a rat model of moderate prenatal ethanol exposure, we have observed subtle but persistent neurochemical changes in brain of offspring. These changes occur in specific brain regions involved in the consolidation of memory, both in rats as well as in humans. The neurochemical alterations caused by prenatal ethanol exposure decrease activity-dependent potentiation of synaptic communication between neurons that leads to functional deficits in these brain regions. We believe that these changes may contribute to the learning disabilities observed in children whose mothers drank during pregnancy. Our current studies include preclincial screening of putative therapeutic agents for treating prenatal ethanol-induced learning deficits, and the development of novel biomarkers for the early detection of prenatal alcohol-induced functional brain damage.