Brady Atwood, Ph.D.
Brady Atwood, Ph.D.
|Personal Statement||Drugs of abuse affect behavior and cognition by ultimately altering the ways in which brain cells communicate with one another. Our work analyzes the impact that drugs of abuse have on synaptic plasticity in the dorsal striatum (caudate-putamen in primates), a brain region involved in the control of goal-directed and habitual actions. The dorsal striatum also plays a significant role in addiction, Parkinson’s disease, Huntington’s disease, and obsessive compulsive disorder, among others. We use cutting-edge tools such as optogenetics, mutant mice, electrophysiology, neurochemistry, and mouse models of human alcohol use. We hope that by understanding how drugs of abuse alter normal neuronal communication that we can lay the groundwork for future discoveries to identify new therapeutics for treating drug abuse.|
Undergraduate: Brigham Young University, Neuroscience
Post-doctoral: National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health
|Current Academic Interests||Teaching: I am very enthusiastic about the great opportunity it is to mentor students in the laboratory.
Research: I am currently interested in the synapse-specific effects that alcohol and prescription painkillers, such as oxycodone, have on opioid and cannabinoid receptor-mediated synaptic plasticity in the dorsal striatum. I use optogenetics to probe specific inputs to this brain region and electrophysiological and neurochemical measurements of alterations in synaptic transmission following drug exposure. I also am interested in the role that dorsal striatal opioid receptors play in alcohol consumption and use mouse models of alcohol self-administration to study this.
Atwood BK, Kupferschmidt DA, Lovinger DM. Opioids induce dissociable forms oflong-term depression of excitatory inputs to the dorsal striatum. Nature Neuroscience.17(4): 540-548 (2014). http://www.ncbi.nlm.nih.gov/pubmed/24561996
Atwood BK, Lovinger DM, Mathur BM. Presynaptic long-term depression mediated byGi/o-coupled receptors. Trends in Neurosciences. 37(11): 663-673 (2014). http://www.ncbi.nlm.nih.gov/pubmed/25160683
Atwood BK, Straiker A, Mackie K. CB(2) cannabinoid receptors inhibit synaptictransmission when expressed in cultured autaptic neurons. Neuropharmacology. 63(4):514-523 (2012). http://www.ncbi.nlm.nih.gov/pubmed/22579668
Atwood BK, Wager-Miller J, Haskins C, Straiker A, Mackie K. Functional selectivity inCB(2) cannabinoid receptor signaling and regulation: implications for the therapeuticpotential of CB(2) ligands. Molecular Pharmacology. 81(2): 250-263 (2012). http://www.ncbi.nlm.nih.gov/pubmed/22064678
Atwood BK, Lee D, Straiker A, Widlanski TS, Mackie K. CP47,497-C8 and JWH073,commonly found in 'Spice' herbal blends, are potent and efficacious CB(1) cannabinoidreceptor agonists. European Journal of Pharmacology. 659(2-3): 139-145 (2011). http://www.ncbi.nlm.nih.gov/pubmed/21333643
Atwood BK, Huffman J, Straiker A, Mackie K. JWH018, a common constituent of'Spice' herbal blends, is a potent and efficacious cannabinoid CB receptor agonist.British Journal of Pharmacology. 160(3): 585-593 (2010). http://www.ncbi.nlm.nih.gov/pubmed/20100276