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Brady Atwood, Ph.D.

Brady Atwood, Ph.D.
Assistant Professor of Psychiatry

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.
Education 

Undergraduate: Brigham Young University, Neuroscience

Graduate School: University of Washington, Neurobiology & Behavior

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.
Recent Publications 

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, Straiker A, Mackie K. CB(2): Therapeutic target-in-waiting. Progress in Neuro-Psychopharmacology and Biological Psychiatry. 38(1): 16-20 (2012). http://www.ncbi.nlm.nih.gov/pubmed/22197668

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, Mackie K. CB2: a cannabinoid receptor with an identity crisis. BritishJournal of Pharmacology. 160(3): 467-479 (2010). http://www.ncbi.nlm.nih.gov/pubmed/20590558

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


Brady Atwood, Ph.D.

Department of Psychiatry | 355 W. 16th St., Suite 4800 | Indianapolis, IN 46202 | Ph: (317) 963-7288 | Fax: (317) 963-7313