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Brady Atwood, PhD

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


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.

Selected 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

 


Department of Pharmacology and Toxicology | 635 Barnhill Drive, MS A401 | Indianapolis, IN 46202