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Brady Atwood, Ph.D.

Assistant Professor of Psychiatry, and Pharmacology & Toxicology

Education/Training:
Postdoctoral, Synaptic Pharmacology, National Institute on Alcohol Abuse & Alcoholism, NIH, Rockville, MD (2016)
Ph.D., Neurobiology & Behavior, University of Washington, Seattle, WA (2010) 

The impact of drugs of abuse on synaptic plasticity in brain regions associated with goal-directed and habitual actions.
Drugs of abuse, such as alcohol and prescription painkillers, affect behavior and cognition by ultimately altering the ways in which brain cells communicate with one another. Synaptic plasticity is the process by which neurotransmission between neurons is strengthened or weakened and this plasticity underlies learning and memory. 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 goaldirected and habitual actions. This brain region is involved in drug use and addiction as well as other diseases and disorders such as Parkinson’s disease, Huntington’s disease, and obsessive compulsive disorder, among others. We seek to understand the mechanisms of plasticity at specific synapses in the dorsal striatum and how drugs of abuse can have synapse-specific effects. 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.

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Selected Publications:

  • Atwood BK, Lovinger DM, Mathur BM. Presynaptic long-term depression mediated by Gi/o-coupled receptors. Trends in Neurosciences. 37(11): 663-673 (2014).
  • Atwood BK, Kupferschmidt DA, Lovinger DM. Opioids induce dissociable forms of long-term depression of excitatory inputs to the dorsal striatum. Nature Neuroscience. 17(4): 540-548 (2014).
  • Atwood BK, Straiker A, Mackie K. CB(2) cannabinoid receptors inhibit synaptic transmission when expressed in cultured autaptic neurons. Neuropharmacology. 63(4):514-523 (2012).
  • Atwood BK, Straiker A, Mackie K. CB(2): Therapeutic target-in-waiting. Progress in Neuro-Psychopharmacology and Biological Psychiatry. 38(1): 16-20 (2012). 
  • Atwood BK, Wager-Miller J, Haskins C, Straiker A, Mackie K. Functional selectivity in CB(2) cannabinoid receptor signaling and regulation: implications for the therapeutic potential of CB(2) ligands. Molecular Pharmacology. 81(2): 250-263 (2012).
  • 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) cannabinoid receptor agonists. European Journal of Pharmacology. 659(2-3): 139-145 (2011).
  • Atwood BK, Mackie K. CB2: a cannabinoid receptor with an identity crisis. British Journal of Pharmacology. 160(3): 467-479 (2010).
  • 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).

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