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Staff Scientist

David A Kupferschmidt, Ph.D.

Integrative Neuroscience Section

Porter Neuroscience Research Center
Building 35 Room 1C-905
35 Convent Drive
Bethesda MD 20892-3702
Office: (301) 402-7209
Lab: (301) 402-7209

david.kupferschmidt@nih.gov

Dr. Kupferschmidt earned his M.A. (2007) and Ph.D. (2012) in Psychology from the University of Toronto, where he studied the neurochemistry of stress and relapse to drug seeking. During his postdoctoral fellowship at the National Institute on Alcohol Abuse and Alcoholism, Dr. Kupferschmidt combined neurophysiology with optical, viral, and transgenic tools to assess synaptic and circuit mechanisms of skill and habit learning. Dr. Kupferschmidt also established novel approaches to monitor in vivo calcium dynamics in discrete projections from prefrontal and sensorimotor cortices to the striatum to probe real-time circuit function during action learning. Dr. Kupferschmidt joined NINDS in 2017 as the lead scientist in the lab of NIMH Director, Dr. Joshua A. Gordon. In consultation with Dr. Gordon, Dr. Kupferschmidt guides research into the neural circuit basis of cognitive functions such as working memory, and their dysfunction in mouse models of genetic susceptibility to neuropsychiatric disease, particularly schizophrenia.



Working memory, the storing of behaviorally relevant information on a timescale of seconds, is a central component of cognition. Working memory deficits also feature prominently in many psychiatric disorders, including schizophrenia. Complex networks of neurons across the brain appear to work in concert to produce normal working memory. Dysfunction of this cognitive domain in schizophrenia may therefore arise from the widespread neural circuit dysconnectivity observed in patients with, and models of, this disorder. Importantly, however, the neural computations that give rise to normal and disordered working memory function, and the micro- and macro-circuits of neurons that subserve these computations, are largely unknown.

In the Integrative Neuroscience Section (INS), there are two principal goals: [1] probe the neural circuit basis of normal cognition, including working memory; and [2] characterize the neural circuit and cognitive dysfunction in mouse models of genetic susceptibility to schizophrenia and related disorders to both understand their pathophysiology and identify novel treatment targets. The section uses in vivo electrophysiology and other neural circuit tools (e.g. in vivo fiber photometry, fluorescence imaging) to record the function of discrete cells and circuits in freely moving animals, and use optogenetic tools to control this function in real-time during behavior. The work focuses on the neural computations within, and circuit-level interactions between, the prefrontal cortex, hippocampus, thalamus, and amygdala. The section also aims to identify molecular targets that influence connectivity within and between these structures, and plasticity mechanisms that may be leveraged to counteract circuit dysconnectivity in psychiatric disease-related models.

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  • Emily Alway, B.S.
    Post baccalaureate IRTA Fellow

  • Joshua Gordon, M.D., Ph.D.
    Lead Investigator

  • Sofiya Hupalo, Ph.D.
    Postdoctoral IRTA Fellow

  • Rachel Mikofsky, B.A.
    Post baccalaureate IRTA Fellow

  • Maxym Myroshnychenko, Ph.D.
    Postdoctoral IRTA Fellow

  • Johannes Passecker, Ph.D.
    Visiting Scientist

  • 1) Kupferschmidt DA, Gordon JA (2018)
  • The dynamics of disordered dialogue: Prefrontal, hippocampal and thalamic miscommunication underlying working memory deficits in schizophrenia
  • Brain and Neuroscience Advances
  • 2) Kupferschmidt DA, Juczewski K, Cui G, Johnson KA, Lovinger DM (2017)
  • Parallel but dissociable processing in discrete corticostriatal inputs encodes skill learning
  • Neuron , 96(2), 476-489
  • 3) Kupferschmidt DA, Lovinger DM (2015)
  • Inhibition of presynaptic calcium transients in cortical inputs to the dorsolateral striatum by metabotropic GABA(B) and mGlu2/3 receptors
  • J Physiol , 593(10), 2295-310
  • 4) Atwood BK, Kupferschmidt DA, Lovinger DM (2014)
  • Opioids induce dissociable forms of long-term depression of excitatory inputs to the dorsal striatum
  • Nat Neurosci , 17(4), 540-8
  • 5) Kupferschmidt DA, Lovejoy DA, Rotzinger S, Erb S (2011)
  • Teneurin C-terminal associated peptide-1 blocks the effects of corticotropin-releasing factor on reinstatement of cocaine seeking and on cocaine-induced behavioural sensitization
  • Br J Pharmacol , 162(3), 574-83
View Pubmed Publication