Donald Kuhn, Ph.D.

Position Title

Professor

Office Address

John D. Dingell VA Medical Center
Research & Development Service
4646 John R
Detroit, MI 48201

Office Phone

313-576-4457

Biography

Dr. Kuhn is a Professor of Psychiatry and Behavioral Neurosciences and a VA Research Career Scientist. Research in the Kuhn laboratory has been funded by the National Institutes of Health, Department of Veterans Affairs and the Department of Defense. Dr. Kuhn continues to serve on numerous federal grant review committees and he is called on frequently to review submitted manuscripts for numerous peer reviewed neuroscience journals.

Education Training

  • Presbyterian College, Clinton, SC, BS (Biopsychology), 1972
  • University of South Carolina, Columbia, SC, PhD (Behavioral Pharmacology), 1976

Postgraduate Training

  • Postdoctoral Fellow, Princeton University, Princeton, NJ, 1976-1977
  • Staff Fellow, Section on Biochemical Pharmacology, National Institutes of Health, Intramural Research Program, Bethesda, MD, 1977-1986

Research Interests

Neurobiology
  • Damage to the brain caused by injury, drugs and disease (e.g., Parkinson’s disease) and the resultant neuropsychiatric outcomes. Research in this area concentrates on repetitive, mild traumatic brain injury using an animal model that simulates head impacts sustained by athletes. This model imparts results in little or no evidence of behavioral or neuropathological dysfunction acutely. However, with the passage of time, significant alterations in behavior (e.g., psychiatric-like conditions) and neuropathology (e.g., chronic traumatic encephalopathy or CTE; increases in reactive gliosis and neuroinflammation). This model is being used to study therapeutic interventions that can delay or prevent the delayed and progressive emergence of behavioral dysfunction and CNS damage after repetitive, mild head impacts. Our laboratory also studies the neuropharmacological and neurochemical effects of the neurotoxic amphetamines (e.g., methamphetamine, MDMA) and the synthetic cathinone drugs (e.g., mephedrone, methcathinone). These two classes of drugs share significant structural similarities yet one class causes neurotoxicity (methamphetamine and related drugs) whereas the other (cathinone related drugs) do not. A wide variety of approaches is used to increase the understanding of the neuronal damage caused by these drugs of abuse. Last, we study the non-motor symptoms of Parkinson’s disease using various animal models that reflect the CNS pathology of this neurodegenerative condition to include its characteristic psychiatric-like symptoms (e.g., depression, obsessive-compulsive disorder, cognitive decline).
  • Studies on the role of the neurotransmitter serotonin in neuropsychiatric conditions, neurochemistry and physiology. We have developed a knockout mouse lacking the gene for tryptophan hydroxylase 2 (TPH2), the enzyme responsible for the synthesis of serotonin in brain, to facilitate studies of the role of serotonin in neurodevelopmental disorders such as autism. In addition, the TPH2 knockout mouse has opened numerous avenues of translational study into behavioral dysfunction to include depression, OCD, impulsivity/disinhibition and aggression. Using both constitutive and inducible (i.e., tamoxifen-induced) knockout models, we study the role of serotonin in behavior using extensively validated tests of psychiatric-like conditions across the life-span.
  • The gut microbiome and gut-brain axis communication. Our laboratory was recently funded to purchase an Illumina MiSeq system to study the gut microbiome. We are using 16S rRNA sequencing to analyze how psychiatric drugs and drugs of abuse alter the diversity and composition of the microbiota. In addition, our laboratory is also investigating how the gut microbiome, as well as altered communication along the gut-brain axis, contributes to psychiatric conditions like depression and PTSD. Finally, we are focusing attention on Gulf War Illness. This chronic disorder is characterized by both CNS and gastrointestinal symptoms that may reflect a dysbiosis in the gut microbiome. Using a mouse model of Gulf War Illness, we are observing significant alterations in the gut microbiome and its metabolomics profile. These alterations open new avenues of research into the use of probiotics and microbiota transfer to treat Gulf War Illness and the psychiatric conditions associated with it.

     

Clinical/Research Interests

  • Delirium
  • Gulf War Illness

Publications

Complete List of Published Work in MyBibliography

 

 

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