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James I Koenig
 

James I Koenig Ph.D.

Academic Title: Adjunct Professor
Primary Appointment: Psychiatry
jkoenig@mprc.umaryland.edu
Location: MPRC,
Phone: (410) 402-7319

Personal History:

My doctoral work in neuroendocrinology was performed at the University of Texas Southwestern Medical School in the laboratory of Dr. Ladislav Krulich.  Our laboratory was a part of the Neuroendocrinology Group headed by Dr. SM McCann.  After receiving my Ph.D. degree in 1983, I did post-doctoral work with Drs. Herbert Meltzer and Gary Gudelsky at the University of Chicago School of Medicine.  My studies as a post-doc included sophisticated neuroendocrine studies of neuropeptide release using hypophysial portal blood collection techniques and evaluating effects of antipsychotic and antidepressant drugs on neuroendocrine endpoints.  After a brief period at Case Western University, I took a faculty position at Massachusetts General Hospital/Harvard Medical School working on hypothalamic neuropeptide systems with Dr. JB Martin.  Much of our work at this time focused on a newly identified peptide called galanin.  In 1994, I spent two years as a program director at the National Science Foundation in Arlington, VA where I directed the Neuroendocrinology and Neuronal and Glial Mechanisms Programs.  Subsequently in 1996, I joined the faculty at the MPRC.  Because of the integrative nature of studying neuropsychiatric disorders, I have been able to use my diverse neuroscience training to probe more deeply into the pathophysiology of schizophrenia and the role of stress in the etiology of the disease.

Research Interests:

The primary focus of my research is the neurobiology of stress. Stress can be loosely defined as the inability of an organism to control its internal or external environment in response to a physical or psychological challenge. This lack of control triggers a series of preprogrammed neurobiological, behavioral and neuroendocrinological responses, which are collectively known as the stress response. Neuropsychiatric disorders, such as depression and schizophrenia, appear to be triggered or exacerbated by inappropriate responses to stress. My laboratory is investigating the neurochemical, neuroanatomical and molecular biological events initiated by stress, to better understand the etiology of schizophrenia and depression. On-going studies utilize modern molecular biological, biochemical and organismal techniques to determine the involvement of neuropeptides and neurotransmitters in the sexually-dimorphic response to stress. Additional studies focus on the effects of stress during development and how this influences adult behaviors.

Lab Techniques and Equipment:

Because of the multidisciplinary approach we are using to study the brain and how stress affects it, an array of biochemical, molecular biological and behavioral techniques are being used.  These techniques include recombinant DNA techniques; DNA microarrays; molecular neuroanatomical techniques, such as in situ hybridization histochemistry; techniques to study proteins, such as RIA and western blotting; and a host of in vivo techniques to investigate behavior especially directed toward social behavior and cognitive function.


Laboratory Personnel:

  • Dana Bell
  • Ashley Holmes
  • Christina Wilson

Publications:

Koenig JI, Kirkpatrick B, Lee P.  Stress and early brain development in schizophrenia.  Neuropsychopharmacology 2002; 27:309-318 (PMID: 12093605).

Lee PR, Brady DL, Shapiro R, Dorsa DA, Koenig JI Prenatal stress induced deficits in social behaviors:  role of central oxytocin.  Brain Res. 2007; 1156:152-167 (PMID: 17540347).

Taylor AR*, Markham JA*, Taylor SB, Brady-Bell D, Koenig JI.  Characterization of the cognitive impairments induced by prenatal exposure to stress in the rat.  Frontiers in Behavioral Neuroscience 2010; 4:173 (* - Co-first authors, PMID: 21151368).

Markham JA, Koenig JI.  Prenatal stress:  Role in psychotic and depressive diseases.  Psychopharmacology (Berl) 2011; 214:89-106 (PMID: 20949351).

Taylor SB, Taylor AR, Markham JA, Koenig JI.  Disruption of the neuregulin 1 gene in the rat alters HPA axis activity and behavioral responses to environmental stimuli.  Physiology and Behavior 2011; 104:205-214 (PMID: 21092742).

Taylor SB, Markham JA, Taylor AR, Kanaskie BZ, Koenig JI.  Sex specific neuroendocrine and behavioral phenotypes in hypomorphic Type II neuregulin 1 rats.  Behavioral Brain Res.  2011; 224:223-232 (PMID: 21620900).

Markham JA, Mullins SE, Koenig JI.  Peri-adolescent maturation of the prefrontal cortex is sex-specific and disrupted by prenatal stress.  J. Comp. Neurol. 2012 (in press; doi: 101002/cne.23262) (PMID: 23172080).

Taylor SB, Taylor AR, Koenig JI.  The interaction of disrupted Type II neuregulin 1 and chronic adolescent stress on anxiety-like behavior in adult rats.  Neuroscience 2012 (doi: 10.1016/j.neuroscience2012.09.045) (PMID: 23022220).

Taylor AR, Taylor SB, Koenig JI.  Specific cognitive deficits in rats with genetically decreased neuregulin 1:  possible relevance for schizophrenia.  Neuroscience Lett. 2012;  531:131-135 (PMID: 23098760).