SOM Faculty Profile : James I Koenig

James I Koenig

James I Koenig Ph.D.

Academic Title: 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 Brady

Jill Sharifi

Adam Taylor

Publications

Lee PR, Brady D, Shapiro RA, Dorsa DM, Koenig JI. Prenatal stress generates deficits in rat social behavior: reversal by oxytocin. Brain Res. 2007; 1156:152-167.

Silverman JL, Koenig JI. Evidence for involvement of ER-Î² and RGS9-2 in 17-Î² estradiol enhancement of amphetamine-induced place preference behavior. Hormones and Behavior 2007; 52:146-155.

Koenig JI. Schizophrenia: a new translational opportunity in behavioral neuroendocrinology. Hormones & Behavior 2006; 50; 602-611.

Lee PR, Brady D, Shapiro RA, Dorsa DM, Koenig JI. Social interaction deficits caused by chronic phencyclidine administration are reversed by oxytocin Neuropsychopharmacology 2005; 30:1883-1894.

Koenig JI, Elmer GI, Shepard P, Lee PR, Mayo C, Joy B, Hercher E, Brady D. Stress during gestation produces alterations in adult rat behavior: relevance to schizophrenia.Behav. Brain Res. 2005; 156:251-261.

Sharifi JL, Koenig JI. Regulators of G-protein signaling (RGS) mRNA expression in nucleus accumbens is controlled by estrogen and drugs of abuse. Neuroreport 2004; 15:2433-2436.

Sarpal D, Koenig JI, Adelman JP, Brady D, Clerkin L, Shepard PD. Regional distribution of SK3 mRNA-containing neurons in the adult and adolescent rat ventral midbrain and their relationship to dopamine-containing cells. Synapse 2004; 53:104-113.

Kinnunen A, Koenig JI, Bilbe G. Analysis of differential gene expression in the rat brain induced by prenatal stress. J. Neurochemistry 2003; 86:736-742.

Lee PR, Brady DB, Koenig JI. Corticosterone affects NMDA receptor expression before the onset of puberty. Mol. Brain Res. 2003;115:55-62.

Lee PR, Koenig JI. Thyroid hormone regulation of NMDA receptor subunit expression in adult brain. J. Neuroendocrinology., 2003; 15:87-92

Koenig JI, Kirkpatrick B, Lee P. Glucocorticoid hormones and early brain development in schizophrenia. Neuropsychopharmacology 2002; 27:309-318 (available on line at www.acnp.org).

Arango C, Kirkpatrick B, Koenig JI. Stress, hippocampal neuronal turnover and neuropsychiatric disorders. Schizophrenia Bull., 2001; 27:477-480.

Nillni EA, Bartnick A, Aird F, Seidah NG, Todd RB, Koenig JI. PreproTRH178-199 and two novel peptides (PFQ7 and PSE14) derived from its processing, which are produced in the paraventricular nucleus of the rat brain, are regulated during suckling. Endocrinology 2001; 142:896-906.

Faculty members: Click here to update your contact information and create a profile.