515-271-1089 (Office Phone)
Dr. Duric received a PhD in Pharmacology from the University of Kansas Medical Center (KUMC) in Kansas City under the mentorship of Dr. Kenneth McCarson in the field of Pain Neurobiology (2000-2005). His predoctoral work focused on characterization of brain events that link chronic pain state and development of comorbid mood disorders such as the major depression. In 2006, Dr. Duric completed a one year postdoctoral fellowship in Neurophysiology with Dr. Randy Nudo at the KUMC studying brain stroke in squirrel monkeys. From 2007 through 2012, Dr. Duric completed a second postdoctoral fellowship in Molecular Psychiatry with Dr. Ronald Duman at the Yale University School of Medicine focusing on neurobiology of stress and mood disorders, including genetic analysis of human depressed brains. In 2012, Dr. Duric joined the faculty in the Department of Physiology and Pharmacology at Des Moines University, where he currently utilizes a variety of biochemical, pharmacological and preclinical behavioral approaches to study neural mechanisms that underlie the development and treatment of depression as well as its comorbidity with other neurological and physical illnesses.
|Postdoctoral training: Molecular Psychiatry, Yale University School of Medicine, 2007-2012|
|Postdoctoral training: Neurophysiology, University of Kansas Medical Center, 2006|
|Ph.D., Pharmacology, University of Kansas Medical Center, 2005|
|B.A., Biochemistry and Chemistry, Gustavus Adolphus College, 2000|
Depression is one the most common and debilitating psychiatric disorders that affects up to 17% of U.S. population and is one of the leading causes of long-term disability worldwide. Clinically, depression is characterized as a heterogeneous mental illness associated with a broad range of symptoms such as excessive sadness, despair, inability to experience pleasure (i.e., anhedonia), alterations in cognition, sleep, and appetite. The etiology of depression and the underlying brain events are not well understood, however, they are thought to involve a combination of environmental (e.g., stress or trauma) and genetic factors that result in functional and structural abnormalities of several brain regions that regulate mood and cognitive function (e.g., hippocampus, prefrontal cortex).
Our current research is directed towards characterization of central nervous system (CNS) mechanisms including changes in intracellular signaling and synaptic plasticity that are relevant to depressed state. We are particularly interested in studying the role of phosphatase enzymes such as MKP-1, which are powerful negative regulators of cellular pathways responsible for development, growth and survival of neurons. Activity of MKP-1 is robustly increased in the brains of depressed human subjects and rodents exposed to chronic stress, which, in part, may contribute to atrophy and loss of function observed in these brains. Through utilization of a variety of cellular, molecular and pharmacological approaches in combination with preclinical behavioral models, the overall goal of this research is to identify potential biomarkers and promising new drug targets for treating depression and possibly other mood disorders.
In addition, we are also interested in studying neural mechanisms linking depression and other CNS illnesses, such as chronic pain. Clinical reports indicate that over 50% of patients suffering from chronic pain also express clinically diagnosable symptoms of depression. Like depression, chronic pain is not a single disease as it spans a broad spectrum of pathophysiological and psychological etiologies that may result from activation of brain areas that regulate the cognitive and emotional aspects of pain. This idea is further supported by our previous studies showing that chronic pain mimics stress-like molecular and cellular alterations in the CNS, such as attenuation of the rate of production of new neurons (i.e., neurogenesis) in the hippocampus of an adult rat brain. Our current research is focused on elucidating common neural mechanisms linking chronic pain conditions and depression, in particular, the role of immune-inflammatory reactions. The results of this project may ultimately contribute towards the development of new clinical strategies to prevent or diminish the mental health consequences of chronic pain.
- Jeanneteau F, Barrere C, Vos M, De Vries CJM, Rouillard C, Levesque D, Dromard Y, Duric V, Franklin TC, Duman RS, Lewis DA, Ginsberg SD, Arango-Lievano M. Stress-driven adaptation of pyramidal neurons via the nuclear receptor NR4A1 pathway leads to mitochondrial uncoupling and dendritic spine loss (2018). Journal of Neuroscience 7;38(6):1335-1350.
- Banasr M, Lepack A, Fee C, Duric V, Maldonado-Aviles JG, DiLeone R, Sibille E, Duman RS, Sanacora GS. Characterization of GABAergic marker expression in the chronic unpredictable stress model of depression (2017). Chronic Stress [Epub Aug 2017].
- Duric V, Banasr M, Franklin T, Lepack A, Adham N, Kiss B, Gyertyan I, Duman RS. Cariprazine exhibits anxiolytic and dopamine D3 receptor-dependent antidepressant effects in the chronic stress model (2017). International Journal of Neuropsychopharmacology 20(10):788-796.
- Yuan LL, Wauson E, Duric V. Kinase-mediated signaling cascades in mood disorders and antidepressant treatment (2016). Journal of Neurogenetics 30(3-4): 178-184.
- Duric V, Clayton S, Leong ML, Yuan LL. Comorbidity factors and brain mechanisms linking chronic stress and systemic illness (2016). Neural Plasticity 2016:5460732 [Epub Feb 2016].
- Iwata M, Ota KT, Li XY, Sakaue F, Li N, Dutheil S, Banasr M, Duric V, Yamanashi T, Kaneko K, Rasmussen K, Glasebrook A, Koester A, Song D, Jones KA, Zorn S, Smagin G, Duman RS. Psychological Stress Activates the Inflammasome via Release of Adenosine Triphosphate and Stimulation of the Purinergic Type 2X7 Receptor (2016). Biological Psychiatry 80(1): 12-22.
- Licznerski P, Duric V, Banasr M, Alavian KN, Ota KT, Kang HJ, Jonas EA, Ursano R, Traumatic Stress Brain Study Group, Krystal JH, Duman RS. Decreased SGK1 expression and function contributes to behavioral deficits induced by traumatic stress (2015). PLOS Biology 13(10): e1002282.
- Ota KT, Liu R-J, Voleti B, Maldonado-Aviles JG, Duric V, Iwata M, Dutheil S, Duman C, Boikess S, Lewis DA, Stockmeier CA, DiLeone RJ, Rex C, Aghajanian GK, Duman RS. REDD1 is essential for stress-induced synaptic loss and depressive behavior (2014). Nature Medicine 20(5): 531-5.
- Duric V and Duman RS. Depression and treatment response: dynamic interplay of signaling pathways and altered neural processes (2013). Cellular and Molecular Life Sciences 70(1): 39-53.
- Duric V, Banasr M, Stockmeier CA, Simen AA, Newton SS, Overholser JC, Jurjus GJ, Dieter L, Duman RS. Altered expression of synapse and glutamate related genes in post-mortem hippocampus of depressed subjects (2013). International Journal of Neuropsychopharmacology 16(1): 69-82.
- Elsayed M, Banasr M, Duric V, Fournier NM, Licznerski P, Duman RS. Antidepressant effects of fibroblast growth factor-2 in behavioral and cellular models of depression (2012). Biological Psychiatry 72(4): 258-65.
- Duman RS, Li N, Liu RJ, Duric V, Aghajanian G. Signaling pathways underlying the rapid antidepressant actions of ketamine (2011). Neuropharmacology 62(1): 35-41.
- Duric V, Banasr M, Licznerski P, Schmidt HD, Newton SS, Stockmeier CA, Simen AA, Duman RS. A negative regulator of MAP kinase causes depressive behavior (2010). Nature Medicine 16(11): 1328-32.
- Okamoto H, Voleti B, Banasr M, Sarhan M, Duric V, Girgenti MJ, DiLeone R, Newton SS, Duman RS. Wnt2 expression and signaling is increased by different classes of antidepressant treatments (2010). Biological Psychiatry 68(6): 521-527.
- Dancause N, Duric V, Barbay SH, Frost SB, Stylianous A, Nudo RJ. An additional motor-related field in the lateral frontal cortex of monkeys (2008). Cerebral Cortex 18(12): 2719-28.
- Duric V and McCarson KE. Hippocampal mechanisms linking chronic pain and depression (2008). Journal of Neuropathic Pain & Symptom Palliation 2(4): 15-32.
- Duric V, McCarson KE. Neurokinin-1 (NK-1) receptor and brain-derived neurotrophic factor (BDNF) gene expression is differentially modulated in the rat nociceptive sensory and affective systems during inflammatory pain (2007). Molecular Pain 3 (32): 1-9.
- Duric V and McCarson KE. Effects of analgesic or antidepressant drugs on pain- or stress-evoked hippocampal and spinal neurokinin-1 (NK-1) receptor and brain-derived neurotrophic factor (BDNF) gene expression in the rat (2006). Journal of Pharmacology and Experimental Therapeutics 319 (3): 1235-43.
- Duric V and McCarson KE. Persistent pain produces stress-like alterations in hippocampal neurogenesis and gene expression (2006). Journal of Pain 7 (8): 544-55.
- McCarson KE, Duric V, Reisman SA, Winter M, Enna SJ. GABAB receptor function and subunit expression in the rat spinal cord as indicators of stress and the antinociceptive response to antidepressants (2006). Brain Research 1068 (1): 109-17.
- Duric V and McCarson KE. Hippocampal neurokinin-1 receptor and brain-derived neurotrophic factor gene expression is decreased in rat models of pain and stress (2005). Neuroscience 133 (4): 999-1006.
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