Volker Neugebauer, M.D., Ph.D., Professor and Vice Chair
- Director, Neuroscience Graduate Program
- Affiliations: Department of Neuroscience & Cell Biology
- Route: 1069, 2.104-D Medical Research Building (MRB)
- Tel: (409) 772-5259
- Fax: (409) 762-9382
- Neugebauer CV
Volker Neugebauer, M.D., Ph.D.
M.D., University of Wuerzburg,
Ph.D. (equivalent, Physiology), University of Wuerzburg, Germany, 1992
Internship, University of Wuerzburg, Germany, 1991-1992
Postdoctoral Fellowship, Physiology, University of Wuerzburg, Germany, 1992-1995
Postdoctoral Fellowship, Pharmacology, UTMB, 1995-1997
Postdoctoral Fellowship, Neuroscience, UTMB, 1997-1998
Emotional-affective and cognitive brain functions. The focus of my research over the past two decades has been on synaptic and cellular neuroplastic changes in higher brain functions and dysfunctions. Of particular interest are neurobiological mechanisms of emotional-affective and cognitive behaviors related to pain and neuropsychiatric disorders. Pain research is a prime example of the translational potential of basic science because of its clinical significance and usefulness for mechanistic studies of higher brain functions. The close interaction between pain and anxiety/depression is clinically relevant but poorly understood. Pain can also impair cognitive functions and in turn is modulated by cognitive processes, but the underlying mechanisms are largely unknown. Thus, there is a need for the study of cellular and molecular brain mechanisms, utilizing expertise from outside the field. As a consequence, collaborations have expanded our pain-research program into studies of brain mechanisms of neurodegenerative disorders, depression and drug addiction.
Accomplishments. Our work pioneered the field of pain-related neuroplasticity in the amygdala, a brain center for emotions. In recent years our attention turned to the interactions between the amygdala and cortical areas such as the medial prefrontal cortex. We showed that abnormal amygdala activity in pain impairs mPFC function, causing cognitive deficits. In turn, failure to engage cortical control of the amygdala allows the persistence of pain and its transition to a chronic state. The mechanistic analysis of emotional-affective and cognitive brain mechanisms of pain is a key contribution of our work to the field of pain research and neuroscience. Collaborative research projects on neuropsychiatric disorders (neurodegenerative disorders, depression and drug addiction) focus on neural mechanisms of cognitive dysfunctions and long-term synaptic plasticity in affected brain areas such as the amygdala, hippocampus, striatum and prefrontal cortex. Our research projects use an integrative approach of state-of-the-art electrophysiology, optogenetics, live cell imaging, innovative behavioral assays, and pharmacology for the mechanistic analysis of neuroplasticity and nervous system disorders.
Goals. The overall goal of our research program is the better understanding of brain plasticity and homeostatic imbalance in clinically relevant disorders. We are particularly interested in cortico-limbic interactions that play an important role in the cognitive control of emotions and in emotional influences on cognitive functions. The better understanding of higher brain functions and dysfunctions in pain and neuropsychiatric disorders is an important benefit to medical school education and graduate training. It also provides exciting opportunities for interdisciplinary collaborations.
Ren, W., Kiritoshi, T., Grégoire, S., Ji, G., Guerrini, R., Calo, G, and Neugebauer, V. Neuropeptide S: a novel regulator of pain-related plasticity in the amygdala and behaviors. J. Neurophysiol., 2013. PMID: 23883857 (in press).
Grégoire, S. and Neugebauer, V. 5-HT2CR blockade in the amygdala conveys analgesic efficacy to SSRIs in a rat model of arthritis pain. Mol. Pain 9:41-52, 2013. PMID: 23937887. PMC3751088.
Ji, G., Fu, Y., Adwanikar, H. and Neugebauer, V. Non-pain-related CRF1 activation in the amygdala facilitates synaptic transmission and pain responses. Mol. Pain 9:2-17, 2013. PMID: 23410057. PMC3583817.
Kiritoshi, T., Sun, H., Ren, W., Stauffer, S.R., Lindsley, C.W., Conn, P.J. and Neugebauer, V. Modulation of pyramidal cell output in the medial prefrontal cortex by mGluR5 interacting with CB1. Neuropharmacology 66:170–178, 2013. PMID: 22521499. PMC3568505.
Ji, G. and Neugebauer, V. Modulation of medial prefrontal cortical activity using in vivo recordings and optogenetics. Mol. Brain 5:36-45, 2012. [Identified as “Highly accessed”]. PMID: 23044043. PMC3565915.
Ji, G. and Neugebauer, V. Pain-related deactivation of medial prefrontal cortical neurons involves mGluR1 and GABAA receptors. J. Neurophysiol. 106:2642-2652, 2011. PMID: 21880942. PMC3214095
Sun, H. and Neugebauer, V. mGluR1, but not mGluR5, activates feed-forward inhibition in the medial prefrontal cortex to impair decision-making. J. Neurophysiol. 106:960-973, 2011. PMID: 21613584. PMC3154822.
Li, Z., Ji, G. and Neugebauer, V. Mitochondrial reactive oxygen species are activated by mGluR5 through IP3 and activate ERK and PKA to increase excitability of amygdala neurons and pain behavior. J. Neurosci. 31:1114-1127, 2011. PMID: 21248136. PMC3073477.
Ji, G. and Neugebauer, V. Reactive oxygen species are involved in group I mGluR-mediated facilitation of nociceptive processing in amygdala neurons. J. Neurophysiol. 104:218-229, 2010. PMID: 20463194. PMC2904214.
Ji, G., Sun, H., Fu, Y., Li, Z., Pais-Vieira, M., Galhardo, V. and Neugebauer, V. Cognitive impairment in pain through amygdala-driven prefrontal cortical deactivation. J. Neurosci. 30: 5451–5464, 2010. PMID: 20392966. PMC2868074.
Neugebauer, V., Galhardo, V., Maione, S. and Mackey, S.C. Forebrain Pain Mechanisms. Brain Res. Rev. 60:226-242, 2009. PMID: 19162070. PMCID: PMC2700838.
Pernía-Andrade, A.J., Kato, A., Witschi, R., Nyilas, R., Katona, I., Freund, T.F., Watanabe, M., Filitz, J., Koppert, W., Schüttler, J., Ji, G., Neugebauer, V., Marsicano, G., Lutz, B., Vanegas, H., Zeilhofer, H.U. Spinal endocannabinoids and CB1 receptors mediate C-fiber-induced heterosynaptic pain plasticity. Science 325:760-764, 2009. [Editor’s Choice, P. R. Stern, Plastic Pain Perception. Sci. Signal. 2, ec269 (2009) and featured in M.J. Christie and C. Mallet, Sci. Signal. 2: ep57 (2009)]. PMID: 19661434. PMC2835775.
Ji, G. and Neugebauer, V. Hemispheric lateralization of pain processing in amygdala neurons. J. Neurophysiol. 102:2253-2264, 2009. PMID: 19625541. PMC2776996.
Fu, Y. and Neugebauer, V. Differential mechanisms of CRF1 and CRF2 receptor functions in the amygdala in pain-related synaptic facilitation and behavior. J. Neurosci. 28:3861-3876, 2008. PMID: 18400885. PMC2557030.
Ji, G. and Neugebauer, V. Differential effects of CRF1 and CRF2 receptor antagonists on pain-related sensitization of neurons in the central nucleus of the amygdala. J. Neurophysiol. 97: 3893-3904, 2007. PMID: 17392412.
Li, W. and Neugebauer, V. Differential changes of group II and group III mGluR function in central amygdala neurons in a model of arthritic pain. J. Neurophysiol. 96: 1803-1815, 2006. PMID: 16760343.
Han, J.S., Li, W. and Neugebauer, V. Critical role of CGRP1 receptors in the amygdala in synaptic plasticity and pain behavior. J. Neurosci. 25:10717-10728, 2005. PMID: 16291945.
Bird, G.C., Lash, L.L., Han, J.S., Zou, X., Willis, W.D. and Neugebauer, V. PKA-dependent enhanced NMDA receptor function in pain-related synaptic plasticity in amygdala neurons. J. Physiol. 564.3:907–921, 2005. PMID: 15760935. PMC1464474.
Neugebauer, V., Li, W., Bird G.C. and Han, J.S. The amygdala and persistent pain. The Neuroscientist 10: 221-234, 2004. PMID: 15155061.
Neugebauer, V., Li., W., Bird, G.C., Bhave, G. and Gereau, R.W. Synaptic plasticity in the amygdala in a model of arthritic pain: differential roles of metabotropic glutamate receptors 1 and 5. J. Neurosci. 23:52-63, 2003. PMID: 12514201.