D. P. Mohapatra, Ph.D.

Associate Professor

Neurosciences Program
Molecular Cell Biology Program
Biochemistry, Biophysics, and Structural Biology Program

  • 314-362-8229

  • 314-362-8244

  • 314-362-8334

  • 8054

  • 5502-CSRB

  • d.p.mohapatra@wustl.edu

  • http://elysium.wustl.edu/mohapatra_lab/mohapatra_lab/Home.html

  • Neuronal Excitability, Ion Channels, GPCR, Membrane Biology, Neurophysiology, Pain, Cancer, Rodent Behavior, Cellular Signaling, Neuroprotection

  • Basic and Translational Pain Biology (Cancer Pain, Neuropathic Pain and Inflammatory Pain)

Research Abstract:

My research group investigates the adaptive and plastic properties of mammalian neurons that are critical to the intrinsic homeostatic control of cellular excitability, neuronal activity and the overall cellular survival process in response to diverse pathological insults. The intrinsic excitability of mammalian neurons reflects the complex but fine interplay between the inward and outward membrane conductance, which underlies the unique electrical activity pattern in individual types of neurons within the central and peripheral nervous system (CNS and PNS). In mammalian nervous system these processes are homeostatically regulated during development and aging, and in response to short- and long-term changes in neuronal activity in the face of sustained alterations in synaptic stimulations, which otherwise could drive the neuronal activity towards extreme excitation or quiescence. These processes are primarily governed by the expression, localization and activity of voltage-gated ion channels. However, the ligand-gated ion channels that are activated by neurotransmitters, second messengers and a number of physiological and pathological mediators bring-in changes in membrane potentials, thereby providing the essential voltage change or electrical trigger to activate the voltage-gated ion channels. In addition to ionic channels, a plethora of plasma membrane receptors, such as G-protein coupled receptors (GPCRs) and growth factor receptors (GFRs), are expressed in mammalian neurons and connective/support cell types in the nervous system. These receptors are activated by endogenous ligands under physiological conditions, resulting in the activation/inhibition of multiple intracellular signaling events that ultimately contribute to cell growth, proliferation/differentiation, migration and survival. However, under pathological conditions over-activation of a majority of such receptor signaling events in neurons and other cells in the nervous system threatens the normal functioning, cellular excitability and overall survival of neurons. Our studies are geared towards studying distinct intrinsic regulatory processes of membrane excitability and cellular survival in neurons at the face of neuropathological insults operating via dynamic intracellular crosstalk between enhanced GPCR/GFR signaling and neuronal ion channel expression/localization/functions. We utilized rodent models of human diseases/pathologies such as metastatic bone cancer pain, inflammatory pain, chronic pain associated with obesity, ischemic stroke-reperfusion injury, and HIV-induced neurodegeneration.

Selected Publications:

Mickle A.D., Shepherd, A.J., Loo L., and Mohapatra D.P.: Induction of thermal and mechanical hypersensitivity by parathyroid hormone-related peptide (PTHrP) through upregulation of TRPV1 function and trafficking. Pain, 2015 [In Press]. PMID: 25970319

Mickle A.D.*, Shepherd, A.J.*, and Mohapatra D.P.: Sensory TRP channels: the key transducers of nociception and pain. Progress in Molecular Biology and Translational Science 131:73-118, 2015. PMID: 25744671

Shepherd A.J., Loo L., and Mohapatra D.P.: Chemokine co-receptor CCR5/CXCR4-dependent modulation of Kv2.1 channel confers acute neuroprotection to HIV-1 glycoprotein gp120 exposure. PLoS ONE 8: e76698, 2013. PMCID: PMC3782454

Sowers L.P., Loo L., Wu Y., Campbell E., Ulrich J.D., Wu S., Paemka L., Wassink T., Meyer K., Bing X., El-Shanti H., Usachev Y.M., Ueno N., Manak J.R., Shepherd A.J., Ferguson P.J., Darbro B.W., Richerson G.B., Mohapatra D.P., Wemmie J.A., and Bassuk A.G. (2013). Disruption of the non-canonical Wnt gene PRICKLE2 leads to autism-like behaviors with evidence for hippocampal synaptic dysfunction. Molecular Psychiatry. Vol. 18(10): 1077-1089, 2013. PMCID: PMC4163749

Shepherd A.J., Loo L., Gupte R.P., Mickle A.D., and Mohapatra D.P.: Distinct modifications in Kv2.1 channel via chemokine receptor CXCR4 regulate neuronal survival-death dynamics. Journal of Neuroscience 32(49):17725-17739, 2012. PMCID: PMC3544972

Loo L., Shepherd A.J., Mickle A.D., Lorca R.A., Shutov L., Usachev Y.M., and Mohapatra D.P.: The C-type natriuretic peptide induces thermal hyperalgesia through a non-canonical Gβγ-dependent modulation of TRPV1 channel. Journal of Neuroscience 32(35):11942-11955, 2012. PMCID: PMC3461320

Bocksteins E., Labro A.J., Snyders D.J., and Mohapatra D.P. (2012). The electrically silent Kv6.4 subunit confers hyperpolarized gating charge movement in Kv2.1/Kv6.4 heterotetrametic channels. PLoS One. Vol. 7(5): e37143, 2012. PMCID: PMC3462578

Shepherd A.J., and Mohapatra D.P. (2012). Tissue preparation and immunostaining of mouse sensory nerve fibers innervating skin and limb bones. Journal of Visualized Experiments. Vol. 59, e3485, 2012. PMCID: PMC3355112

Kalashnikova E., Lorca, R.A., Li B.H., Kaur I., Ishimaru T., Trimmer J.S., Mohapatra D.P., and Diaz E.D.: SynDIG1: a novel activity regulated postsynaptic protein that directs formation of AMPA receptor containing synapses. Neuron 65(1):80-93, 2010. PMCID: PMC2822728

Last Updated: 5/25/2017 9:14:33 AM

Human Dorsal Root Ganglia Tissue Section Showing CGRP-labeled Sensory Neurons and Nerve Fibers (in red)
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