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Dr. Mark D. Womble

Dr. Mark D. Womble
Professor
Anatomy and Physiology
Graduate Program Director

330-941-4727
mdwomble AT ysu DOT edu
WBSH 4063

B.S.   Texas Christian University, 1975
M.S.   University of Kentucky, 1978
Ph.D.  University of Michigan, Anatomy and Cell Biology, 1983


 

Research Interests

Neurons display a wide variety of ion channels that selectively allow charged ions (K+, Na+, Ca+2, Cl-) to cross the cell membrane. These channels open or close in response to a variety of influences, including membrane potential (voltage), the binding of neurotransmitters or other chemical messengers to cell surface receptors, or activation of intracellular signal transduction (2nd messenger) systems. The primary regulators of neuronal activity are thus the particular population of ion channels expressed by an individual neuron, and the functional behavior (open vs. closed) of these channels on a moment to moment basis.

As a cellular neurophysiologist, my primary interest is the mechanisms by which neurotransmitters, hormones, or drugs act to modulate ion channel activity and thus alter neuronal firing behavior. This work utilizes the whole-cell patch-clamp recording technique to monitor the electrical responses from an individual neuron. With this technique, not only can the resting potential and action potentials be recorded, but different ionic conductances may also be isolated and individually examined.

My projects at YSU utilize acutely isolated neurons from bullfrog sympathetic ganglia. These cells are easy to obtain and may be used immediately or maintained in culture for several days. One ionic conductance found in these cells is a voltage-gated K+ current known as the M-current. This current is an important regulator of the resting potential and action potential firing behavior not only in bullfrog neurons, but also in a wide variety of peripheral and central mammalian neurons. Current or recent projects in my lab have examined the modulation of the M-current by the neurotransmitter Substance P or the anti-convulsant drug Retigabine.

Another project involves the identification and biophysical characterization of all of the ionic conductances expressed by bullfrog neurons and the determination of how these contribute to the control of neuronal activity. The data obtained from neurophysiological experiments in my lab will be utilized to construct a mathematical model of the neuron. This work is part of the MBUR (Math and Biology Undergraduate Research) project and is being done in collaboration with Dr. Jalics of the Department of Mathematics and Statistics at YSU.

I also collaborate with Dr. Simmons in the Department of Integrated Medical Sciences at the Northeastern Ohio Universities College of Medicine (NEOUCOM). Work in his laboratory examines the actions of the neurotransmitter Neurokinin B on neurons of the mammalian prefrontal cortex. This neurotransmitter induces depolarization and increased action potential firing and I am investigating the ionic conductances and intracellular pathways involved in this modulation.

Selected Publications

Riblet, R., Kaur, A., Kaur, H., and Womble, M.D. (2008). The anticonvulsant drug retigabine enhances M-current and reduces neuronal excitability in bullfrog sympathetic neurons. BIOS (submitted).

Womble, M.D., Andrews, J.A., and Crook, J.J. (2002). 17-ß Estradiol reduces excitatory postsynaptic potential (EPSP) amplitude in rat basolateral amygdala neurons. Neuroscience Letters 331: 83-86.

Mark D. Womble and Gary R. Walker (2001). Teaching Biology to a Visually Impaired Student. Journal of College Science Teaching 30(6):394-396

Womble, M.D. (1999). Anatomy and computers: A new twist to teaching the oldest medical course. Bioscene: Journal of College Biology Teaching 25: 15-17.

Moises, H.C., Womble, M.D., Washburn, M.S. & Williams, L.R.(1995). Nerve growth factor facilitates cholinergic neurotransmission between nucleus basalis and the amygdala: An electrophysiological study. Journal of Neuroscience 15: 8131-8142.

Womble, M.D. and Moises, H.C. (1994). Metabotropic glutamate receptor agonist ACPD inhibits some, but not all, muscarinic-sensitive K+ conductances in basolateral amygdaloid neurons. SYNAPSE 17: 69-75.

Womble, M.D. and Moises, H.C. (1993). Hyperpolarization-activated currents in neurons of the rat basolateral amygdala. Journal of Neurophysiology 70: 2056-2065.

Womble, M.D. and Moises, H.C. (1993). Muscarinic modulation of conductances underlying the afterhyperpolarization in neurons of the rat basolateral amygdala. Brain Research 621: 87-96.

Womble, M.D. and Moises, H.C. (1992). Muscarinic inhibition of M-current and a potassium leak conductance in neurons of the rat basolateral amygdala. Journal of Physiology 457: 93-114.

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