Mark D. Womble Dr. Mark D. Womble

Associate Professor
Anatomy and Physiology Division
Dept. of Biological Sciences
Youngstown State University
Youngstown, OH 44555-3601
Phone: (330) 941-4727
E-mail: mdwomble@cc.ysu.edu

Education

Courses I Teach

Research

Dr. Womble at his physiology recording rig. The cellular and molecular mechanisms of learning and memory formation in the mammalian brain are just beginning to be understood. One of the most important brain neurotransmitters in relation to learning and memory is acetylcholine. Much of my work has concentrated on the mechanisms by which neuronal functioning is altered by acetylcholine. This work is broadly related to Alzheimer's disease, a neurodegenerative disorder in which there is a specific and progressive loss of acetylcholine-releasing neurons. The resulting disruption of cholinergic functioning may underlie the memory loss and other cognitive and emotional dysfunctions associated with this disease.

Recently, steroid hormones have also been found to have actions in the brain related to memory. Clinical evidence indicates that estrogen may enhance memory formation and help protect against Alzheimer's disease, while stress hormones such as cortisol may promote forgetting.

My research utilizes intracellular electrophysiological techniques to investigate how neurotransmitters or steroid hormones generate changes in neuronal activity during memory formation. Ongoing projects in my laboratory are investigating the mechanisms by which neurotransmitters, such as acetylcholine or norepinephrine, or steroid hormones, such as estrogen or cortisol, have on the cellular and molecular mechanisms of neuronal functioning.

Selected Publications

Moises, H. C., and Womble, M. D. 1995. Acetylcholine operated ionic conductances in central neurones. In: CNS Neurotransmitters and Neuromodulators: Acetylcholine, T. W. Stone, ed., CRC Press, Boca Raton, FL, pp. 129-148.

Moises, H. C., M. D. Womble, M. S. Washburn, & L. R. Williams. 1995. Nerve growth factor facilitates cholinergic neurotransmission between nucleus basalis and the amygdala: An electrophysiological study, Journal of Neuroscience 15:831-842.

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

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

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

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