ºù«ÍÞÊÓƵ

Daniel Barth is professor of neuroscience in the Department of Psychology. He received his Ph.D. in psychology from the University of California at Los Angeles and was a faculty member in their Department of Neurology before moving to the University of Colorado in 1990.

Dr. Barth is a member of a number of professional organizations in neuroscience. He has served as a member and chair of various committees for the National Institutes of Health and the National Science Foundation. He has also served as peer reviewer for these organizations, as well as numerous other national and international funding agnecies and professional journals.

Dr. Barth's primary research interests are in the electrophysiology and neurophysiology of sensory systems, as well as the neural mechanisms controlling brain excitability, particularly as it applies to the treatment of human epilepsy. He is currently working on three research projects. The first examines the cellular basis and functional significance of fast electrical oscillations in the sensory cortex. The second is concerned with areas of cerebral cortex uniquely dedicated to combining information from different sensory modalities. Finally, Dr. Barth is conducting a collaborative study with doctors at the Denver Health Sciences Center to use high speed computers for the detection and treatment of epileptic seizures in humans.

Selected Publications:

Alem, O., Benison, A.M., Barth, D.S., Kitching, J. and Knappe, S. Magnetoencephalography of epilepsy with a microfabricated atomic magnetrode. J. Neurosci. 2014, 34(43):14324-14327.

Rodgers, K.M., Dudek, F.E. and Barth, D.S. Progressive, seizure-like, spike-wave discharges are common in both injured and uninjured Sprague-Dawley rats: Implications for the fluid percussion injury model of post-traumatic epilepsy. J. Neurosci. 2015, 35(24):9194-9204.

Bercum, F.M, Rodgers, K.M., Benison, A.M., Smith, Z.Z., Taylor, J., Kornreich, E., Grabenstatter, H.L., Dudek, F.E. and Barth, D.S. Maternal stress combined with terbutaline leads to comorbid autistic-like behavior and epilepsy in a rat model. .J. Neurosci. 2015, 35(48): 15894-15902.