My interest in Neuroscience developed while carrying out electron microscopical studies comprising my M.Sc. studies at the University of Western Ontario. Subsequently during Ph.D. research at York University in Toronto, I utilized electrical stimulation of nervous tissue to increase neurohormone release as studied ultrastructurally and biochemically. From these studies I decided to learn more about neurophysiological techniques as research tools. As a post-doc at the Tulane Medical School with Dr. Ed Dudek, I studied the electrophysiology of mammalian neuroendocrine cells and used live hippocampal slices to examine electrotonic coupling among neurons.
My lab is currently demonstrating that our higher brain is susceptible to global ischemia, while our brainstem is dramatically resistant, despite the fact that all regions are equally lose their blood flow http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0096585. This provides an explanation as to why the brain-injured patient often enters a `persistent vegetative state`: the subject is left with only a functioning hypothalamus and brainstem and so is awake but not aware. We propose that this is because the higher brain has developed a `shutdown` mode (i.e., spreading depolarization) to bypass epileptiform and seizure activity immediately following brain injury. This induces a lie-low response to brain injury that has several advantageous. For example, movement attracting attention immediately post-injury is suppressed.
Most recently we are carrying out single cnannel recordings in mammalian neurons undergoing ischemia to discover the fundamental molecular mechanisms underlying acute neuronal death that can quickly develop following spreading depolarization.