Michael I. Sandstrom is a professor in both Psychology and the Neuroscience Program. He joined the faculty of the Central Michigan University Psychology Department in Spring 2004. Before that he held a postdoctoral position at Indiana University, Bloomington campus since receiving his Ph.D. in Neuroscience from Ohio State University in 1998.
Dr. Sandstrom's research interests focus on the physiological side of behavioral neuroscience. Specifically, experiments explore mechanisms that underlie plasticity and recovery of the mammalian brain following neuronal deterioration-induced deficits that disrupt behavior. Most of Dr. Sandstrom's earlier work has explored compensatory changes in basal ganglia function related to either Parkinson's disease (PD) or Huntington's disease (HD) using animal models. While the behavioral deficits in movement and cognition are a hallmark of the psychological attributes, Dr. Sandstrom is far more focused on the underlying physiological mechanisms that both generate disrupted neuronal activity and engage restorative actions in his explorations, as neuronal modifications are likely precursors to outward behavior restoration. Currently, Dr. Sandstrom is processing the nature of stem cell-supported recovery. To this end, he renders stem cells into dopaminergic neural cells using sophisticated in-vitro techniques. These dopaminergic cells then are transplanted, incorporate themselves into the network of the dorsal striatum of rats modeling PD (following removal of their natural dopamine innervation), and support improved movement capacities among transplant recipients (yet with notable limits). Dr. Sandstrom's lab recognizes that while cerebral dopamine restoration is crucial in this disease, temporal control of dopamine release may be necessary for circumstantial behavioral control. Experiments utilizing optogenetics to provide a means of stimulating transplanted dopaminergic cells in awake unrestrained animals are being used to explore this notion. Other techniques include in-vivo microdialysis, single unit electrophysiology, iontophoresis, local intracranial infusions, immunohistochemistry, and sophisticated molecular and neurochemical analysis strategies.
Wolfram, A.M., Altemus, M., Wickwire, J.H., (2014) Presymptomatic Glutamate levels in Prefrontal Cortex in the Hdh(CAG150) Mouse Model of Huntington's Disease, Journal of Huntington's Disease, 3(4), 387-99; doi: 10.3233/JHD-140114.
Sandstrom, M.I., Steffes, S.K., Jayaprakash, N., Wolfram-Aduan, A., and Dunbar, G.L., Book Chapter: Early Dysfunction of Neural Transmission and Cognitive Processing, in Huntington’s Disease, In Huntington’s Disease - Core Concepts and Current Advances, Nagehan Ersoy Tunali Ed., (February 2012),ISBN:978-953-307-953-0,InTech,Open Source & available from: http://www.intechopen.com/books/huntington-s-disease-core-concepts-and-current-advances/early-dysfunction-of-neural-transmission-and-cognitive-processing-in-huntington-s-disease
Dey N.D., Bombard M.C., Roland B.P., Davidson S., Lu M., Rossignol J., Sandstrom M.I., Skeel R.L., Lescaudron L., & Dunbar G.L., Genetically engineered mesenchymal stem cells reduce behavioral deficits in the YAC 128 mouse model of Huntington's disease. Behavioural Brain Research. (2010), 214(2), 193-200.
Sandstrom, M.I., and Steffes, S., Constructing inexpensive, flexible, and versatile microdialysis probes in an undergraduate microdialysis research lab, Journal of Undergraduate Neuroscience Education (JUNE), (2008), Fall Quarter, 7(1), A33-A47.