Website: www.chsbs.cmich.edu/michael_sandstrom/
Bio:
Michael I. Sandstrom is an associate 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.
Research Interest:
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 Parkinson's disease with an animal model. He is currently investigating transgenic mice that model Huntington's disease (HD) to delineate neurochemical deficits in both basal ganglia and limbic structures using operant tasks and concurrent microdialysis to track changes in monoamine neurotransmitters (dopamine and serotonin) related to strategy switching. Patients suffering with HD and related animal model expressions tend to have trouble switching strategies to gain access to behavioral reward more efficiently. His goal is to narrow down on key physiological disruptions to explain the earlier stages of brain deterioration that occur before neurons begin dying in transgenic mouse models of HD, and then use this insight to develop practical strategies to assess putative treatments. Techniques include in-vivo microdialysis, single unit electrophysiology, iontophoresis experiments using awake and unrestrained animals, immunohistochemistry, local intracranial infusions, operant behavior training, and sophisticated molecular and neurochemical analysis strategies.
Recent Research:
Fink KD, Rossignol J, Crane AT, Davis KK, Bavar AM, Dekorver NW, Lowrance SA, Reilly MP, Sandstrom MI, von Hörsten S, Lescaudron L, Dunbar GL. (2012-Jun) Early cognitive dysfunction in the HD 51 CAG transgenic rat model of Huntington's disease.. Behavioral Neuroscience 126(3), 479-487.
Lowrance, S.A., Matchynski1, J., Rossignol, J., Dekorver, N., Sandstrom, M., and Dunbar, G. (2012). CXB-909 Attenuates Cognitive Deficits in the mu-p-75 Saporin Mouse Model of Alzheimer’s Disease. Neuroscience and Medicine, (2012), 3, 65-68.
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.
H.-Martines, K., Shear, D.A., Hargrove, C., Patton, J., Mazei-Robison, M., Sandstrom, M.I., and Dunbar, G.L., 7-nitroindazole attenuates 6-hydroxydopamine-induced spatial learning deficits and dopamine neuron loss in a presymptomatic animal model of Parkinson's disease, Experimental & Clinical Psychopharmacology, 16(2), (2008) 178-189.