Michael Sandstrom Ph.D.
 |
Address: Email: sands1m@cmich.edu |
Bio:
Michael I. Sandstrom is a new assistant professor joining the faculty of the Central Michigan University Psychology Department in Spring 2004. He has 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:
Dey, N. D., Boersen, A. J., Myers, R. A., York, L. R., Bombard, M. C., Lu, M., Sandstrom, M. I., Hulce, V. D., Lescaudron, L., & Dunbar, G. L. (2007). The novel substituted pyrimidine, KP544, reduces motor deficits in the R6/2 transgenic mouse model of Huntington’s disease. Restorative Neurology and Neuroscience, 25, 485-492.
Rebec, G. V., & Sandstrom, M. I. (2007). Extracellular Ascorbate Modulates Glutamate Dynamics: Role of Behavioral Activation, BMC Neuroscience, 8:32.
Rebec, G. V., Witowski, S. R., Sandstrom, M. I., Rostand, R. D., & Kennedy, R. T. (2005). Extracellular ascorbate modulates cortically evoked glutamate dynamics in rat striatum, Neuroscience Letters, 378(3), 166-170.
Sandstrom, M., Nelson, C. L., & Bruno, J. P. (2003). Neurochemical correlates of sparing from motor deficits in rats depleted of striatal dopamine as weanlings, Developmental Psychobiology 43, 373-383.
Sandstrom, M. I., & Rebec, G. V. (2003). Characterization of striatal activity in conscious rats: Contribution of both NMDA and AMPA/kainate receptors to both spontaneous and glutamate-driven firing. Synapse, 47, 91-100.
Bruno, J. P., Sandstrom, M., Arnold, H. M., & Nelson, C. L. (1998). Age-dependent neurobehavioral plasticity following forebrain dopamine depletions. (Review) Developmental Neuroscience.
Soghomonian, J. J., Laprade, N., Sandstrom, M., & Bruno, J. P. (1998). c-fos gene expression is induced in a subpopulation of striatal neurons following a single administration of a dopamine D1-receptor agonist in adult rats lesioned with 6-OHDA as neonates. Molecular Brain Research.
Sandstrom, M., & Bruno, J. P. (1997). Sensitivity to the motoric effects of a dopamine antagonist differ as a function of age at the time of dopamine depletion. Developmental Psychobiology.