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Faculty Detail    
Name MICHELLE L OLSEN
 
Campus Address MCLM 958A Zip 0005
Phone 205-975-2715
E-mail molsen@uab.edu
Other websites
     


Faculty Appointment(s)
Appointment Type Department Division Rank
Primary  Cell, Developmntl, & Integrative Biology  Cell, Developmntl, & Integrative Biology Assistant Professor
Secondary  Neurobiology  Neurobiology Assistant Professor
Center  General Clinical Research Center  Comprehensive Neuroscience Center Assistant Professor
Center  Ctr for Glial Bio in Med  Ctr for Glial Bio in Med Assistant Professor

Graduate Biomedical Sciences Affiliations
Cell, Molecular, & Developmental Biology 
Genetics and Genomic Sciences 
Neuroscience 
Pathobiology and Molecular Medicine 

Biographical Sketch 
PhD (Neurobiology) University of Alabama at Birmingham 2005

Society Memberships
Organization Name Position Held Org Link
2000 - present Society for Neuroscience   Member   
2013 - present American Society for Neurochemistry  Member   

Research/Clinical Interest
Title
Glial potassium channels and glutamate transporters in injury and abnormal development
Description
The focus of Dr. Olsen's research is to enhance our understanding of the role of astrocytes in brain and spinal cord function. Astrocytes are the most numerous cells in the central nervous system yet the role of astrocytes in injury, particularly pediatric injury, and neurodevelopmental disorders is highly understudied. Her work focuses on two essential functions of astrocytes; buffering of extracellular K+ and glutamate. These functions are thought to be largely mediated by two astrocytic proteins, Kir4.1, an inwardly rectifying potassium channel and excitatory amino acid transporter, GLT-1. These two proteins function to dampen neuronal excitability. Following injury, persistent alterations in the biophysical properties of astrocytes hinder their ability to perform these basic altruistic functions. The resulting dysregulation of extracellular K+ and glutamate are associated with increased neuronal excitability and changes in synaptic physiology and plasticity in the adult. In the developing central nervous system, loss of these functions may profoundly impact neuronal development. Indeed, the immature brain is intrinsically more excitable which may be due in part to lower levels of expression of these two proteins. Surprisingly, little is known regarding the regulation of either protein in normal brain, following injury or during abnormal development. The current research projects span from understanding the regulation of Kir4.1 and GLT-1 gene transcription in pathophysiology, examining protein expression, function and activity, to understanding how the loss of extracellular K+ and glutamate regulation impact neuronal development. To do this work requires a multitude of techniques including functional assays, such as electrophysiology and glutamate uptake assays, confocal and wide field fluorescent imaging, protein biochemistry, and molecular biology. We use tissue and cultured cells derived from several animal models as well as human autopsy and surgical resection tissue.

Selected Publications 
Publication PUBMEDID
1. M.L. Olsen, S. Schade, S.A. Lyons, M.D. Amaral, H. Sontheimer. Expression of Voltage-Gated Chloride Channels in Human Glioma Cells, Journal of Neuroscience 23(13)5572-5582, 2003, PMID: 12843258-5 year impact factor = 8.1
2. M.L. Olsen, H. Sontheimer. Mislocalization of Kir Channels in Malignant Glia, Glia 46:63-73, 2004, PMCID: 2548404-5 year impact factor = 5.5
3. M.L. Olsen, A.K. Weaver, P. Ritch, H. Sontheimer. Modulation of Glioma BK (gBK) Channels via erbB2, Journal of Neuroscience Research 15;81(2):179-89, 2005, PMID: 15948146-5 year impact factor = 3.2
4.M.L. Olsen, H Higashimori, S.L. Campbell, J.J. Hablitz and H. Sontheimer. Functional Expression of Kir4.1 Channels in Spinal Cord Astrocytes, Glia 53(5):516-28, 2006, PMCID: 2553202--5 year impact factor = 5.5
5.M.L. Olsen, S.L. Campbell and H. Sontheimer. Differential Distribution of Kir4.1 in Spinal Cord Astrocytes Suggests Regional Differences in K+ Homeostasis, Journal of Neurophysiology, 98(2):786-93 , 2007, PMCID: 2040512-5 year impact factor =3.7
6.A.K. Weaver, M.L. Olsen, M. B. McFerrin and H. Sontheimer. BK Channels are Coupled to IP3-receptors via Lipid Rafts: a Novel Mechanism for Coupling [Ca2+]i to Channel Activation, Journal of Biological Chemistry, 26;282(43):31558-68, 2007, PMID: 2227909 -5 year impact factor =5.5
7. C.M. Habela, M.L. Olsen and H. Sontheimer. ClC3 Is a Critical Regulator of Cell Cycle in Normal and Malignant Cells, Journal of Neuroscience, 28(37):9205-17, 2008, PMID: 18784301-5 year impact factor =8.1
8. M.L. Olsen and H. Sontheimer. Functional Implications for Kir4.1 Channels in Glial Biology: From K+ Buffering to Cell Differentiation, Journal of Neurochemistry, 107, 589–601, 2008-5 year impact factor =4.5
9. M.L. Olsen, S.L. Campbell, C.L. Floyd, H. Sontheimer, Spinal Cord Injury in vivo Causes Wide-Spread, Persistent Loss of Kir4.1 and GLT-1: Potential Benefits of Treatment with 17β-Estradiol, Brain, 133(Pt 4):1013-25, 2010, PMID: 20375134 5 year impact factor = 10.1
10. R. Raphemot, R. Kadakia, M. L. Olsen, S. Banerjee, E. Days, S S. Smith, C. D. Weaver and J. S. Denton. Development and validation of fluorescence- and automated patch clamp-based functional assays for the inward rectifier potassium channel Kir4.1. in press Assay and Drug Development Technologies, 2013 Assay Drug Dev Technol. 2013 Nov-Dec;11(9-10):532-43. PMID: 24266659 5 year impact factor = 2.0
11. S.E. Nwaobi, S.R. Peramsetty, E. Lin and M.L. Olsen, DNA methylation is a critical regulator of Kir4.1 in CNS development, Glia. Mar;62(3):411-27, 2014 PMID:2441522 5 year impact factor = 5.4
12*. V. A. Cuddapah, R. B. Pillai, K. V. Shekar, J. B. Lane, K. J. Motil, S. A. Skinner, G. McGwin2, D. C. Tarquinio5, D. G. Glaze, W. E. Kaufmann, A. K Percy, J. L. Neul, M. L. Olsen. Methyl-CpG-binding protein 2 (MEPC2) mutation type is associated with disease severity in Rett Syndrome, J Med Genet. 2014 Mar;51(3):152-8, PMID 24399845 5 year impact factor = 5.8
13. X. Tong, Y. Ao, GC Faas, SE Nwaobi, J Xu, MD Haustein, MA Anderson, I Mody, ML Olsen, MV Sofroniew, BS Khakh. Astrocyte Kir4.1 ion channel deficits contribute to neuronal dysfunction in Huntington's disease model mice. Nat Neurosci. 2014 Mar 30. PMID:24686787 5 year impact factor 16.0

 
2548404 

Keywords
brain injury, neurodevelopmental disorders, spinal cord, astrocyte, potassium channel, glutamate transporter, epigenetics