Skip to Main Content
 

Global Search Box

 
 
 
 

Files

File List


Masters Thesis .pdf (4.93 MB)

ETD Abstract Container

Abstract Header

Exploring the Role of Calcium-Binding Protein Calreticulin in the Mouse Suprachiasmatic Nucleus

Birkholz, Tyler M.
http://rave.ohiolink.edu/etdc/view?acc_num=bgsu1562689789471245

Abstract Details

2019, Master of Science (MS), Bowling Green State University, Biological Sciences.
The master circadian clock in the hypothalamic suprachiasmatic nucleus of vertebrates receives information from the retina that entrains the clock to cycles of light and darkness in the animal’s environment. This timing signal is important for maintaining the appropriate organization of circadian rhythms generated throughout the body, which have many effects on health, development, and aging. One potential influence on entrainment is from retinal light signals acting on SCN cells that have protein expression patterns typical of stem cells. These stem-like cells may have plasticity in their interactions allowing circadian rhythms generated in the SCN to be modified when needed to adapt to changing environmental or internal conditions. Calcium-binding proteins in SCN cells have important functions in the entrainment process, but the role of one of these proteins, calreticulin (CALR), has not been examined in the SCN. This study characterized the spatial pattern of CALR-expressing SCN cells and their distribution among neurons (MAP2-positive), glial cells (GFAP-positive), and stem-like cells (SOX2-positive) by using immunocytochemistry and confocal fluorescence microscopy. Cells expressing significant levels of CALR were found throughout most of the SCN, with fewer in the core region. In the SCN, 86.9% of CALR cells were classified as neurons, 19.1% as astrocytic glial cells, and 60.33% as stem-like cells according to immunofluorescence imaging. To determine whether CALR expression can be induced by a stimulus that can entrain the SCN circadian clock a group of mice were exposed to two hours of light in the early portion of the night and were compared with mice remaining in darkness. Although SCN neurons did not show a significant response to the stimulus, non-neuronal cells including glial cells did, showing a two-fold increase in percentage of CALR-positive cells. We conclude that a substantial number of the CALR cells, 98.6%, express stem-marker SOX2 elevated, suggesting CALR could have an important role in this enigmatic cell type. We also conclude that SCN glial cells respond to the excitation from an entraining light signal with an increase in number that express elevated CALR, suggesting a role for this ubiquitous protein in Ca2+-regulated events during entrainment.
Michael Guesz, Dr. (Advisor)
Verner Bingman, Dr. (Committee Member)
Raymond Larsen, Dr. (Committee Member)
59 p.
Biology; Molecular Biology; Neurosciences
circadian; calcium; calcium-binding proteins; calreticulin; stem cells; calregulin; neuroscience; induction

Recommended Citations

Citations

  • Birkholz, T. M. (2019). Exploring the Role of Calcium-Binding Protein Calreticulin in the Mouse Suprachiasmatic Nucleus [Master's thesis, Bowling Green State University]. OhioLINK Electronic Theses and Dissertations Center. http://rave.ohiolink.edu/etdc/view?acc_num=bgsu1562689789471245

    APA Style (7th edition)

  • Birkholz, Tyler. Exploring the Role of Calcium-Binding Protein Calreticulin in the Mouse Suprachiasmatic Nucleus . 2019. Bowling Green State University, Master's thesis. OhioLINK Electronic Theses and Dissertations Center, http://rave.ohiolink.edu/etdc/view?acc_num=bgsu1562689789471245.

    MLA Style (8th edition)

  • Birkholz, Tyler. "Exploring the Role of Calcium-Binding Protein Calreticulin in the Mouse Suprachiasmatic Nucleus ." Master's thesis, Bowling Green State University, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=bgsu1562689789471245

    Chicago Manual of Style (17th edition)

bgsu1562689789471245
402
© 2019, all rights reserved.
This open access ETD is published by Bowling Green State University and OhioLINK.