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dc.contributor.advisorJ. Troy Littleton.en_US
dc.contributor.authorMelom, Jan E. (Jan Elizabeth)en_US
dc.contributor.otherMassachusetts Institute of Technology. Department of Biology.en_US
dc.date.accessioned2013-06-17T19:04:17Z
dc.date.available2013-06-17T19:04:17Z
dc.date.copyright2013en_US
dc.date.issued2013en_US
dc.identifier.urihttp://hdl.handle.net/1721.1/79160
dc.descriptionThesis (Ph. D.)--Massachusetts Institute of Technology, Dept. of Biology, 2013.en_US
dc.descriptionThis electronic version was submitted by the student author. The certified thesis is available in the Institute Archives and Special Collections.en_US
dc.descriptionCataloged from student-submitted PDF version of thesis.en_US
dc.descriptionIncludes bibliographical references.en_US
dc.description.abstractGlial cells exhibit spontaneous and activity-dependent fluctuations in intracellular Ca²+, yet it is unclear whether glial Ca²+ oscillations are required during neuronal signaling. Somatic glial Ca²+ waves are primarily mediated by the release of intracellular Ca²+ stores, and their relative importance in normal brain physiology has been disputed. Recently, near-membrane microdomain Ca²+ transients were identified in fine astrocytic processes and found to arise via an intracellular store- independent process. Here, we describe the identification of rapid, near-membrane Ca²+ oscillations in Drosophila cortex glia of the central nervous system. In a screen for temperature-sensitive conditional seizure mutants, we identified a glial-specific Na+/Ca²+, K+ exchanger (zydeco) that is required for microdomain Ca²+ oscillatory activity. We found that zydeco mutant animals exhibit increased susceptibility to seizures in response to several environmental stressors, and that zydeco is required acutely in cortex glia to regulate seizure susceptibility. We also found that glial expression of calmodulin is required for stress-induced seizures in zydeco mutants, suggesting a Ca²+/calmodulin-dependent glial signaling pathway is involved in acute glial-neuronal communication. These studies demonstrate that microdomain glial Ca²+ oscillations require NCKX-mediated plasma membrane Ca²+ flux, and are essential for normal neuronal excitability.en_US
dc.description.statementofresponsibilityby Jan E. Melom.en_US
dc.format.extent160 p.en_US
dc.language.isoengen_US
dc.publisherMassachusetts Institute of Technologyen_US
dc.rightsM.I.T. theses are protected by copyright. They may be viewed from this source for any purpose, but reproduction or distribution in any format is prohibited without written permission. See provided URL for inquiries about permission.en_US
dc.rights.urihttp://dspace.mit.edu/handle/1721.1/7582en_US
dc.subjectBiology.en_US
dc.titleMicrodomain calcium oscillations in Drosophila glia regulate seizure susceptibility and require NCKXen_US
dc.typeThesisen_US
dc.description.degreePh.D.en_US
dc.contributor.departmentMassachusetts Institute of Technology. Department of Biology
dc.identifier.oclc844348732en_US


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