Molecular Mechanisms in Pathophysiology of Migraine Aura
| dc.contributor.advisor | Elfring, Lisa | en |
| dc.contributor.author | Mayer, Lisa | |
| dc.creator | Mayer, Lisa | en |
| dc.date.accessioned | 2017-08-07T22:28:34Z | |
| dc.date.available | 2017-08-07T22:28:34Z | |
| dc.date.issued | 2017 | |
| dc.identifier.citation | Mayer, Lisa. (2017). Molecular Mechanisms in Pathophysiology of Migraine Aura (Bachelor's thesis, University of Arizona, Tucson, USA). | |
| dc.identifier.uri | http://hdl.handle.net/10150/625087 | |
| dc.description.abstract | Cortical spreading depression (CSD), the underlying mechanism behind migraine aura, occurs when neurons become depolarized and lose function, while releasing signaling molecules that propagate this condition. Spreading depression occurs when abnormal flow of ions across the cell membranes of a neural cell depolarizes the cell and activates detrimental signaling pathways that cause the same disruptive ion flow to occur in nearby neural or glial cells. After depolarization, cells affected by CSD are not able to return to their normal state and remain nonfunctional for some time. This lack of function causes symptoms of migraine aura. Calcium and glutamate signaling may be primary drivers of the CSD; inhibition of either tends to prevent CSD, whereas their activation promotes it. Cerebral blood flow and oxygen consumption are considered measures of cell function during CSD and further demonstrate the significance of CSD on a larger scale. This is a review of current research about these elements of migraine aura. | |
| dc.language.iso | en_US | en |
| dc.publisher | The University of Arizona. | en |
| dc.rights | Copyright © is held by the author. Digital access to this material is made possible by the University Libraries, University of Arizona. Further transmission, reproduction or presentation (such as public display or performance) of protected items is prohibited except with permission of the author. | en |
| dc.rights.uri | http://rightsstatements.org/vocab/InC/1.0/ | |
| dc.title | Molecular Mechanisms in Pathophysiology of Migraine Aura | en_US |
| dc.type | text | en |
| dc.type | Electronic Thesis | en |
| thesis.degree.grantor | University of Arizona | en |
| thesis.degree.level | bachelors | en |
| thesis.degree.discipline | Honors College | en |
| thesis.degree.discipline | Molecular and Cellular Biology | en |
| thesis.degree.name | B.S. | en |
| refterms.dateFOA | 2018-06-14T04:43:15Z | |
| html.description.abstract | Cortical spreading depression (CSD), the underlying mechanism behind migraine aura, occurs when neurons become depolarized and lose function, while releasing signaling molecules that propagate this condition. Spreading depression occurs when abnormal flow of ions across the cell membranes of a neural cell depolarizes the cell and activates detrimental signaling pathways that cause the same disruptive ion flow to occur in nearby neural or glial cells. After depolarization, cells affected by CSD are not able to return to their normal state and remain nonfunctional for some time. This lack of function causes symptoms of migraine aura. Calcium and glutamate signaling may be primary drivers of the CSD; inhibition of either tends to prevent CSD, whereas their activation promotes it. Cerebral blood flow and oxygen consumption are considered measures of cell function during CSD and further demonstrate the significance of CSD on a larger scale. This is a review of current research about these elements of migraine aura. |
