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dc.contributor.authorReiss, Jenny
dc.date.accessioned2014-03-04T02:47:25Z
dc.date.available2014-03-04T02:47:25Z
dc.date.issued2007-08
dc.identifier.otherreiss_jenny_i_200708_ms
dc.identifier.urihttp://purl.galileo.usg.edu/uga_etd/reiss_jenny_i_200708_ms
dc.identifier.urihttp://hdl.handle.net/10724/24260
dc.description.abstractStudies have demonstrated that exercise decreases the symptoms of a variety of neurological disorders, but the mechanism through which exercise provides this protection is unknown. Excitotoxicity is a common cause of cell death underlying a number of brain disorders. Neuronal hyperexcitability is reduced by the neuropeptide galanin, and galanin mRNA is up-regulated by 3 weeks of activity wheel running. The following studies tested whether activity wheel running can reduce excitability and seizure behaviors induced by kainic acid. The importance of exercise-induced up-regulation of galanin was determined by injecting the galanin antagonist M-40 prior to administration of kainic acid. Seizure-induced behaviors and excitability were decreased in exercising animals following intraperitoneal and intracerebroventricular (ICV) administration of kainic acid. This effect was significantly attenuated when M-40 was injected prior to ICV kainic acid. These findings indicate that exercise induced up-regulation of galanin is a necessary factor in exercise-induced neuroprotection against excitotoxicity.
dc.languageeng
dc.publisheruga
dc.rightspublic
dc.subjectPhysical activity
dc.subjectKainic Acid
dc.subjectGalanin
dc.subjectNeuroprotection
dc.subjectSeizure
dc.titleExercise-induced neuroprotection against kainic acid-induced seizures in the rat
dc.title.alternativerole of galanin
dc.typeThesis
dc.description.degreeMS
dc.description.departmentPsychology
dc.description.majorNeuroscience
dc.description.advisorPhilip Holmes
dc.description.committeePhilip Holmes
dc.description.committeeRodney Dishman
dc.description.committeeAndrea Hohmann


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