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dc.contributor.advisorSchulz, Davideng
dc.contributor.advisorGarcia, Michaeleng
dc.contributor.authorLett, Kawasi M.eng
dc.date.issued2014eng
dc.date.submitted2014 Falleng
dc.descriptionAbstract from public.pdf.eng
dc.description.abstract[ACCESS RESTRICTED TO THE UNIVERSITY OF MISSOURI AT AUTHOR'S REQUEST.] Neural networks need to generate appropriate output regardless of external stimuli, to ensure survival of the organism. We utilize the crustacean stomatogastric ganglion (STG) and the mouse major pelvic ganglion (MPG) to investigate why perturbations to such networks induce homeostatic compensation, and how this affects the network�s ability to generate appropriate output. We assessed whether changes in expression of select transcripts constitute homeostatic compensation for loss of afferent input or disease. We use the STG as proof of concept to investigate impacts of loss of neuromodulation and subsequent compensatory responses, then utilize the MPG to implicate these kinds of responses as general characteristics across nervous systems. The STG is dependent on neuromodulation from anterior ganglia for proper output. Previous studies showed that deafferentation of the pyloric network attenuates output. We investigated whether reconnected input to the STG restored normal pyloric output. We found that the deafferented pyloric pacemaker responds differentially to restored inputs as well as exogenously applied neurotransmitters. Normal bladder function requires coordination of the central and peripheral nervous system. Peripheral nerve injury can be caused by surgery in the pelvic region or spinal cord injury. The main sequela is loss of bladder control. We will investigate if injury or disease alter gene expression patterns in MPG neurons. Using quantitative PCR on whole MPG, we observed changes in a select group of channel and receptor genes. These data demonstrate that perturbations to neural networks that alter their neuromodulatory input cause them undergo changes in transcription and functional output.eng
dc.identifier.urihttps://hdl.handle.net/10355/45807
dc.languageEnglisheng
dc.publisherUniversity of Missouri--Columbiaeng
dc.relation.ispartofcollectionUniversity of Missouri--Columbia. Graduate School. Theses and Dissertations.eng
dc.relation.ispartofcommunityUniversity of Missouri--Columbia. Graduate School. Theses and Dissertationseng
dc.rightsAccess is limited to the campuses of the University of Missouri.eng
dc.sourceSubmitted by the University of Missouri--Columbia Graduate School.eng
dc.subject.FASTNeurotransmitter receptorseng
dc.subject.FASTNeurons -- Physiologyeng
dc.subject.FASTHomeostasiseng
dc.subject.FASTIon channelseng
dc.titleLoss of afferent input alters voltage gated ion channel and neuromodulator receptor expression in crustacean and mammalian neuronseng
dc.typeThesiseng
thesis.degree.disciplineBiological sciences (MU)eng
thesis.degree.grantorUniversity of Missouri--Columbiaeng
thesis.degree.levelDoctoraleng
thesis.degree.namePh. D.eng


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