[-] Show simple item record

dc.contributor.advisorMcClellan, Andreweng
dc.contributor.authorKovalenko, Mykolaeng
dc.date.issued2008eng
dc.date.submitted2008 Summereng
dc.descriptionThe entire dissertation/thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file (which also appears in the research.pdf); a non-technical general description, or public abstract, appears in the public.pdf file.eng
dc.descriptionTitle from title screen of research.pdf file (viewed on August 12, 2009)eng
dc.descriptionThesis (M.A.) University of Missouri-Columbia 2008.eng
dc.description.abstractAfter spinal cord injury in larval lamprey, RS neurons regenerate their axons (Davis and McClellan, 1994a,b), restore synaptic contacts and most of the original locomotor functions (McClellan, 1998). It was previously demonstrated that calcium influx in RS neurons in culture results in inhibition of neurite outgrowth (Ryan et al., 2007). There is a hypothesis that injured RS neurons may undergo a number of changes in their electrical properties to maintain relatively low intracellular calcium concentrations and to promote axonal regeneration (Ryan et al., 2007; McClellan et al., 2008). For uninjured RS neurons, blocking calcium channels with various calcium channel blockers significantly reduced or eliminated the sAHP and produced changes in firing patterns in response to applied depolarizing current pulses that mimicked some of the effects of SCI. Furthermore, blocking SKKCa channels with apamin significantly reduced the sAHP compared to control values. However, blocking calcium and SKKCa channels in injured RS neurons did not have an apparent effect on sAHP and firing properties of the neurons. In addition, computer modeling shown that the AHP and firing properties of axotomized RS neurons could be obtained by substantially reducing calcium and SKKCa channel conductances compared to those in computer model of control RS neurons. This work provides additional information for understanding changes in ion channel expression in RS neurons that might be important to promote axonal regeneration in higher vertebrates, including humans.eng
dc.description.bibrefIncludes bibliographical referenceseng
dc.identifier.merlinb70625591eng
dc.identifier.oclc430230224eng
dc.identifier.urihttps://doi.org/10.32469/10355/5651eng
dc.identifier.urihttps://hdl.handle.net/10355/5651
dc.languageEnglisheng
dc.publisherUniversity of Missouri--Columbiaeng
dc.relation.ispartofcommunityUniversity of Missouri--Columbia. Graduate School. Theses and Dissertationseng
dc.rightsOpenAccess.eng
dc.rights.licenseThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivs 3.0 License.
dc.sourceSubmitted by University of Missouri--Columbia Graduate School.eng
dc.subject.lcshIon channelseng
dc.subject.lcshSpinal cord -- Wounds and injurieseng
dc.subject.lcshNervous system -- Regenerationeng
dc.subject.lcshLampreys -- Larvaeeng
dc.titleSpinal cord injury induces changes in ion channels of reticulospinal neurons in larval lampreyeng
dc.typeThesiseng
thesis.degree.disciplineBiological sciences (MU)eng
thesis.degree.grantorUniversity of Missouri--Columbiaeng
thesis.degree.levelMasterseng
thesis.degree.nameM.A.eng


Files in this item

[PDF]
[PDF]
[PDF]

This item appears in the following Collection(s)

[-] Show simple item record