Glia-neuron signaling

dc.contributor.advisor Philip G. Haydon
dc.contributor.author Parpura, Vladimir
dc.contributor.department Zoology and Genetics
dc.date 2018-08-23T00:30:00.000
dc.date.accessioned 2020-06-30T07:08:07Z
dc.date.available 2020-06-30T07:08:07Z
dc.date.copyright Fri Jan 01 00:00:00 UTC 1993
dc.date.issued 1993
dc.description.abstract <p>This dissertation deals with release of neurotransmitter from glia. It has been demonstrated that bradykinin causes a receptor-mediated release of excitatory amino acids (EAAs), glutamate and aspartate, from glial cultures obtained from dorsal root ganglia (DRG) together with an increase in the cytoplasmic level of glial free calcium. Perturbations which inhibited bradykinin-induced calcium mobilization prevented the release of EAAs from glia. The addition of ionomycin caused a calcium-dependent release of EAAs. Taken together, these data demonstrate that calcium is both necessary and sufficient for stimulating the release of EAAs from DRG glia;Bradykinin was applied to mixed neuron-glial cultures derived from rat cerebral cortex while monitoring calcium levels. Bradykinin elevated calcium levels in neurons only when neurons contacted glia. The general glutamate receptor antagonist, D-glutamylglycine (DGG), prevented bradykinin-induced neuronal calcium elevation. These data indicate that bradykinin elevates neuronal calcium levels through the action of glutamate that is released from glia. While addition of bradykinin to mixed neuron-glial culture is the simplest experimental method of testing the hypothesis that glia can signal to neurons, a second technique allowed a more direct test of this hypothesis. Direct photo-stimulation of glia was used to increase glial calcium levels. A portion of glia was exposed to focal application of UV light while monitoring the calcium response. Photo-stimulation reliably raised the level of calcium in the glial cell. Since elevated calcium is sufficient to stimulate the release of glutamate from glia, this perturbation induced the calcium-dependent release of glutamate. By monitoring calcium levels from adjacent neurons, it was possible to determine that photo-stimulation of glia caused an elevation in calcium levels of adjacent unstimulated neurons. This effect was greatly reduced by DGG. Thus, glia can regulate neuronal calcium levels through glutamate-mediated actions.</p>
dc.format.mimetype application/pdf
dc.identifier archive/lib.dr.iastate.edu/rtd/10849/
dc.identifier.articleid 11848
dc.identifier.contextkey 6418542
dc.identifier.doi https://doi.org/10.31274/rtd-180813-10052
dc.identifier.s3bucket isulib-bepress-aws-west
dc.identifier.submissionpath rtd/10849
dc.identifier.uri https://dr.lib.iastate.edu/handle/20.500.12876/64040
dc.language.iso en
dc.source.bitstream archive/lib.dr.iastate.edu/rtd/10849/r_9414010.pdf|||Fri Jan 14 18:29:22 UTC 2022
dc.subject.disciplines Cell Biology
dc.subject.disciplines Neuroscience and Neurobiology
dc.subject.disciplines Neurosciences
dc.subject.keywords Zoology and genetics
dc.subject.keywords Zoology (Neurobiology)
dc.subject.keywords Neuroscience
dc.subject.keywords Neurobiology
dc.title Glia-neuron signaling
dc.type article
dc.type.genre dissertation
dspace.entity.type Publication
relation.isOrgUnitOfPublication 4a2929da-5374-4338-b62f-f5fd9e156ef9
thesis.degree.level dissertation
thesis.degree.name Doctor of Philosophy
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