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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