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dc.contributor.advisorDravid, Shashank M.en_US
dc.contributor.authorSuryavanshi, Pratyushen_US
dc.date.accessioned2013-08-20T20:27:54Z
dc.date.available2018-01-01T09:40:19Z
dc.date.issued2013-08-15en_US
dc.identifier.urihttp://hdl.handle.net/10504/45446
dc.description.abstractThe delta family of ionotropic glutamate receptors consists of glutamate delta-1 (GluD1) and glutamate delta-2 (GluD2) receptors. These receptors are unique in that they do not exhibit ion channel currents in response to typical glutamate receptor agonists. GluD1 receptors are expressed throughout the forebrain during development with high expression in hippocampus during adulthood. Although the function of GluD2 in cerebellum is well understood, the role of GluD1 in the CNS remains elusive. GRID1, the gene for GluD1, is shown to be associated with a number of neuropsychiatric disorders including autism spectrum disorder (ASD). ASD is characterized by core features namely social interaction and communication deficits and repetitive behaviors as well as variable symptoms such as aggression, depression and hyperactivity. We have recently shown that GluD1 knockout mice exhibit social interaction deficits, repetitive behaviors, hyperactivity, hyperaggression and depression-like behavior which mimic both the core and variable symptoms in ASDs. GluD1 knockout mice also exhibit deficit in reversal learning in the Morris water maze which is analogous to resistance to change behavior in ASDs. Glutamate delta receptor subunits GluD1 and GluD2 have been shown to play a crucial role in neuronal synapse formation and regulation. Interestingly, we also find that loss of GluD1 leads to increased number of immature dendritic spines similar to the characteristic observations of higher immature spine number in ASD and Fragile-X syndrome human patients and Fragile-X mental retardation protein (FMRP) knockout mice. This morphological difference may be associated with abnormal group 1 metabotropic glutamate receptor (mGluR) signaling found in the animal models of autism spectrum disorder. In this study, we tested the effect of deletion of GluD1 on regulation of metabotropic glutamate receptor function. Our results demonstrate that GluD1 is necessary for normal mGluR signaling.en_US
dc.language.isoen_USen_US
dc.publisherCreighton Universityen_US
dc.rightsCopyright is retained by the Author. A non-exclusive distribution right is granted to Creighton University and to ProQuest following the publishing model selected above.en_US
dc.subject.meshReceptors, Glutamate--geneticsen_US
dc.subject.meshChild Development Disorders, Pervasive ǂx geneticsen_US
dc.subject.meshHippocampus ǂx physiopathology.en_US
dc.titleRegulation of metabotropic glutamate receptor 5 signaling by glutamate delta-1 receptor in the hippocampus.en_US
dc.typeThesis
dc.rights.holderPratyush Suryavanshien_US
dc.publisher.locationOmaha, Nebraskaen_US
dc.description.noteProQuest Traditional Publishing Optionen_US
dc.description.pages97 pagesen_US
dc.contributor.cuauthorSuryavanshi, Pratyushen_US
dc.embargo.terms2015-08-30
dc.degree.levelMS (Master of Science)en_US
dc.degree.disciplinePharmaceutical Science (graduate program)en_US
dc.degree.nameM.S. in Pharmaceutical Sciencesen_US
dc.degree.grantorGraduate Schoolen_US
dc.degree.committeeMurray, Thomasen_US
dc.degree.committeeSimeone, Timothyen_US


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