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Effect of drugs which alter NMDA receptor function on in vivo neurochemical changes following acute and repeated antidepressant drug treatment in the freely moving ratSmith, Jenny Claire Elizabeth January 2001 (has links)
No description available.
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Neurotransmitter interactions within the rat neostratumCrawford, Martin January 1989 (has links)
No description available.
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Kif5b interaction with NMDA receptors regulates neuronal functionLin, Raozhou, 林饒洲 January 2012 (has links)
Intracellular transportation is an essential cellular event controlling neuronal development, morphology, function and survival. Kinesin-1 is the molecular motor conveying cargo along microtubule by utilizing the chemical energy from ATP hydrolysis. This motor consists of two heavy chains and two light chains. Both heavy and light chains are responsible for cargo bindings. There are three kinesin-1 heavy chains in eukaryotic cells. Kif5a and Kif5c are neuronal specific, while Kif5b is ubiquitously expressed. Kif5b carries various cargos essential for neuronal functions, and the early embryonic death of Kif5b null mice suggests the importance of Kif5b in vivo.
N-methyl-d-aspartate receptors (NMDARs) are glutamate elicited channel, which is permeable to calcium and crucial for synaptic plasticity in the central nervous system. NMDARs are heteromeric assemblies consisting of NR1, NR2 and NR3 subunits. These transmembrane subunits contain three parts. Other than the transmembrane domain, the extracellular domain serves as the ligand binding site while the intracellular domain interacts with various partners regulating downstream signaling and receptor trafficking. Synaptic NMDAR activation regulates synaptic plasticity, while extrasynaptic NMDAR activation leads to excitotoxicity.
In this project, I find that kinesin-1 directly interacts with NMDAR subunit, NR1, NR2A and NR2B in vivo. NMDAR colocalizes with kinesin-1 in the cell body and neurites. By GST-pull-down assays with different Kif5b fragments, the cytoplasmic domains of NR1, NR2A and NR2B are found to directly bind with Kif5b via a Kif5b C-terminal region independent of kinesin light chains.
To examine the role of Kif5b in NMDAR trafficking, dominant negative Kif5b fragments are expressed in cell lines together with NR1-1a and GFP-NR2B. Overexpression of dominant negative Kif5b significantly disrupts GFP-NR2B forward trafficking and prevents it from entering into Golgi apparatus. Furthermore, the surface NR1 and NR2B levels are significantly reduced whilst the NR2A levels are not affected in Kif5b+/- mice in which the Kif5b protein level is reduced by 50% compared with the wild-type littermates. Consistent with this observation, the NR1 and NR2B levels are decreased in fractions containing synaptosomal membrane but not the one containing only postsynaptic densities, suggesting that the extrasynaptic NMDAR levels are affected in Kif5b+/- mice.
NMDARs are highly permeable to calcium while activated, thereby activating neuronal nitric oxide synthases (nNOS) to produce nitric oxide (NO). It is found that NMDA triggered calcium influx is perturbed in Kif5b+/- neurons, while the synaptic NMDA receptor mediated calcium influx is normal. In Kif5b+/- slices, the production of NO reduces significantly. Calcium ionophore, A23187, rescue this NO defect, indicating insufficient supply of calcium as the main contribution to this defect. Therefore, Kif5b-dependent extrasynaptic localization of NMDA receptors mediates calcium influx upon NMDA stimulation and controls NO production.
In the summary, above results suggest kinesin-1 as a novel motor involving in NMDA receptor trafficking. This interaction may contribute to the extrasynaptic distribution of NMDARs. By regulating NO production through interaction with NMDARs, Kif5b may mediate neuronal survival in cerebral ischemia and certain aggressive behaviors. This provides a novel target for therapy development against stroke and schizophrenia. / published_or_final_version / Biochemistry / Doctoral / Doctor of Philosophy
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Functional investigation of NMDA receptor molecular evolutionRyan, Tomás John January 2010 (has links)
No description available.
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Properties of NMDA receptors in Substantia nigra pars compacta dopaminergic neuronesBrothwell, Shona Lindsay Crawford January 2008 (has links)
No description available.
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Control of Aspartate Transcarbamylase activity by Norit-A adsorbable compounds during synchronous growth of Chlorella pyrenoidosa /Cole, Francis Eugene, January 1964 (has links)
Thesis (Ph. D.)--Virginia Polytechnic Institute, 1964. / Vita. Abstract. Includes bibliographical references (leaves 29-30). Also available via the Internet.
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NMDA receptor mediated toxicity in primary neuronal cultures from rodent cerebral cortex /Yu, Chi Wang. January 2004 (has links)
Thesis (M.Phil.)--Hong Kong University of Science and Technology, 2004. / Includes bibliographical references (leaves 64-78). Also available in electronic version. Access restricted to campus users.
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Dopamine D1-like receptor-mediated regulation of NMDA receptor sensitivity to ethanol in the nucleus accumbensZhang, Tao, Morrisett, Richard A., January 2005 (has links) (PDF)
Thesis (Ph. D.)--University of Texas at Austin, 2005. / Supervisor: Richard A. Morrisett. Vita. Includes bibliographical references.
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Modulation of N-methyl-D-aspartate receptor expression in neuronal cell cultureLui, Pik Wa 01 January 2002 (has links)
No description available.
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The role of the N-methyl-D-aspartate receptor (NMDAR)--NR2b subunit in female reproductive agingMaffucci, Jacqueline Ann. January 1900 (has links)
Thesis (Ph. D.)--University of Texas at Austin, 2008. / Vita. Includes bibliographical references.
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