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Dissertations / Theses on the topic 'Excitatory amino acid'

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Published: 4 June 2021

Last updated: 20 February 2023

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1

Agarwal, Shailesh Ramjilal. "Pharmacological modeling and regulation of excitatory amino acid transporters (EAATS)." CONNECT TO THIS TITLE ONLINE, 2007. http://etd.lib.umt.edu/theses/available/etd-09262007-111510/.

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2

Martin, David. "In vitro studies of excitatory amino acid pharmacology." Thesis, Royal Veterinary College (University of London), 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.519528.

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3

Palmer, Andrew John. "Pharmacological modulation of excitatory amino acid receptors 'invitro'." Thesis, Royal Veterinary College (University of London), 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.519539.

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4

McGowan, Eileen M. "Excitatory amino acid neurotransmission in the hippocampus after ischaemia." Thesis, University of Cambridge, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.321403.

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5

Smith, Adam Luke. "Characterization of excitatory amino acid receptors using novel structural analogues." Thesis, University of Oxford, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.302953.

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6

Neville, Lewis Frederic. "Pre-synaptic modulation of cortical excitatory amino acid neurotransmitter release." Thesis, University of Southampton, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.328909.

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7

Goundry, William R. F. "The synthesis of hachijodine F and excitatory amino acid analogues." Thesis, University of Oxford, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.409794.

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8

Chatha, B. Tracey. "Localization of excitatory amino acid receptors in the basal ganglia." Thesis, University of Oxford, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.365693.

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9

Bolonna, Anusha Antoinette. "A genetic study of excitatory amino acid receptors in schizophrenia." Thesis, King's College London (University of London), 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.248467.

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10

Gill, Ramanjit. "Neuroprotective studies of excitatory amino acid antagonists in focal cerebral ischaemia." Thesis, Royal Veterinary College (University of London), 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.522532.

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11

Kortzak, Daniel [Verfasser]. "Mechanismus der K+ Kopplung in excitatory amino acid transporters / Daniel Kortzak." Düsseldorf : Universitäts- und Landesbibliothek der Heinrich-Heine-Universität Düsseldorf, 2018. http://d-nb.info/1151383198/34.

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12

Badman, G. T. "The synthesis and pharmacology of some novel excitatory amino acid analogues." Thesis, London Metropolitan University, 1986. http://repository.londonmet.ac.uk/3278/.

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Certain amino acids, notably L-glutamate and L-aspartate, are believed to fulfil a role as excitatory neurotransmitters in the mammalian Central Nervous System (CNS). Investigation has revealed the presence of three, and possibly a fourth, type of receptor for such neurotransmitters. These receptors have been named after the most potent and selective agonist of each; thus they are usually referred to as N-methyl-D-aspartate (A1), quisqualate (A2), kainate (A3) and 2-amino, 4-phosphono butyric acid (A4); the designations in brackets being that of the nomenclature of Fagg and Foster.

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13

Mavencamp, Terri Lynn. "Design, synthesis and biological evaluation of a family of excitatory amino acid transporter 3 (EAAT3) preferring inhibitors." [Missoula, Mont.] : The University of Montana, 2008. http://etd.lib.umt.edu/theses/available/etd-03212009-152926/unrestricted/Mavencamp_umt_0136D_10009.pdf.

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14

Euler, Mia von. "Experimental spinal cord injuries : a histopathological, neurological, and pharmacological study in the rat /." Stockholm, 1999. http://diss.kib.ki.se/1999/91-628-3461-4/.

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15

Okonkwo, P. I. "The synthesis and pharmacological evaluation of quisqualic acid and some novel excitatory amino acid mimetics." Thesis, London Metropolitan University, 1992. http://repository.londonmet.ac.uk/2965/.

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L-Glutamic acid and L-aspartic acid are believed to be the principal initiators of excitatory synaptic neurotransmission in the mammalian central system. A number of molecules of either natural or synthetic origin have been identified as possessing agonist or antagonist properties at glutamate binding sites. One of the most potent agonist is quisqualic acid (69), and this thesis features two aspects of the synthetic organic chemistry and the pharmacology of quisqualic acid and some of its analogues.

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16

Richmond, Saul Alexander. "Characterization of excitatory amino acid receptors in the mammalian central nervous system." Thesis, University of Oxford, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.308536.

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17

Fowkes, Adrian Francis Stewart. "Synthesis and Evaluation of Skeletally Diverse Inhibitors of Excitatory Amino Acid Transporters." Thesis, University of Leeds, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.534428.

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18

Richards, Dannette Shanon. "CHARACTERIZATION OF EXCITATORY AMINO ACID NEUROTRANSMITTERS AT MOTONEURON SYNAPSES CONTACTING RENSHAW CELLS." Wright State University / OhioLINK, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=wright1260896604.

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19

Allan, Stuart McRae. "Excitatory amino acid-mediated modulation of synaptic transmission in rat hippocampal slices." Thesis, University of Aberdeen, 1993. http://digitool.abdn.ac.uk/R?func=search-advanced-go&find_code1=WSN&request1=AAIU540765.

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The whole-cell patch-clamp technique was established in the laboratory in order to investigate the modulation of excitatory amino acid-mediated synaptic transmission in the rat hippocampal slice. Following the successful development of the technique the basic properties of excitatory amino acid-mediated synaptic transmission in the CA3-CA1 pathway were studied. Stimulation of the SCCFs (Schaffer collateral-commissural fibres) under conditions in which the inhibitory transmission was blocked resulted in a compound EPSC (excitatory postsynaptic current) mediated by AMPA (-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid) and NMDA (N-methyl-D-aspartic acid) receptors. Application of a brief high-frequency stimulus to the SCCFs resulted in a long-lasting potentiation of the EPSC. Various compounds were applied to the slice to establish whether tetanus-induced potentiation could be mimicked pharmacologically. No potentiation was observed with perfusion of the ionotropic glutamate-receptor agonists L-glutamate, NMDA or AMPA, the latter two producing a transient depression of the EPSC. Following this a series of experiments were performed that investigated the consequences of mGluR (metabotropic glutamate receptor) activation. Perfusion with the selective agonist 1S,3R-ACPD ((1S,3R)-1-aminocyclopentane-1,3-dicarboxylic acid) resulted in a small depression of both the compound EPSC and the isolated NMDA receptor-mediated EPSC. In the presence of AA (arachidonic acid (10M)), 1S,3R-ACPD produced a slight potentiation of the response that was not blocked by the NMDA receptor antagonist D-AP5 (D-(-)-2-amino-5-phosphonopentanoic acid). The co-application of 1S,3R-ACPD and NMDA also produced a slight enhancement of the EPSC, as did AA when applied alone. These findings are consistent with an involvement of mGluRs in the induction of LTP, when activated in the presence of AA.

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20

Rousseau, Stephen John. "Nicotinic modulation of excitatory amino acid release in the rat frontal cortex." Thesis, University of Bath, 2004. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.398609.

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21

Jones, Martyn Gwynne. "Pharmacological studies of ionotropic excitatory amino acid receptors on rat central neurones 'invitro'." Thesis, Royal Veterinary College (University of London), 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.519542.

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22

Rosin, Claudia. "Excitatory amino acid-induced oligodendrocyte cell death in vitro : mechanisms and protective strategies." Thesis, University of Nottingham, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.408626.

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23

Collins, Dawn R. "Excitatory amino acid induced enhancement of synaptic transmission in the rat hippocampal slice." Thesis, University of Aberdeen, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.386216.

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The effects of exogenous application of excitatory amino acids on synaptic transmission was investigated in the CA1 region of the rat hippocampal slice preparation using two methods of application: iontophoresis and perfusion. Iontophoretic application of N-methyl-D-aspartate (NMDA) evoked a short lasting form of potentiation, whereas application of the proposed endogenous excitatory transmitter substance L-glutamate induced a slowly-forming and long lasting potentiation of the response by both techniques. Surprisingly, brief perfusion of 50μM NMDA elicited only a long-lasting depression of the response. Application of 10μM α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) showed no long-term effects on synaptic transmission. Perfusion of (1S,3R) 1-aminocyclopentane-1,3-dicarboxylic acid (ACPD) induced only a marginal form of synaptic enhancement under normal conditions and depression of the response in conditions of low Mg²⁺ or in the presence of low doses (1μM) of picrotoxin. However, in the presence of the GABA_A antagonist picrotoxin (1μM), perfusion of 100μM ACPD evoked a slowly-forming enhancement of the response. Application of the proposed retrograde transmitter arachidonic acid (10μM) elicited a slowly-forming depression of the response when perfused alone. Co-application of arachidonic acid (10μM) and ACPD (50μM) evoked a rapidly inducible and long-lasting form of synaptic enhancement.

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24

Magnuson, David Stuart Keith. "Analysis of excitatory amino acid receptors in the rat spinal cord in vivo and in vitro." Thesis, University of British Columbia, 1988. http://hdl.handle.net/2429/29017.

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Several endogenous amino acids including L-glutamate and L-aspartate have potent excitatory effects in the central nervous system. They are thought to act as synaptic transmitters in many neural pathways including those in the spinal cord. Three distinct receptors have been described through which these excitatory amino acids exert their effects. These are referred to as quisqualate, kainate and N-methyl-D-aspartate (NMDA) receptors, after the exogenous excitants most specific for each. In addition, sub-types of the NMDA receptor have been proposed to account for differences observed in the actions of the endogenous excitant quinolinate (2,3-pyridine dicarboxylate) in various regions of the nervous system. The characterization of excitant amino acid receptors has been accomplished primarily using two or more potent antagonists which include D-(-)-2-amino-5-phosphonovalerate (APV), a specific NMDA antagonist, and kynurenate, a compound related to quinolinate which potently attenuates the actions of NMDA- and kainate-like excitants. Structure-activity studies of amino acid receptors were undertaken using standard extracellular recording and iontophoretic techniques in the dorsal horn of the spinal cord in vivo, and compared with the neocortex of the rat. In addition, a spinal cord slice preparation was developed wherein dorso-ventral longitudinal slices were prepared from the lumbar enlargement of weanling rats (50 - 125 g). The slices were maintained in an "interface" tissue bath of novel design. Extracellular recording of several hours duration and up to 8 hours after slice preparation were routinely possible. Conformationally restricted analogues of glutamate, aspartate and quinolinate were examined for agonist and antagonist actions in the rat spinal cord in vivo and in vitro. Compounds found to be excitants were compared directly with quisqualate, kainate, and NMDA for sensitivity to blockade by APV and kynurenate applied both iontophoretically and in the bathing medium; antagonist dose-response curves were constructed for the actions of APV and kynurenate against quisqualate, kainate, quinolinate and NMDA. The conformationally restricted compounds found to be antagonists were examined to determine their potency and specificity against excitations elicited by quisqualate, kainate, quinolinate and NMDA. Although quinolinate is known to be NMDA-like in the hippocampus and cortex, when compared to quisqualate, kainate and NMDA in the spinal cord in vitro, it proved to be unique. A fourth receptor (the "QUIN" receptor) is proposed to account for its actions in the spinal cord. Three of the isomers of 1-amino-1,3-cyclopentane dicarboxylate (ACPD), conformationally restricted analogues of glutamate, were potently blocked by APV and KYNA and were therefore classified as NMDA-like. The fourth, D-trans-ACPD. was indistinguishable from quinolinate in terms of both potency and sensitivity to antagonists. The (-) isomer of trans-1-amino-1,2-cyclopentane dicarboxylate proved to be an antagonist with greater potency against excitations elicited by quisqualate and kainate than those of NMDA. These findings are, in many ways, different from what has been observed in the hippocampal slice. Several pyridine derivatives were examined; 2,5- and 2,6-pyridine dicarboxylate were weak excitants behaving like quisqualate in the presence of APV and kynurenate. No other pyridines were excitatory; however 2,4-pyridine dicarboxylate was observed to be a weak, non-specific antagonist similar in action to acridinate (an antagonist closely related to kynurenate). None of the pyridine derivatives, save quinolinate, are excitatory in the hippocampus. Structural analysis of the active compounds tested, in consideration of previous studies, shows that three points of attachment (two carboxyl and one amino group) are necessary for activation of NMDA, quisqualate and quinolinate receptors in the spinal cord. The location of the distal or y-carboxyl group relative to the a ionic groups appears to be the primary factor determining the activity of a conforrnationally restricted compound. The absolute distance between the Y-carboxyl and α-carbon appears to play a secondary role in determining the action of a compound.
Medicine, Faculty of
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25

Albo, Angelus Zimbul. "Excitatory amino acid receptor changes induced by neonatal bilateral ventral hippocampus lesion in rats." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/tape16/PQDD_0002/MQ37087.pdf.

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26

Ye, Ran. "Mass Spectrometric Characterization and Fluorophore-Assisted Light Inactivation of Human Excitatory Amino Acid Transporter." The University of Montana, 2009. http://etd.lib.umt.edu/theses/available/etd-05192009-104425/.

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Glia-expressing excitatory amino acid transporter 2 (EAAT2) mediates the bulk of glutamate re-uptake in the human central nervous system (CNS) and is associated with a variety of neurological disorders. Our understanding of the structure and mechanism of this integral membrane protein is limited. The goal of this study was to use pharmacological, mass spectrometric (MS) and photochemical approaches to probe EAAT2. For MS characterization, a hexahis epitope was incorporated into the N-terminus of human EAAT2. The recombinant protein was functionally expressed in HEK 293T cells and purified through a single-step nickel column. In-gel and in-solution trypsin digestions were conducted on the isolated protein. Overall, eighty-nine percent sequence coverage of the protein was achieved. An 88-amino acid tryptic peptide covering the proposed substrate binding site was revealed after N-deglycosylation. This study provided an efficient and simple method to purify, digest and characterize integral membrane proteins by MS. In addition, the EAAT2 peptide fingerprint obtained by digestion offered a template for later protein modification studies. In an effort to design photoaffinity labels for hEAAT2, a series of aryl diaminopropionic acids and aryl aspartylamide compounds were synthesized and characterized as potent EAAT inhibitors. Compounds containing 9-fluorenone groups were found to be able to irreversibly inactivate EAATs under UV-A illumination. The mechanism underlying the photo-inactivation was shown to be singlet oxygen mediated protein oxidation. The specificity of the photo-inactivation was illustrated by the protection effects of inhibitors, as well as the proximity between the transporter and ligands. Trypsin digestion and MS analyses revealed a mass change of a peptide from hEAAT2 binding pocket in the photo-inactivated protein. Molecular docking results supported our speculation that a tryptophan residue was oxidized during the photo-inactivation. The identification of possible EAAT2 photo-inactivation site provided additional information for the location of the EAAT2 lipophilic interaction domain.

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27

Gravenstede, Sarah Louise. "The role of excitatory amino acid receptors in regulating excitability of sympathetic preganglionic neurones." Thesis, University of Aberdeen, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.367479.

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The role of excitatory amino acid receptors in the regulation of excitability of sympathetic preganglionic neurones was investigated. Whole-cell patch-clamp recordings were made from sympathetic preganglionic neurones in transverse slices of the rat (8 to 14 days). Sympathetic preganglionic neurones were identified by their characteristic membrane properties and morphology. Perfusion of α-amino-3-hydroxy-5-methyl-4-isoxazole proprionic acid (AMPA; 1 to 10 μM; n = 25), kainate (10 to 50 μM; n = 66), and domoic acid (0.5 to 10 μM; n = 10) evoked concentration-dependent excitatory depolarisation in all SPNs tested. Domoic acid was significantly more potent on sympathetic preganglionic neurones than either AMPA or kainate. Responses to AMPA were reduced by 6-cyano-7-nitroquinoxaline-2, 3-dione (CNQX; 10 μM) and completely abolished by GYKI 52466 (50 μM). By contrast responses to kainate and domoic acid were reduced by CNQX (10 μM) and reduced but not abolished by GYKI 52466 (50 μM). Cyclothiazide (100 μM) selectively potentiated AMPA-induced responses and Concanavalin A selectively potentiated kainate-induced responses in sympathetic preganglionic neurones. Excitatory postsynaptic potentials (EPSPs) were evoked in sympathetic preganglionic neurones by electrical stimulation of the lateral funiculus. EPSPs were differentially sensitive to GYK1 52466 and CNQX suggesting a differential role for AMPA and kainate receptors in sympathetic preganglionic neurones. These results demonstrate that non-NMDA receptors, which form pharmacologically distinct AMPA and kainate receptor populations, are found on sympathetic preganglionic neurones. Domoic acid appears to excite sympathetic preganglionic neurones via kainate receptors. Differential roles were also discovered for AMPA and kainate receptors in synaptic transmission.

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28

Suchak, Sachin Kirit. "Molecular studies of the excitatory amino acid transporters in the rodent central nervous system." Thesis, King's College London (University of London), 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.399082.

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29

Leinenweber, Ariane [Verfasser]. "Regulation of Excitatory Amino Acid Transporter 2 (EAAT2) by Carboxy-terminal Domains / Ariane Leinenweber." Hannover : Bibliothek der Tierärztlichen Hochschule Hannover, 2010. http://d-nb.info/100962427X/34.

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30

Dickinson, Jane A. "Cellular mechanisms of presynaptic nAChR-mediated excitatory amino acid release from rat prefrontal cortex." Thesis, University of Bath, 2007. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.486644.

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Nicotine-mediated activation of nicotinic acetylcholine receptors (nAChRs) located in the prefrontal cortex (PFC) has been associated with the augmentation of attention and working memory. Whilst studies have implicated a.7 and p2* nAChRs in nicotine-elicited cognitive enhancement, the cellular mechanisms underlying these effects have yet to be elucidated. The aim of this project was to characterise the cellular mechanisms bywhich presynaptic a.7 and p2* ~ChRs mediate excitatory amino acid (EAA) release from rat PFC. The first part of this project established the suitability of PFC P2 synaptoso~es and [3H]D-aspartate for measuring presynaptic mechanisms of EAA release, as well as confirming the presence of a.7 and p2* nAChRs in the PFC. Initial experiments showed that nicotine could evoke EAA release via both a.7 and p2* nAChRs, this was confirmed following the characterisation of selective nAChR subtype agonists, (R)-N-(1-azabicyclo[2.2.Z]oct-3-yl)(5-(Zpyridyl) thiophene-2-c~rboxamide) (compound A) and 5-iodo-A-85380. Having established that compound A and 5-iodo-A-85380 evoke EAA release via a.7 and pZ* nAChRs, respectively; investigations into the cellular mechanisms mediating this release were carried out. Whilst higher concentrations of KCI application revealed that EAA release can be mediated by EAA transporter reversal and a Ca2+-dependent mechanism, EAA release mediated by a.7 or p2* nAChRs was entirely Ca2+-dependent. The use of voltage-operated Ca2+ channel (VOCC) inhibitors and modulators of intracellular Ca2+storesdetermined that a.7 and p2* nAChR-mediated EAA release was elicited via distinct pathways. Whilst p2* nAChR-mediated responses were dependent upon VOCC activation, a.7 nAChR-mediated responses required Ca2+-induced Ca2+release (CICR) with no VOCC involvement. To establish whether this distinct coupling of a.7 and pZ* nAChRs was a widespread phenomenon, a.7 and pZ* 0 nAChR subtype selective tools were used to alter Ca2+ levels in PCIZ cells. As seen at the presynaptic terminal, a.7 and pZ* nAChRs were coupled to VOCCs and CICR, respectively. The segregation of these two nAChR subtypes to separate Ca2+pathways may constitute a method by which they regulate different neuronal events. Intracellular Ca2+ stores have recently been implicated in synaptic plasticity, and may provide a mechanism by which a.7 nAChRs mediate their effects on cognition. One possible pathway that can translate presynaptic Ca2+ release into synaptic plasticity is the extracellular regulated kinase cascade. The use of inhibitors and western blotting revealed that this pathway was activated in PFC synaptosomes following a.7 nAChR activation and was essential for a.7 nAChR-mediated EAA release, consistent with a,possible role for this receptor in nicotine-evoked synaptic plasticity in the PFC.

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31

Pook, P. C. K. "Ligand binding and electrophysiological studies of excitatory amino acid receptors in the rat central nervous system." Thesis, University of Bristol, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.381675.

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32

Tian, Guilian. "The molecular mechanisms of the loss of glial glutamate transporter EAAT2 in neurodegenerative diseases." Columbus, Ohio : Ohio State University, 2007. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1187038549.

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33

Connell, Barry James. "The pharmacological effects of intrathecally administered excitatory amino acid receptor ligands in the formalin test." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1996. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp04/mq22182.pdf.

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34

Garry, Emer. "Excitatory amino acid receptors implicated in neuropathic pain : the role of receptor phosphorylation and adapter proteins." Thesis, University of Edinburgh, 2002. http://hdl.handle.net/1842/24603.

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35

Layer, Richard T. "Modulation of hyperactivity and reward by excitatory amino acid, serotonin, and opiate receptors in nucleus accumbens /." The Ohio State University, 1992. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487759914761242.

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36

Chen, Zhiguo. "Excitotoxic neurodegeneration in mouse brain : roles of immune cells and cytokines /." Stockholm, 2004. http://diss.kib.ki.se/2004/91-7349-873-4/.

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37

S, Mathew Seena. "Kainate receptor modulation of synaptic transmission in neocortex." Thesis, Birmingham, Ala. : University of Alabama at Birmingham, 2007. https://www.mhsl.uab.edu/dt/2007p/mathew.pdf.

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38

Sattler, Rita. "Effects of moderate and profound hypothermia on excitatory amino acid-induced neuronal injury in cortical cell cultures." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1996. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/MQ51597.pdf.

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39

Mavencamp, Terri Lynn. "Design, Synthesis and Biological Evaluation of a Family of Excitatory Amino Acid Transporter 3 (EAAT3) Preferring Inhibitors." The University of Montana, 2009. http://etd.lib.umt.edu/theses/available/etd-03212009-152926/.

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This work describes the synthesis and initial characterization of the biological activity of a family of EAAT3 preferring inhibitors, L-β-benzyl aspartate (L-β-BA) and L-β-BA derivatives. L-β-BA and derivatives were initially synthesized in an approximate 2:1 ratio of diasteromers (threo:erythro), using base promoted enolate addition. Kinetic analysis of 3H-D-aspartate uptake into C17.2 cells expressing the hEAATs demonstrated that L-threo-β-BA is the more potent diastereomer (Ki values of 9 µM for EAAT1, 10.0 µM for EAAT2 and 0.8 µM for EAAT3), acts competitively, and exhibits a 10-fold preference for EAAT3 compared to EAAT1 and EAAT2. Electrophysiological recordings of EAAT-mediated currents in Xenopus oocytes further identified L-β-BA as a non-substrate inhibitor. Derivatives of L-β-BA were prepared and characterized for the ability to inhibit 3H-D-aspartate uptake into hEAAT1-3 expressing C17.2 cells. Computational modeling and analysis of structure activity data suggest the area the aromatic moiety of L-β-BA derivatives probe is 1) 3-dimentionally confined, 2) more tolerant of substitutions at the 3 and 5 positions than the 4 position, 3) at least partially distinct from the area probed by L-TBOA and 4) more accessible in the EAAT3 protein than EAAT1 and EAAT2. Computational modeling supports the pharmacological data and lends insight into the selectivity observed with L-β-BA derivatives. Docking studies suggest that H-bonding interactions of L-β-BA derivatives with key residues in the binding site position L-β-BA analogues in a unique manner that is better tolerated in the EAAT3 protein than in the EAAT1 and EAAT2 proteins.

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40

Hwa, Granger G. C. (Guo-Chiang). "An in vitro study on the role of excitatory amino-acid receptors in normal and epileptic neocortices." Thesis, McGill University, 1992. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=39355.

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The putative neurotransmitters L-glutamate and L-aspartate can exert their excitatory action by activating the N-methyl-D-aspartate (NMDA) and non-NMDA receptors. The objective of this thesis is to investigate the physiological role of these excitatory amino-acid receptors in neocortical slices of normal rats and epileptic patients. My experiments in the rat neocortex indicate that excitatory synaptic transmission in normal artificial cerebrospinal fluid (ACSF) is primarily mediated by non-NMDA receptors, whereas the NMDA receptor is only activated when synaptic inhibition mediated by gamma-aminobutyric-acid-A receptors is reduced or blocked. Under such conditions, I found that the NMDA receptor participates in neuronal synchronization through polysynaptic circuits and contributes to the depolarization underlying the epileptiform discharge. In the epileptogenic human neocortex, I discovered that both NMDA and non-NMDA receptors are responsible for excitatory synaptic transmission in normal ACSF. Furthermore, their activation can lead to the appearance of epileptiform discharges. Together, the findings reported in this thesis suggest that the function of NMDA and non-NMDA receptors might be enhanced in the epileptogenic human neocortex, and lend further support to the hypothesis that excitatory amino acids are involved in epileptogenesis.

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41

Smith, Stuart Ernest. "Excitatory amino acid antagonists and related agents as potential therapies in focal cerebral ischaemia in the rat." Thesis, King's College London (University of London), 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.281943.

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42

Hotzy, Linda Sabrina Jasmin [Verfasser]. "Fluorometric approaches to analyze the structure-function relationship of excitatory amino acid transporters (EAATs) / Linda Sabrina Jasmin Hotzy." Hannover : Technische Informationsbibliothek und Universitätsbibliothek Hannover (TIB), 2013. http://d-nb.info/1032720204/34.

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43

Jones, Philip Leslie St John. "Structure-activity studies of novel compounds acting at metabotropic excitatory amino acid receptors in neonatal rat spinal motoneurons." Thesis, University of Bristol, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.385687.

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Barcelona, Stephanie Suazo. "Investigation of the Mechanism of Substrate Transport by the Glutamate Transporter EAAC1." Scholarly Repository, 2007. http://scholarlyrepository.miami.edu/oa_theses/91.

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The activity of glutamate transporters is essential for the temporal and spatial regulation of the neurotransmitter concentration in the synaptic cleft which is critical for proper neuronal signaling. Because of their role in controlling extracellular glutamate concentrations, dysfunctional glutamate transporters have been implicated in several neurodegenerative diseases and psychiatric disorders. Therefore, investigating the mechanism of substrate transport by these transporters is essential in understanding their behavior when they malfunction. A bacterial glutamate transporter homologue has been successfully crystallized revealing the molecular architecture of glutamate transporters. However, many important questions remain unanswered. In this thesis, I will address the role of D439 in the binding of Na+, and I will identify other electrogenic steps that contribute to the total electrogenicity of the transporter cycle. The role of D439 in the binding of Na+ to the transporter was explored previously in this lab. While it was proposed that the effect of D439 in Na+ binding is indirect, the results described in this thesis provides added support to this work. Here, I will show that the D439 mutation changed the pharmacology of EAAC1 such that THA was converted from a transported substrate to a competitive inhibitor. I will also show that Na+ binding to the substrate-bound mutant transporter occurred with the same affinity as that of Na+ to the substrate-bound wild-type transporter. Therefore, based on these results, D439 is not directly involved in the binding of Na+ to the substrate-bound transporter, but that its effect is rather indirect through changing the substrate binding properties. Na+ binding steps to the empty transporter and to the glutamate-bound EAAC1 contribute only 20% of the total electrogenicity of the glutamate transporter reactions cycle. While K+-induced relocation has been proposed to be electrogenic, there is no experimental evidence that supports it. In this work, I will show that the K+-induced relocation of the empty transporter is electrogenic. Moreover, the results in this work show that the K+-dependent steps are slower than the steps associated with the Na+/glutamate translocation suggesting that the K+-induced relocation determines the transporter?s properties at steady state.

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Gerfin-Moser, Andrea Michaela. "Excitatory amino acid receptor expression : localisation in pigeon brain and modulation in rat hippocampal explant cultures by epileptiform activity /." [S.l.] : [s.n.], 1994. http://e-collection.ethbib.ethz.ch/show?type=diss&nr=10918.

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46

Scott, George. "Excitatory amino acid and monoamine mediated neurotransmission in the rat dorsolateral geniculate nucleus in vivo : modulation by BTS 54 505." Thesis, University of Nottingham, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.357974.

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47

Szebeni, Katalin, Attila Szebeni, Michelle J. Chandley, Craig A. Stockmeier, E. Lutz, and Gregory A. Ordway. "Low Gene Expression of Excitatory Amino Acid Transporters in Astrocytes of the Locus Coeruleus From Subjects With Major Depressive Disorder." Digital Commons @ East Tennessee State University, 2009. https://dc.etsu.edu/etsu-works/8629.

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Glutamate is a major stress-sensitive excitatory input to the noradrenergic locus coeruleus (LC) and pathology of both glutamatergic and noradrenergic systems is strongly implicated in major depressive disorder (MDD). Glutamatergic innervation of the LC originates in the frontal cortex and in local brainstem nuclei. Stress increases the release of glutamate in the LC which results in activation of noradrenergic LC neurons. Previous research has demonstrated abnormalities in the levels of glutamate receptor proteins and gene expressions in the postmortem LC of subjects with MDD as compared to normal control subjects providing further evidence for disruption of glutamate-norepinephrine communication in MDD. A principal mechanism for the termination of the action of neuronally-released glutamate is by reuptake via excitatory amino acid transporters (EAAT) located on glia, cells which express both EAAT1 and EAAT2. Here, the potential contribution of glia to glutamate pathology in the LC in MDD was studied by measuring gene expression of EAAT1 and EAAT2 in astrocytes captured from the immediate region of the postmortem LC from 6 pairs of subjects with MDD and psychiatrically normal control subjects. MDD and control subjects were carefully matched for age, RIN value (RNA integrity number), gender, cigarette smoking or non-smoking, and brain tissue pH. Laser capture microdissection was used to capture astrocytes from tissue sections labeled with a modified rapid GFAP-immunostaining, and gene expression levels were analyzed by quantitative PCR. Three reference genes were used as internal controls and the quality of the capture of astrocytes was confirmed by examining the gene expression of cell-type specific markers, including markers for noradrenergic neurons and oligodendrocytes. The gene expression of EAATs was significantly lower (EAAT1, -60%; p<0.001; EAAT2, -25%, P<0.01) in LC astrocytes from MDD subjects as compared to normal control subjects. To determine the regional specificity of these findings, gene expression levels of EAAT1 and EAAT2 were measured in homogenates of both gray and white matter from Brodmann’s area 10 of the cortex. No differences in EAAT gene expression in these cortical tissues were observed comparing MDD to control subjects. These findings indicate that disrupted glial transport of glutamate may contribute to altered glutamatergic transmission in the noradrenergic LC in MDD.

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Linderholm, Klas. "Kynurenic acid in psychiatric disorders studies on the mechanisms of action /." Stockholm, 2010. http://diss.kib.ki.se/2010/978-91-7409-818-1/.

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Butchbach, Matthew E. R. "Regulation of glutamate transport by GTRAP3-18 and by lipid rafts." Connect to this title online, 2003. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1054650123.

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Thesis (Ph. D.)--Ohio State University, 2003.
Title from first page of PDF file. Document formatted into pages; contains xviii, 160 p.; also includes graphics Includes bibliographical references (p. 132-160). Available online via OhioLINK's ETD Center

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Svensson, Erik. "Modulatory effects and interactions of substance P, dopamine, and 5-HT in a neuronal network /." Stockholm, 2003. http://diss.kib.ki.se/2003/91-7349-524-7/.

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