Dissertations / Theses: 'Brain chemistry'

1

Kiritsis, Nikolaos. "Modeling of microdialysis processes and systems used for in vitro experiments /." Digital version accessible at:, 1999. http://wwwlib.umi.com/cr/utexas/main.

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Boyes, Barry Edward. "An immunochemical and immunocytochemical study of the S-100b protein." Thesis, University of British Columbia, 1985. http://hdl.handle.net/2429/24485.

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This thesis describes an immunochemical and immunocytochemical study of the bovine brain S-lOOb protein. The two major forms of the S-100 isoproteins (S-lOOa and S-lOOb) were purified to apparent homogeneity from bovine brain. A polyclonal rabbit antiserum to the S-lOOb protein was prepared. The antiserum was characterized by solid phase immunochemical methods. The S-lOOb derived antiserum displayed a high degree of specificity for S-lOOb, but also crossreacted with the purified S-lOOa protein. The characteristics of the immunochemical reactivity of the antiserum towards these two isoproteins suggests the antiserum has specificity for the 6-subunit of the S-100 proteins. An immunohistochemical analysis of the cellular localization of S-lOOb immunoreactivity was undertaken. In the adult rat brain only the astrocytes were S-lOOb immunoreactive. This conclusion is supported by the morphological characteristics of the immunolabelled cells, as well as the observed co-localization of the immunoreactivities for S-lOOb and the Glial Fibrillary Acidic protein (GFAP), the major protein of the astrocyte intermediate filaments. These two antigens were always found to coexist. The immunolabelling of rat brain astrocytes by the S-lOOb derived antiserum stained the entire cell, yielding more complete morphological detail than is possible with the GFAP immunohistochemistry, which only labels the filamentous glial processes. It is concluded that S-lOOb immunohistochemistry could be of general utility in the investigation of astrocyte morphology. The present results also determine that the as yet unknown biological function(s) of the S-100 proteins must be related to a property of astrocytes.
Medicine, Faculty of
Graduate

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3

Bengtson, Colin Peter. "Serotonin and dopamine actions on basal forebrain neurons in the ventral pallidum in vitro /." [St. Lucia, Qld.], 2001. http://www.library.uq.edu.au/pdfserve.php?image=thesisabs/absthe16862.pdf.

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Cada, Amy Marie. "Brain energy metabolism and spatial memory dysfunction /." Digital version accessible at:, 1998. http://wwwlib.umi.com/cr/utexas/main.

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5

Malak, Ramez. "2D gel analysis on CNP-overexpressing mouse brain." Thesis, McGill University, 2002. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=79041.

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2',3'-Cyclic nucleotide 3 '-phosphodiesterase (CNP) is an early marker for oligodendrocytes, and it is suspected to be implicated in the expansion of membranes during myelination. We have previously generated transgenic mice that overexpress CNP. These mice showed altered oligodendroyte development, produced aberrant myelination, and had less MBP accumulated in myelin. More interestingly, ODCs isolated from those mice had a tremendous increase in the process extension formation. The purpose of the present study is to compare the protein expression pattern in the myelin isolated from control and CNP overexpressing mice (L191), using two-dimensional gel electrophoresis. We found that CNP overexpression increases HSC70, and HSP70, and decreases MAG expression in myelin. We also found that the mRNA for MAG, in L191 brain was identical to control brain during all stages of development. These findings suggest that CNP may be implicated with HSC70 in vesicular transport, and this may explain the mechanism of process extension mediated by CNP.

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Jäverfalk-Hoyes, Emmy. "Development of methods in CE, CE-MS and MS/MS : applications in pharmaceutical, biomedical and forensic sciences /." Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2001. http://publications.uu.se/theses/91-554-5107-1/.

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7

Laitinen, Päivi. "Antizyme in the regulation of mouse brain ornithine decarboxylase." Oulu : University of Oulu, 1986. http://catalog.hathitrust.org/api/volumes/oclc/16882622.html.

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8

Schweinsburg, Brian Christopher. "Neurochemical correlates of blood oxygen level dependent signal changes in abstinent alcoholics /." Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2004. http://wwwlib.umi.com/cr/ucsd/fullcit?p3130210.

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9

PINTO, LUCIANA DORNELAS. "STUDY OF COPPER(II) COMPLEXES CONTAINING AMINO ACIDS OF INTEREST FOR BRAIN CHEMISTRY." PONTIFÍCIA UNIVERSIDADE CATÓLICA DO RIO DE JANEIRO, 2010. http://www.maxwell.vrac.puc-rio.br/Busca_etds.php?strSecao=resultado&nrSeq=16189@1.

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CONSELHO NACIONAL DE DESENVOLVIMENTO CIENTÍFICO E TECNOLÓGICO
Foram sintetizados 16 complexos de cobre(II) coordenados com seis aminoácidos presentes na placa b-amilóide, que está associada à Doença de Alzheimer - ácido aspártico, ácido glutâmico, metionina, glicina, serina e arginina, outros dois aminoácidos também encontrados no cérebro - cisteína e homocisteína, além da L-carnitina e acetil-L-carnitina que vêm sendo utilizados como suplemento alimentar em pacientes com doenças neurodegenerativas. Nosso objetivo foi verificar a afinidade do cobre(II) com estes aminoácidos, uma vez que o envelhecimento provoca aumento no cérebro tanto das concentrações de íons cobre como dos níveis de todos estes aminoácidos (que são consequência de fragmentações peptídicas). Por esta razão, procurou-se trabalhar in vitro com condições próximas ao meio biológico utilizando apenas água deionizada como solvente. Os complexos obtidos foram caracterizados pelas seguintes técnicas: análise elementar (espectrometria de absorção atômica e CHN), condutimetria, análise termogravimétrica, ressonância paramagnética eletrônica, voltametria cíclica e espectroscopia no infravermelho. Foi possível verificar que, exceto a acetil-L-carnitina, todos se comportam como ligantes bidentados e complexam facilmente ao cobre(II). Ácido aspártico, ácido glutâmico, serina, metionina, glicina e arginina se coordenaram através do átomo de oxigênio do grupo carboxilato e do átomo de nitrogênio do grupo amino, cisteína e homocistéina através do átomo de enxofre e do átomo de nitrogênio do grupo amino, L-caritina através do átomo de oxigênio do grupo carboxilato e do átomo de oxigênio alcoólico e acetil-L-carnitina se coordena monodentadamente através do átomo de oxigênio do grupo carboxilato.
Sixteen complexes of copper(II) with six amino acids that are present in the b-amyloid peptide, which is associated with Alzheimer’s disease - aspartic acid, glutamic acid, methionine, glycine, serine and arginine -, two amino acids also found in the brain - cysteine and homocysteine -, as well as L-carnitine and acetyl-L-carnitine, which have been used as food supplement in patients with neurodegenerative diseases, were studied. Our aim was to determine the affinity of copper(II) with these amino acids, since aging causes an increase in brain concentrations of copper ions as well as in the level of all of these amino acids, as a consequence of peptide fragmentation. For this reason, we decided to do an in vitro study in similar conditions as the biological environment, using only deionized water as solvent. These compounds were characterized through the following techniques: elementary analysis (atomic absorption spectrometry and CHN), conductimetry, thermogravimetric analysis, electron paramagnetic resonance, electrochemical analysis, and infrared spectroscopy. It was possible to verify that, except for acetyl-L-carnitine, all amino acids behaved as bidentate ligands. They all form complexes with copper(II) easily. Aspartic acid, glutamic acid, serine, methionine, glycine and arginine coordinate through the oxygen atom of the a-carboxylate group and the nitrogen atom of the amine group. Cysteine and homocysteine coordinate through the sulfur atom and the nitrogen atom of the amine group, L-Carnitine coordinates through one oxygen atom of the carboxylate group and one oxygen atom of the alcohol group, and acetyl-L -carnitine coordinates through the oxygen atom of the carboxylate group.

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10

Charlton, Stuart Thomas. "Drug delivery to the brain via intranasal administration." Thesis, University of Nottingham, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.275962.

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11

Chen, Zheng-wang. "Isolation and characterization of novel intestinal polypeptides of the enteroinsular and brain-gut axes and of macrophages /." Stockholm, 1997. http://diss.kib.ki.se/1997/19971212chen.

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Migues, Paola Virginia. "Role of neurosteroids on memory formation in the chick." Thesis, Open University, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.367225.

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13

Kuhnell, Pierce. "Evaluating the relationship between brain chemistry and postural balance in the Cincinnati Lead Study." University of Cincinnati / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1409065672.

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Rich, Clive George. "Morphine-like compounds in brain tissue and dietary materials." Thesis, University of Sunderland, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.328983.

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Maurya, Manisha. "The effect of antidepressants on rodent brain glucocorticoid systems." Thesis, Open University, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.368872.

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16

Olsson, Hans. "In vivo quantification of extrastriatal dopamine D2 receptors in the human brain /." Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-290-X/.

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17

McClelland, Alan R. "Event-related brain potential correlates of nicotine and smoking behaviour." Thesis, Queen's University Belfast, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.317560.

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18

Wagner, Michael R. "The Nitroxidative Response to Traumatic Brain Injury." Ohio University / OhioLINK, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=ohiou1584179902783766.

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19

Giddins, R. E. "Behavioural and biochemical correlates of melatonin action in the rodent brain." Thesis, University of Bradford, 1985. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.371472.

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20

Harder, Hubert Werner. "Metabolism of arachidonic and adrenic acids in molecular species of gycerophospholipids in mouse brain /." The Ohio State University, 1986. http://rave.ohiolink.edu/etdc/view?acc_num=osu14872651431456.

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21

Pedada, Kiran K. Mr. "GRADIENT CHROMATOFOCUSING AND REVERSED PHASE HPLC IN PROTEIN ANALYSIS AND LC-MS/MS DETERMINATION OF THIAZOLIDINEDIONE NL-1 IN MOUSE SERUM AND BRAIN." Cleveland State University / OhioLINK, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=csu1390322545.

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22

Dobrucki, Wawrzyniec L. "Nitrogen and Oxygen Radicals in Ischemic and Hypoxic Injury of the Brain." Ohio University / OhioLINK, 2003. http://rave.ohiolink.edu/etdc/view?acc_num=ohiou1057171850.

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23

Tavares, Adriana A. S. "Development of novel radiotracers as tools for imaging the human brain." Thesis, University of Glasgow, 2011. http://theses.gla.ac.uk/2919/.

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Introduction: Brain imaging using single photon emission computed tomography (SPECT) or positron emission tomography (PET) can be used to study the processes underlying neurological and psychiatric disorders. In addition, in vivo brain imaging using SPECT or PET may provide new approaches for drug target identification, pre-clinical testing and occupancy studies, and therefore improve drug discovery. The utility of in vivo brain imaging using SPECT or PET relies on the ability of different radiotracers (typically organic compounds labelled with radionuclides) to bind to a wide variety of targets, including receptors, transporters and enzymes. Therefore the development of novel radiotracers for in vivo brain imaging using SPECT of PET is of vital importance. This thesis is focused on the process of developing novel radiotracers as tools for imaging the human brain, where the radiotracer discovery and development pipeline is discussed and each step prior to clinical trials investigated. Radiotracer discovery: Previously, discovery of novel brain radiotracers has largely relied on simplistic screening tools. Improved selection methods at the early stages of radiotracer discovery and an increased understanding of the relationships between in vitro physicochemical and in vivo radiotracer properties are needed. This thesis investigated if high performance liquid chromatography (HPLC) methodologies could provide criteria for lead candidate selection by comparing HPLC measurements with radiotracer properties in humans. In this study, ten molecules, previously used as radiotracers in humans, were analysed to obtain the following measures: partition coefficient (Log P); permeability (Pm); percentage of plasma protein binding (%PPB); and membrane partition coefficient (Km). Relationships between brain entry measurements (Log P, Pm and %PPB) and in vivo brain percentage injected dose (%ID); and Km and specific binding in vivo (BPND) were investigated. Results showed that HPLC measurements of Pm, %PPB and Km were potentially useful in predicting in vivo performance and hence allow evaluation and ranking of compound libraries for the selection of lead radiotracer candidates at early stages of radiotracer discovery. The HPLC tool developed provides information on in vivo non-specific binding and binding potential that is not possible using conventional screening methods. Another important finding reported in this thesis is that Log P should not be relied on as a predictor of brain entry. The HPLC tool developed, together with competition binding assays, was used to characterise a newly synthesised library of compounds for imaging of the translocator protein (TSPO) in brain using SPECT. Results showed that compound LS 1 was the most likely to succeed within the library investigated, but the high %PPB observed for LS 1 suggested novel compounds with improved %PPB were needed. Thus, a novel library of compounds for imaging of TSPO in brain using SPECT is currently been developed for future testing using the HPLC tool developed here and competition binding assays. Pre-clinical research: radiotracers for imaging the noradrenaline transporter (NAT) in brain using SPECT. In this thesis, NKJ64, a novel iodinated analogue of reboxetine, was successfully radiolabelled via electrophilic iododestannylation and evaluated as a potential SPECT radiotracer for imaging the NAT in brain using rodents and non-human primates. Biological evaluation of the novel radiotracer, 123/125I-NKJ64, in rodents included: in vitro ligand binding assays; in vitro and ex vivo autoradiography; in vivo biodistribution studies and ex vivo pharmacological blocking studies. In rats, 123/125I-NKJ64 displayed saturable binding with nanomolar affinity for the NAT in cortical homogenates, regional distribution consistent with the known density of NAT in the rodent brain and high maximum brain uptake of around 2.93 % of the injected dose. The specific: non-specific ratio (locus coeruleus:caudate putamen) of 123I-NKJ64 uptake was 2.8 at 30 minutes post intravenous injection and prior administration of reboxetine significantly reduced the accumulation of 123I-NKJ64 in the locus coeruleus (> 50% reduction). Data obtained using rodents indicated that further evaluation of 123I-NKJ64 in non-human primates was needed to determine its utility as a SPECT radiotracer for imaging of NAT in brain. Consequently, in vivo kinetic modelling studies using SPECT imaging with 123I-NKJ64 and two baboons were carried out to determine 123I-NKJ64 brain binding kinetics, brain distribution and plasma metabolism in non-human primates. Even though a high brain uptake of around 3.0% of the injected dose was determined, the high non-specific binding observed throughout the brain, a low binding potential (BPND<2) in NAT rich regions and a brain distribution that was inconsistent with the known NAT distribution in non-human primate brain precludes the translation of 123I-NKJ64 into humans. Another NAT radiotracer, 123I-INER, developed by Tamagnan and colleagues at Yale University and Institute for Degenerative Disorders, New Haven, USA, was also investigated as part of this thesis. Kinetic modelling analysis of 123I-INER in baboon brain was investigated for different models, namely invasive and reference tissue models. Bolus plus constant infusion experiments with displacement at equilibrium using six different doses of atomoxetine and four different doses of reboxetine were carried out in several baboons to obtain occupancy measurements as a function of injected dose (mg/kg) for the two NAT selective drugs. Results showed that reference tissue models were able to determine BPND values of 123I-INER in different brain regions. In addition the volume of distribution could be determined by dividing concentration in tissue by the concentration in venous blood at 3 hours post-injection. After administration of atomoxetine or reboxetine, dose-dependent occupancy was observed in brain regions known to contain high densities of NATs. Results supported the translation of 123I-INER into humans studies, despite the slow kinetics determined over the imaging period. Pharmacokinetic properties of 123I-INER described in this thesis may be used to simplify future data acquisition and image processing. Conclusion In conclusion, this thesis reported: (1) the development of novel radiotracers for brain imaging, namely NAT and TSPO; and (2) the development of a new methodology for aiding lead molecule identification at early stages of radiotracer discovery (i.e. prior to radiolabelling). In addition, an overview of radiotracer discovery and development process is provided in a single document, with a focus on brain radiotracers.

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Jogiraju, Harini. "OPTIMIZATION OF GRADIENT CHROMATOFOCUSING FOR THE PROTEIN SEPARATIONANDLC-MS/MS DETERMINATION OF NGP1-01 IN MOUSE SERUM, BRAIN, AND RETINA." Cleveland State University / OhioLINK, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=csu1389704171.

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25

Morin, Mario Y. "Enhancement of neural cell regeneration and survival by altering gap junctional communication following brain injury." Thesis, University of Ottawa (Canada), 2006. http://hdl.handle.net/10393/27397.

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The adult brain is particularly susceptible to injury given that it lacks significant regenerative capacity. The presence of rare neural stem and progenitor cells - cells capable of self-renewal and specification to a neuronal or a glial lineage - in specific areas of the adult central nervous system (CNS) offers new hope for therapeutic cell replacement. Our laboratory has previously implicated connexin32 (Cx32) in participating in neural progenitor cell fate determination to an oligodendrocyte lineage (Melanson-Drapeau et al., 2003; Hebb et al., submitted). Based on these previous findings, I hypothesized that neuronal regeneration might be increased in Cx32 knockout (KO) mice following hippocampal injury. Kainic acid (KA)-induced epileptic seizure was used to elicit loss of hippocampal neurons and study subsequent progenitor cell proliferation and specification to neurons and oligodendrocytes in the hippocampus of adult wild type (WT) and Cx32KO mice. The kinetics of hippocampal cellular degeneration and regeneration were established following seizure by qualitative and quantitative histological analyses. I found that the viability of the granule cell population in the dentate gyrus (DG) was compromised following excitotoxic challenge but that damaged cells recovered four weeks post-injury without undergoing significant cell death. Substantial neuronal loss with both apoptotic and non-apoptotic characteristics was detected in the CA3 field of the hippocampus 0.5 weeks post-injury in both genotypes. Significant progenitor cell amplification (proliferation) was observed in the CA3 field at the same time period. Progenitor cells in Cx32KO mice preferentially committed to a neuronal lineage, increasing neuroregeneration 4.5 weeks following injury. The Morris water maze, a hippocampal dependent spatial memory task, was used to test the functionality of these new neurons four weeks following KA-induced injury. I show that uninjured WT and Cx32KO mice exhibit comparable indices of spatial learning and memory. Following KA-induced seizure, WT mice are behaviourally impaired while Cx32KO mice are not, providing strong evidence of enhanced functional neuroregeneration in the absence of Cx32. Finally, to provide a tool to track the fate of neural progenitors destined to express Cx32 over time following injury, a new transgenic marker mouse, that expresses the enhanced green fluorescent protein (EGFP) in place of Cx32, was engineered for use in future studies.

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26

Fraser, Graeme L. "Characterization of [delta] opioid receptor function in rat brain by pharmacological and antisense techniques." Thesis, McGill University, 2001. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=38454.

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The opioid family of G-protein coupled receptors comprises four known receptor subtype genes (delta, mu, kappa, ORL1) and further receptor heterogeneity within each opioid receptor subfamily has been proposed. All four genes are expressed throughout the central nervous system and are believed to modulate a variety of behavioural responses including analgesia. Opiate drugs such as morphine that are selective for the mu receptor subtype are effective analgesics, but their chronic use is limited by the appearance of side effects such as respiratory depression, constipation and dependence. Consequently, the analgesic potential of agonists selective for other opioid receptors is under investigation. In this regard, previous studies suggest that delta agonists mediate antinociception, yet produce fewer adverse effects than mu agonists. To further investigate the cloned delta opioid receptor (DOR) as a target for novel analgesics, the pharmacological role of DOR in brain was evaluated in rats.
First, we characterized delta agonist binding sites and receptor activation in rat brain membranes. We also introduced a novel antagonist radioligand, [125I]AR-M100613, to label tissues with low delta opioid receptor expression in order to support follow-up studies where radioligand binding was performed on rat brain membranes following antisense treatment. Second, we examined the behavioural response to delta agonists in rats. Deltorphin II and SNC80 (i.c.v.) were shown to induce antinociception in acute pain assays, and to reverse hyperalgesia following tissue inflammation induced by Freund's adjuvant with even greater potency. These findings indicate that delta receptors play an enhanced role in the modulation of descending pain pathways following tissue injury. Deltorphin II and SNC80 (i.c.v. ) were also shown to induce hyperlocomotor activity. Third we used antisense studies to demonstrate that the antinociceptive and locomotor stimulant effects of delta agonists are modulated by the cloned delta opioid receptor (DOR). In contrast to other delta agonists, the antinociceptive effects of DPDPE were not modulated by DOR antisense treatment but rather were blocked by a selective mu antagonist (CTOP) suggesting that DPDPE may activate mu sites in the brain rather than an alternate delta receptor subtype. Finally, we demonstrated that peptide nucleic acids (PNA, i.c.v.) can act as target-specific and sequence-selective antisense agents. In total, these findings demonstrate that DOR is an appropriate target for the development of novel analgesics and that PNA can serve as effective antisense agents for the determination of gene function for CNS targets.

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Ondik, Mercedes Maye. "Detecting the inclusion and exclusion of a neuronal XDP-associated microexon in situ." Thesis, Massachusetts Institute of Technology, 2018. http://hdl.handle.net/1721.1/118130.

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Thesis: S.B. in Chemistry-Biology, Massachusetts Institute of Technology, Department of Brain and Cognitive Sciences, 2018.
This electronic version was submitted by the student author. The certified thesis is available in the Institute Archives and Special Collections.
Cataloged student-submitted from PDF version of thesis. "Submitted to the Department of Brian and Cognitive Sciences in supplement to the requirements for the degree of Bachelor of Science in Chemistry-Biology."
Includes bibliographical references (pages 52-54).
X-linked dystonia parkinsonism (XDP), also known as torsion dystonia type 3 (DYT3), afflicts hundreds of individuals. Under an X-linked mode of inheritance, the DYT3 haplotype occurs in Filipino populations and is of the highest frequency in the Panay Islands of the Philippines. Recently, convincing evidence has shown the causative mutation to be an insertion of the repetitive sequence SINE-VNTR-Alus (SVA). This insertion is associated with misregulation of 3' end exons in the gene TBP-associated factor 1 (TAF1). TAF1, the largest of fourteen TAF proteins, incorporates into a TATA binding complex that promotes transcription by RNA polymerase II. In a collaborative effort, singleplex BaseScope" probes as well as antibodies have been produced to target two TAF1 isoforms, canonical TAF1, C-TAF1, and neuronal TAF1, N-TAF1, separately. N-TAF1 differs from C-TAF1 by the inclusion of a two amino acid microexon, 3' to the SVA insertion, known as 34'. Here, I show that N-TAF1 expression is confined to neurons and interneurons whereas C-TAF1 is widely expressed, particularly by astrocytes, interneurons, neurons, and cells present in other organs including the heart and liver in mouse. Additionally, the antibodies produced show promise for use in human tissue. These results support the hypothesis that C-TAF1 and N-TAF1 have canonical and neuron-specific functions, respectively, and misregulation of N-TAF1 is capable of causing neuronal degeneration. Ultimately these results set the foundation for the study of C-TAF1 and N-TAF1 functions and isoform misregulation in XDP diseased tissue. Furthermore, these probes and antibodies may serve as tools for the validation of XDP models, under development, in which forthcoming XDP therapies may be tested.
by Mercedes Maye Ondik.
S.B. in Chemistry-Biology

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28

Merritt, Rebecca L. "The effects of environmental chemicals on glioblastoma cell growth." Morgantown, W. Va. : [West Virginia University Libraries], 2004. https://etd.wvu.edu/etd/controller.jsp?moduleName=documentdata&jsp%5FetdId=3475.

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Thesis (M.S.)--West Virginia University, 2004.
Title from document title page. Document formatted into pages; contains vii, 78 p. : ill. (some col.). Includes abstract. Includes bibliographical references (p. 70-78).

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29

Powell, R. C. "Evolution of the structure and function of vertebrate brain gonadotropin-releasing hormone." Master's thesis, University of Cape Town, 1986. http://hdl.handle.net/11427/27201.

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In this study, the structure and function of gonadotropin-releasing hormone (GnRH) in different vertebrate species, in the classes Aves, Reptilia and Pisces was investigated. Acetic acid extracts were subjected to gel filtration chromatography and semipreparative high performance liquid chromatography (HPLC) to partially purify the GnRHs. The GnRH immunoreactivity was then characterized by analytical HPLC, and by assaying HPLC fractions by radioimmunoassay with region-specific antisera generated against mammalian GnRH, Gln⁸-GnRH and Trp⁷,Leu⁸-GnRH and assessing luteinizing hormone (LH)-releasing activity of fractions in a chicken dispersed anterior pituitary cell bioassay. Five GnRH molecular forms have thusfar been structurally characterized in vertebrate brain. In mammals a GnRH with the structure pGlu-His-Trp-Ser-Tyr-Gly-Leu-Arg-Pro-Gly-NH₂ has been demonstrated in the hypothalamus (Matsuo et al., 1971; Burgus et al., 1972). Gln⁸-GnRH and His⁵,Trp⁷,Tyr⁸-GnRH were present in chicken hypothalamus (King and Millar, 1982a, 1982c; Miyamoto et al., 1983, 1984), Trp⁷,Leu⁸-GnRH in salmon brain (Sherwood et al., 1983) and Tyr³,Leu⁵,Glu⁶,Trp⁷,Lys⁸-GnRH in lamprey brain (Sherwood et al., 1986). In ostrich (Struthio camelus) hypothalamus two GnRHs with identical properties to Gln⁸-GnRH and His⁵,Trp⁷,Tyr⁸-GnRH have been demonstrated, as well as four other LR-releasing factors with different chromatographic and immunological properties to any of the known naturally-occurring GnRHs. Since Gln⁸-GnRH and His⁵,Trp⁷,Tyr⁸-GnRH were also present in chicken hypothalamus it appears likely that these two GnRHs occur in all birds. In alligator (Alligator mississippiensis) brain only two GnRHs were detected. These forms co-eluted with Gln⁸-GnRH and His⁵,Trp⁷,Tyr⁸-GnRH in two HPLC systems. They cross-reacted similarly to the two synthetic peptides with antisera directed against mammalian GnRH and Gln⁸-GnRH and released LH from chicken dispersed anterior pituitary cells in a similar manner to the synthetic peptides. The Archosaurs (alligators and crocodiles) are believed to be closely related to birds and therefore it seems likely that they should have identical GnRHs. In skink (Calcides ocellatus tiligugu) brain one GnRH, which co-eluted with His⁵,Trp⁷,Tyr⁸-GnRH, was demonstrated. Two other lizards (Cordylis nigra and Pordarcis s. sicula) have been studied (Powell et al., 1985; R.C. Powell, G. Ciarcia, V. Lance, R.P. Millar and J.A. King, submitted). In c. nigra four immunoreactive GnRHs were detected, two of which co-eluted released chicken LH similarly to, Trp⁷,Leu⁸-GnRH and with, and His⁵,Trp⁷,Tyr⁸-GnRH. In P. s. sicula a GnRH molecular form similar to Trp⁷,Leu⁸-GnRH occurred as well as two novel GnRHs. It thus appears that Gln⁸-GnRH does not occur in lower reptiles, but His⁵,Trp⁷,Tyr⁸-GnRH and/or Trp⁷,Leu⁸-GnRH do. His⁵,Trp⁷,Tyr⁸-GnRH appears to he a widespread GnRH, occurring in vertebrates as diverse as birds and elasmobranch fish. In dogfish (Poroderma africanum) brain seven factors, which stimulated release of LH from chicken dispersed anterior pituitary cells, were separated on analytical HPLC. Two of these factors were partially characterized as Trp⁷,Leu⁸-GnRH and His⁵,Trp⁷,Tyr⁸-GnRH. Three of the other forms cross-reacted with GnRH antisera, but appear to be novel GnRHs. In teleost (Coris julis) brain two GnRHs similar to Trp⁷,Leu⁸-GnRH and His⁵,Trp⁷,Tyr⁸-GnRH were present. These two GnRHs therefore appear to occur in both fish species studied. Trp⁷,Leu⁸-GnRH is widespread amongst teleost fish (Jackson and Pan, 1983; Sherwood et al., 1983; Breton et al., 1984; Sherwood et al., 1984; King and Millar, 1985). From these data it seems evident that the mammalian GnRH molecular form occurs only in mammals and amphibians, Gln⁸-GnRH in birds and higher reptiles, and Trp⁷,Leu⁸-GnRH in gnathostomes. His⁵,Trp⁷, Tyr⁸-GnRH appears to he present in numerous different vertebrates. Tyr³,Leu⁵,Glu⁶,Trp⁷,Lys⁸-GnRH has thus far only been detected in lamprey brain. A number of novel GnRHs, whose structures have not been elucidated are present.

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30

Tawati, Ahmed Mohamed. "Neurochemical studies on the role of glycine as a neurotransmitter in rat brain." Thesis, University of Southampton, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.295886.

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31

Myers, Kazimer Rene. "Correlation of membrane glycoconjugates and cell growth with the sensitivity of human glioma and fetal brain cells to natural killer cell cytolysis /." The Ohio State University, 1989. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487670346874684.

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32

Pellerin, Luc. "Studies on arachidonic acid release and metabolism by the 12-lipoxygenase pathway in rat brain slices." Thesis, McGill University, 1992. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=70251.

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The present work was aimed at studying the release of arachidonic acid and formation of lipoxygenase metabolites in rat brain slices maintained in vitro, as well as exploring possible physiological roles for them in the mammalian central nervous system. A particularly active 12-(S)-lipoxygenase activity was found, which could be stimulated by various stimuli including the neurotransmitters norepinephrine and glutamate. Activation of $ alpha$-adrenergic and N-methyl- scD-aspartate (NMDA) receptor subtypes appear responsible for the effect observed in each case. Arachidonic acid on the other hand was found to have profound effects on synaptic transmission, inducing a long-lasting potentiation which appears dependent on the formation of lipoxygenase metabolites. In return, pharmacological conditions which can potentially lead to long-term potentiation (LTP) of synaptic transmission and for most of them activate NMDA receptors also induced arachidonic acid release. As these observations suggest, it is proposed that arachidonic acid and its lipoxygenase metabolites belong to a new group of messengers in the nervous system possibly acting as modulator of synaptic transmission both intra- and transcellularly. This new class of messengers constitutes an essential component of the molecular machinery involved in synaptic plasticity.

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33

Chanda, Mullen. "ANTI-S100B Autoantibodies in Cerebral Small Vessel Disease and Brain Metastasis in a Lung Cancer Population." Cleveland State University / OhioLINK, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=csu1452097886.

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34

Hurley, Michael James. "The localization and regulation of the dopamine D3 receptor in rodent and primate brain." Thesis, King's College London (University of London), 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.339224.

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35

Harrison, Peter Stuart. "The phenomenon of neuronal sensitization by quisqualic acid : a neurochemical investigation in rat brain." Thesis, University of Bristol, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.333960.

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36

El, Kodsi Daniel N. "A Redox Chemistry-based Function for Parkinson Disease-linked Parkin Confers Direct, Anti-oxidant Activities in Mammalian Brain." Thesis, Université d'Ottawa / University of Ottawa, 2020. http://hdl.handle.net/10393/41129.

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Early-onset Parkinson disease, of which the best studied and most common cause are biallelic mutations in the PRKN gene, is characterized by an age of onset before 40 years. Parkin-deficient patients show slow progression, excellent responsiveness to L-dopa therapy, and are generally spared cognitive decline. At autopsy, PRKN-linked Parkinson disease is further distinguished by relative selectivity in cell loss, namely of dopamine producing neurons in the human brainstem, and the general absence of Lewy body inclusions. Since its discovery two decades ago, the field has focused on the function of parkin as an E3 ubiquitin ligase and its related role in mitophagy. However, its essential, neuroprotective function in ageing human midbrain and the mechanisms by which wildtype parkin preserves dopamine cell health in aged humans are yet to be elucidated. I hypothesized that parkin confers neuroprotection due to a redox function by its many cysteines (7.5%). We first focused on parkin’s biochemistry, reporting a shift from solubility to a nearly insoluble, aggregated state in adult control brain after age 40 years. We detected cysteine-based, post-translational modifications of parkin in response to oxidative stress, and characterized a novel, redox chemistry-based function: Through its own oxidation parkin reduced hydrogen peroxide in vitro. I validated this finding by showing its elevation in parkin-deficient, human brain. Wild-type parkin also participated in dopamine metabolism through the conjugation of reactive radicals at several of its cysteines, which augmented the generation of melanin. (Chapter 2). In addition, we demonstrated parkin’s heretofore unknown, antioxidant function in the cytosol using cellular paradigms and select genetic as well as toxin-based mouse models that featured elevated oxidative stress. Moreover, we uncovered parkin’s contribution to the wider thiol network, namely through an apparent feedback loop with glutathione metabolism (Chapter 3). Lastly, I developed and investigated a bi-genic (prkn-/-//Sod2+/-) model in an attempt to restage the pathogenesis of early-onset parkinsonism in mice; there, we detected a rise in systemic, oxidative stress and in total nitrotyrosination profiles of the brain, but did not observe any dopamine neuron loss in the midbrain. In accordance, the behavioural characterization of these animals did not reveal any motor abnormalities (Chapter 4). Based on this previously unknown function for parkin in redox biology, I envision three future research directions: a) additional studies to delineate the full range of oxidative modifications of parkin versus neutralization of radicals; this, to better define the distinct pathogenesis of parkin-linked Parkinson’s when compared to other forms of the disorder; b) structural studies of its oxidative modifications in vitro and renewed attempts of staging parkin-linked dopamine cell death in vivo; and c) and importantly, the exploration of cause-directed therapy based on parkin’s redox functions to preserve dopamine neurons of the human midbrain throughout adulthood.

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37

Ottervald, Jan. "Proteomics in neurological disease." Stockholm, 2009. http://diss.kib.ki.se/2009/978-91-7409-729-0/.

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38

Häidkind, Riina. "Monoaminergic mechanisms in mood-associated behaviours and neurochemistry in rats /." Tartu : Tartu University Press, 2004. http://dspace.utlib.ee/dspace/bitstream/10062/704/5/Haidkind.pdf.

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39

Davidson, Colin H. "The effect of acute and chronic paroxetine treatment on serotonin neurotransmission in rat brain slices." Thesis, Queen Mary, University of London, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.243319.

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40

Chen, Tzu-chin 1965. "Partial purification and characterization of sodium channel phosphatases from rat brain: Similarity to phosphatase 2A." Thesis, The University of Arizona, 1991. http://hdl.handle.net/10150/278004.

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Four distinct serine/threonine protein phosphatases have been purified from and identified in various tissues. They are type 1 and type 2 phosphatases, which are further classified as phosphatase 2A, 2B, and 2C. In this study, endogenous brain phosphatases that dephosphorylate sodium channels were partially purified and characterized. Multiple peaks of sodium channel phosphatase were detected after DEAE-Sephadex chromatography and gel filtration. All peaks were sensitive to a low concentration of okadaic acid (10 nM), which strongly suggests that phosphatase 2A is the major brain phosphatase dephosphorylating sodium channels. Individual fractions containing sodium channel phosphatase activity from both DEAE-Sephadex chromatography and gel filtration were subjected to immunoblot with anti-phosphatase 2Ac antibody. The results indicate that all fractions containing phosphatase activity also contained phosphatase 2Ac immunoreactivity. The fractions which stained most intensely in the immunoblots were the fractions containing the highest phosphatase activity in all cases. The molecular weights of the multiple sodium channel phosphatases estimated by gel filtration were 83 kDa, 147 kDa, and 141 kDa. These may represent isozymes of phosphatase 2A in brain.

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41

Lindblom, Jonas. "The Role of the Melanocortin System in Linking Energy Homeostasis with Reward Mechanisms." Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2002. http://publications.uu.se/theses/91-554-5252-3/.

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42

Lee, Herbert Chi-Ho. "Chemistry and preliminary biological evaluation of novel radioiodinated iodoazomycin arabinoside (IAZA) metabolites as potential SPECT brain and tumor imaging agents." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp02/NQ29061.pdf.

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43

Donaldson, J. "Influence of 1,4-dithiothreitol on histamine H1Ì²-receptor-effector mechanisms in guinea pig brain and ileal smooth muscle." Thesis, University of Nottingham, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.373347.

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44

Barnes, J. C. "Behavioural consequences of chronic disturbance of dopamine function in the nucleus accumbens and amygdala of the rat brain." Thesis, University of Bradford, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.374911.

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45

Williams, Jennifer Nicole. "Metal Containing Nucleosides that Function as Therapeutic and Diagnostic Agents Against Brain Cancer." Cleveland State University / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=csu1409238775.

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46

Siddiqui, Maya. "Development of HPLC-EC Methodology & Its Use in the Determination of the Daily Pattern of Brain Octopamine Levels in Leucophaea Maderae." TopSCHOLAR®, 1992. https://digitalcommons.wku.edu/theses/2866.

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A solid phase extraction technique was developed to aid in removing interfering substances from the cockroach brain extract. Quantitative analysis of octopamine was subsequently achieved by HPLC with amperometric electrochemical detection. The procedure affords 80 to 100 percent recovery of octopamine. The presence of octopamine in brain extract was confirmed by GC-MS. The daily pattern of brain octopamine levels in cockroach Leucophaea maderae was investigated using the HPLC-EC assay procedure. It was concluded that the concentration of brain octopamine in the cockroach L. maderae does not exhibit daily rhythm.

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47

Carletti, Renzo. "Characteristics of NMDA receptor ligands in rodent brain, in vivo and in vitro, under normal conditions and after chronic ischaemia." Thesis, University College London (University of London), 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.243989.

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48

Harris, Jessica Lynn. "INVESTIGATIONS INTO MODULATION OF BRAIN OXIDATIVE STRESS BY VARIOUS INTERVENTIONS." UKnowledge, 2012. http://uknowledge.uky.edu/chemistry_etds/12.

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In this thesis study we examined glycogen synthase kinase-3β (GSK-3β) and its effects over Nrf2 and Pin 1 as it relates to Alzheimer’s disease (AD). AD is a neurodegenerative disease characterized by a prolonged high oxidative environment. Transcription factor Nrf2 is vital in the brain’s defense against oxidative insults through its up-regulation of over 100 antioxidants. Depletion of the brain’s antioxidant defense system results in intolerance to an oxidative environment, contributing to the progression of AD. The regulatory Pin 1 protein promotes cellular homeostasis, and when down-regulated results in increased deposits of neurofibrillary tangles (NFTs) and amyloid-β (Aβ) plaques, the two pathological hallmarks of AD. Using aged SAMP8 mice treated with antisense oligonucleotide (AO) directed at GSK-3β and random AO, the data presented here demonstrate decreased oxidative stress and increased Nrf2 transcriptional activity and Pin 1 levels as a result of the down-regulation of GSK-3β. Collectively, these results implicate GSK-3β activity in the increased oxidative stress of AD and support its inhibition as a possible therapeutic treatment for the disease. Further, we elucidate a possible mechanism connecting GSK-3β to the loss of tolerance to an oxidative environment and increased deposits of NFTs and Aβ plaques observed in AD.

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Lunato, Anthony J. "Part1: Synthesis and in vitro phosphorylation of a homologous series of 5-s-alkylcarboranyl-2'-deoxyuridines and 3-n-alkylcarboranyl- thymidines for use in boron neutron capture therapy of brain cancer ; Part 2: an investigation... /." The Ohio State University, 1996. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487936356160119.

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50

Jones, Glynn. "Application of the L-Tryptophanol assay as an indicator of soluble amyloid aggregates in brain, CSF and plasma." Thesis, University of Aberdeen, 2017. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=232368.

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Alzheimer's disease (AD) is the most common cause of dementia; a problem that is growing in size and cost as the population ages. Early soluble aggregates composed misfolded 'amyloid' peptide sequences have been implicated as key to the initiation and onset of AD pathology, although little is definitively known as to when and how these assemblies form or interact to instigate pathology. The primary focus of this study was to evaluate whether L-Tryptophanol (Trol) signal, which has been shown to be induced via soluble amyloid species, increases with AD severity in a range of ex vivo human samples. Testing of this hypothesis was carried out in several stages: Initially synthetic versions of the amyloid beta (Aβ) peptide were tested in vitro to corroborate Trols propensity to associate to amyloid assemblies and allow for method development. Next, a range of brain lysates from several transgenic mouse lines and aged human AD cases and controls were assessed using the reporter. These experiments demonstrated Trols sensitivity to Aβ and tau, and provided compelling evidence that Trol signal tracks disease progression in brain lysates. During the final stage of testing cerebrospinal fluid (CSF) from AD and Parkinson's disease (PD) patients, and blood plasma samples from PD patients was evaluated. Results from this phase of testing indicated that Trol was able to detect differences in sample composition between healthy and diseased individuals, however differences were not clear cut and could have been affected by confounding factors. Overall, the data presented here suggest that Trol may be able to track disease progression in amyloidopathies when implemented in brain lysates. However, further testing is required to completely validate this finding. These findings highlight the potential of simple techniques for amyloid detection to aid within the diagnosis, evaluation of disease progression and study of AD and other neurodegenerative diseases.

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Dissertations / Theses on the topic 'Brain chemistry'

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