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Dissertations / Theses on the topic 'Central Nervous System Stimulant'

Author: Grafiati

Published: 3 June 2025

Last updated: 1 August 2025

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1

Slattum, Patricia W. "EVALUATION OF QUANTITATIVE ELECTROENCEPHALOGRAPHY FOR ASSESSMENT OF CENTRAL NERVOUS SYSTEM STIMULANT RESPONSE." VCU Scholars Compass, 1992. https://scholarscompass.vcu.edu/etd/5524.

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The objective of this investigation was to evaluate quantitative electroencephalography (EEG) as a measure of CNS stimulation. The reproducibility and sensitivity of quantitative EEG was compared to neuroendocrine, mood, and psychomotor performance measures. The study was conducted in two parts. The ﬁrst part investigated the inter- and intra-individual variability associated with a series of pharmacological response measures under baseline (no drug) conditions. It was an open-label pilot study in which eight healthy male volunteers underwent a series of tests (EEG, visual continuous performan

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2

CONTU, LILIANA. "Influence of Amphetamine-type stimulants in the Central Nervous System: abuse and neurotoxicity." Doctoral thesis, Università degli Studi di Cagliari, 2018. http://hdl.handle.net/11584/255975.

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Amphetamines are synthetic drugs characterized by their psychostimulants effects on the central nervous system (CNS), and include a wide range of substances such as alpha-methylphenethylamine or amphetamine (AMPH), N-methylamphetamine or methamphetamine (METH) and 3,4 methylenedioxymethamphetamine (MDMA) also known as “ecstasy”. The ATS, structurally, are a group of substances related to the compound known as β-phenethylamine (β-PEA), a naturally neurotransmitter in the body. Structural modifications on the aromatic ring of β-PEA create multiple synthetic derivatives with different pharmacolo

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3

Schroeder, Frederick Albert. "A Role for Histone Modification in the Mechanism of Action of Antidepressant and Stimulant Drugs: a Dissertation." eScholarship@UMMS, 2007. https://escholarship.umassmed.edu/gsbs_diss/370.

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Depression and stimulant drug addiction each result in massive losses of health, productivity and human lives every year. Despite decades of research, current treatment regimes for depression are ineffective in approximately half of all patients. Therapy available to stimulant drug addicts is largely ineffective and moreover, dedicated treatments for drug dependence (including abuse of cocaine) are non-existent. Thus, there is a pressing need to further understanding of the molecular mechanisms underlying these disorders in order to develop novel, targeted therapeutic strategies. Chromatin rem

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4

Beaumont, Ross. "The performance and physiological effects of caffeine and octopamine supplementation during endurance cycle exercise." Thesis, Loughborough University, 2017. https://dspace.lboro.ac.uk/2134/25522.

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Caffeine consistently enhances endurance performance in temperate environmental conditions, while far less research has examined its ergogenic and physiological effects during prolonged exercise in the heat. Despite the performance benefit of an acute caffeine doses being less pronounced in regular caffeine users versus those not habituated to the drug, few studies have examined the influence of a prolonged period of controlled caffeine intake on endurance performance. The endogenous trace amine octopamine is purported to possess stimulant-like properties and influence fat metabolism, although

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5

Hedström, Kajsa, and Ulrika Hillbom. "Tillväxt hos barn och ungdomar som behandlats med centralstimulatia : En journalgranskningsstudie." Thesis, Uppsala universitet, Institutionen för folkhälso- och vårdvetenskap, 2011. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-154710.

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Syfte: Att undersöka om det fanns något samband mellan behandling med centralstimulantia ochavvikande tillväxt hos barn och ungdomar med ADHD, samt att undersöka om eventuellt avvikandetillväxt hade något samband med ålder vid insättande, kön eller olika funktionshinder.Metod: 68 barn med ADHD som behandlats med centralstimulantia i minst två år inkluderades.Journalkopior inhämtades från Habiliteringen för barn och vuxna vid Uppsala läns landsting. Dessakopior innehöll barnens tillväxtkurvor, kön, diagnos och ålder. Kurvorna granskades med hjälp av enutformad granskningsmall. Barnens tillväxt

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6

Fagergren, Pernilla. "Cocaine effects on striatal dynorphin and CART neuropeptides : association to mood disorder /." Stockholm, 2003. http://diss.kib.ki.se/2003/91-7349-515-8.

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7

Gauffin, Per. "Underlättar medicinering av barn med ADHD barnets pedagogiska situation i skolan?" Thesis, Karlstad University, Faculty of Arts and Education, 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:kau:diva-1514.

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<p>Persons suffering from Attention deficit/hyperactivity disorder (ADHD) struggle with complications within the functions that regulate and control the brain activities, due to deficiencies in these functions within the affected nerve-paths. ADHD is a cognitive function impairment characterised by inattention, impulsiveness and over activity. According to Diagnostic and Statistic Manual of Mental Disorders, American Psychiatric Association (DSM-IV), certain diagnostic criteria of ADHD must be fulfilled in order for a person to be diagnosed with ADHD. The everyday problems caused by ADHD are i

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8

Strandberg, Joakim. "Toxicological studies of opiate-related death /." Stockholm, 2007. http://diss.kib.ki.se/2007/978-91-7357-191-3/.

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9

Junior, Hercilio Pereira de Oliveira. "Alterações neurocognitivas e morfométricas cerebrais associadas ao uso do crack." Universidade de São Paulo, 2018. http://www.teses.usp.br/teses/disponiveis/5/5142/tde-12092018-082935/.

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INTRODUÇAO: Recentes achados experimentais sugerem que a cocaína na forma crack é mais neurotóxica quando comparada à cocaína inalada. Estes estudos são congruentes com os achados clínicos de que pacientes com transtorno por uso da cocaína e usuários de crack têm pior prognóstico e mais consequências adversas para à saúde. OBJETIVO: Investigar alterações diferenciais em substância cinzenta cerebral (SC) e prejuízos neurocognitivos entre usuários de crack (CRACK), cocaína inalada (COC) e controles. MÉTODOS: 78 indivíduos adultos foram avaliados neste estudo (16 CRACK, 26 COC e 36 controles). To

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10

Martinsson, Louise. "Facilitation of recovery after ischaemic stroke : early dexamphetamine and physiotherapy treatment /." Stockholm, 2003. http://diss.kib.ki.se/2003/91-7349-668-5.

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11

Williams, Michael T., Russell W. Brown, and Charles V. Vorhees. "Neonatal Methamphetamine Administration Induces Region-Specific Long-Term Neuronal Morphological Changes in the Rat Hippocampus, Nucleus Accumbens and Parietal Cortex." Digital Commons @ East Tennessee State University, 2004. https://dc.etsu.edu/etsu-works/6352.

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Previous studies have demonstrated that rats exposed to methamphetamine (MA) during the neonatal period display deficits in spatial learning and memory. The underlying correlates are; therefore, this study was devised to determine whether neuronal changes occur in the dentate gyrus (DG), nucleus accumbens (NAcc) and cortex of adult rats exposed to 10 mg/kg MA administered four times daily from P11-20 using Golgi-Cox staining [Gibb, R. & Kolb, B. (1998) J. Neurosci. Meth., 79, 1-4]. The DG and NAcc demonstrated a decrease in the number of spines per neuron and the NAcc showed an associated decr

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12

Wu, Weiping. "The role of adenosine and its receptor subtypes in nociception and neuropathic pain /." Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-298-5/.

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13

Brown, Russell W., Marla K. Perna, Daniel M. Noel, Jamie D. Whittemore, Julia Lehmann, and Meredith L. Smith. "Amphetamine Locomotor Sensitization and Conditioned Place Preference in Adolescent Male and Female Rats Neonatally Treated with Quinpirole." Digital Commons @ East Tennessee State University, 2010. https://dc.etsu.edu/etsu-works/6341.

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Neonatal quinpirole treatment has been shown to produce an increase in dopamine D2-like receptor sensitivity that persists throughout the subject's lifetime. The objective was to analyze the effects of neonatal quinpirole treatment on effects of amphetamine in adolescent rats using locomotor sensitization and conditioned place preference procedures. Sprague-Dawley rats were treated with quinpirole (1 mg/kg) or saline from postnatal days (P)1 to P11 and raised to adolescence. For locomotor sensitization, subjects were given amphetamine (1 mg/kg) or saline every second day from P35 to P47 and we

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14

Solomon, Thomas. "Central nervous system infections in Vietnam." Thesis, Open University, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.340736.

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15

Zhang, Hui. "Remyelination in the central nervous system." Thesis, University of Edinburgh, 2013. http://hdl.handle.net/1842/8095.

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Multiple Sclerosis (MS) is an inflammatory disease which causes areas of demyelination in the Central Nervous System (CNS) and affects only humans. Current therapies for MS are focused on anti-inflammatory treatment, which reduce the occurrence and clinical relapses of the disease. However, progressive disability of the disease is related to axonal degeneration. After demyelination, remyelination occurs, which helps repair the demyelinated lesions and protects axons from degeneration. However, this endogenous remyelination is inefficient, and currently there are no therapies available to enhan

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16

Poland, Stephen D. "Central nervous system infection with human cytomegalovirus." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/nq21311.pdf.

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17

Bernick, Kristin Briana. "Cell biomechanics of the central nervous system." Thesis, Massachusetts Institute of Technology, 2011. http://hdl.handle.net/1721.1/67202.

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Thesis (Ph. D.)--Massachusetts Institute of Technology, Dept. of Biological Engineering, 2011.<br>Cataloged from PDF version of thesis.<br>Includes bibliographical references (p. 133-153).<br>Traumatic brain injury (TBI) is a significant cause of death and morbidity in both the civilian and military populations. The major causes of TBI, such as motor vehicle accidents, falls, sports concussions, and ballistic and explosive blast threats for military personnel, are well established and extensively characterized; however, there remains much to be learned about the specific mechanisms of damage l

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18

Coutinho, Maria Ester Freitas Barbosa Pereira. "Central nervous system autoimmunity in neuropsychiatric disorders." Thesis, University of Oxford, 2016. https://ora.ox.ac.uk/objects/uuid:389fb830-4b4e-4201-9965-19acb2c63ff3.

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The recent history of autoimmune neurology is marked by the discovery of many central nervous system (CNS) antibody-mediated diseases. These disorders are caused by antibodies that target important proteins expressed in the neuronal surface, which are believed to be directly pathogenic. These antibodies are immunoglobulin G (IgG) isotype and, as such, have the potential to cross the placenta during gestation. Foetal exposure to CNS-targeting antibodies could alter developing neuronal circuits, leading to disease. However, the consequences of exposure to these antibodies during neurodevelopment

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19

Hüppi, Petra Susan. "Serum antibodies to central nervous system antigens /." [S.l : s.n.], 1986. http://www.ub.unibe.ch/content/bibliotheken_sammlungen/sondersammlungen/dissen_bestellformular/index_ger.html.

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20

Piani, Daniela. "Immune-mediated cytotoxicity in the central nervous system /." [S.l.] : [s.n.], 1993. http://e-collection.ethbib.ethz.ch/show?type=diss&nr=10423.

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21

Lamvik, Kate K. "Central Nervous System Associations in Neurofibromatosis Type 1." Cincinnati, Ohio : University of Cincinnati, 2007. http://rave.ohiolink.edu/etdc/view.cgi?acc_num=ucin1179426618.

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Thesis (M.S.)--University of Cincinnati, 2007.<br>Advisor: Dr. Elizabeth K. Schorry. Title from electronic thesis title page (viewed June 30, 2010). Includes abstract. Keywords: Neurofibromatosis type 1 (NF1); optic pathway glioma (OPG); central nervous system (CNS). Includes bibliographical references.

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22

Suzumura, Akio. "Microglia : Immunoregulatory cells in the central nervous system." Nagoya University School of Medicine, 2002. http://hdl.handle.net/2237/5375.

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23

Lee, Yong Beom. "Cytokine network in the human central nervous system." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape7/PQDD_0022/NQ38925.pdf.

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24

Weber, Wilhelm Evert Jacob. "Cellular auto-immunity in central nervous system disease." Maastricht : Maastricht : Rijksuniversiteit Limburg ; University Library, Maastricht University [Host], 1988. http://arno.unimaas.nl/show.cgi?fid=5594.

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25

Jackson, Johanna Sara. "Stem cell tracking in the central nervous system." Thesis, Imperial College London, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.446551.

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26

Bell, Michael David. "Factors regulating inflammation in the central nervous system." Thesis, University of Oxford, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.308694.

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27

Smith, Imogen. "Cannabinoid receptor signalling in the central nervous system." Thesis, University of Reading, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.553656.

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The GPCRs CB1R and CB2R are targets for endocannabinoids, exogenous synthetic agents and phytocannabinoids derived from Cannabis plants. However, the pharmacological properties of many phytocannabinoids remain to be elucidated. The present work focused on activity of cannabinoids at CB1R, and potentially other targets, in brain membrane preparations and a cell culture model of epileptiform activity. The synthetic cannabinoids WIN55,212-2 (CB1/2R agonist) and AM251 (CB1R antagonist), and the phytocannabinoids fl9_THCV, CBO and CBG were investigated using radioligand binding and [35SjGTPyS assay

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28

Sussman, Jonathan David. "Glial lineages in the adult central nervous system." Thesis, University of Cambridge, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.625026.

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29

McQuaid, Stephen. "Measles virus infection of the central nervous system." Thesis, Queen's University Belfast, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.287361.

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30

Davies, M. "5-hydroxytryptamine receptors in the central nervous system." Thesis, Bucks New University, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.382505.

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31

Panni, Moeen. "Neuron-target interactions in the central nervous system." Thesis, University of Cambridge, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.337889.

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32

Staley, Kristina. "Targeting gene expression to the central nervous system." Thesis, University of Cambridge, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.319537.

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33

Galtrey, Clare Margaret. "Central nervous system plasticity and peripheral nerve repair." Thesis, University of Cambridge, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.614254.

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34

Roberts, Malcolm Ian. "Death receptor 3 in the central nervous system." Thesis, University of Cambridge, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.615645.

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35

Rist, Julia Maria. "Rejuvenating remyelination in the ageing central nervous system." Thesis, University of Cambridge, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.608517.

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36

Almeida, Rafael. "Axon-glia interactions during central nervous system myelination." Thesis, University of Edinburgh, 2015. http://hdl.handle.net/1842/21038.

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Myelination drastically speeds up action potential propagation along axons, which is fundamental for the correct function of neuronal circuits. However, axon-oligodendrocyte interactions regulating the onset of myelin formation remain unclear. I sought to determine how reticulospinal axons control myelination, as they are the first myelinated in the zebrafish spinal cord. I genetically manipulated zebrafish in order to either remove such axons from a region of the spinal cord, or to increase their number, and characterized oligodendrocyte-lineage cells following this axonal loss- or gain-of-fu

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37

Gifford, Andrew Neal. "Catecholaminergic neurotransmission in the insect central nervous system." Thesis, University of St Andrews, 1989. http://hdl.handle.net/10023/15042.

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38

Smorodska, O., I. Shandyba, P. Bileckiy, et al. "Affection of central nervous system in MELAS syndrome." Thesis, Karger Publishers, 2017. http://essuir.sumdu.edu.ua/handle/123456789/65352.

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The problem of acute cerebrovascular accident (ACVA) has enormous socio-economic importance due to its significant prevalence. Since the ACVA have clinical and pathogenetic polymorphism, problem of differential diagnosis of diseases that mimic their clinic raised up. This problem was illustrated by the clinical case we present.Difficulty of differential diagnostic illustrated by case with patient who initially hospitalized with a diagnosis of ACVA, but later during dynamic monitoring and additional examinations diagnosis of MELAS syndrome was found. Aim: differential diagnosis of rare mitocho

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39

Wheeler, Natalie A. "Autotaxin in Central Nervous System Development and Disease." VCU Scholars Compass, 2016. http://scholarscompass.vcu.edu/etd/4104.

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During development, oligodendrocytes (OLGs), the myelinating cells of the central nervous system (CNS), undergo a stepwise progression during which OLG progenitors, specified from neural stem/progenitor cells, differentiate into fully mature myelinating OLGs. This progression along the OLG lineage is characterized by well-synchronized changes in morphology and gene expression patterns. The studies presented in this dissertation identified the extracellular factor Autotaxin (ATX) as a novel upstream signal modulating HDAC1/2 activity and gene expression in cells of the OLG lineage. Using the ze

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40

Ebrahimkhani, Saeideh. "Exosomal MicroRNA Signatures in Central Nervous System Diseases." Thesis, The University of Sydney, 2018. http://hdl.handle.net/2123/20208.

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During the last decade there has been a growing interest in studying extracellular vesicles, in particular exosomes and their miRNA contents. Exosomes are released by almost all cell types. They are packed with specific information, stable against degradation processes, are small and flexible enough to cross the blood-brain barrier (BBB), and are readily found in biological fluids including blood. MicroRNAs (miRNAs) are involved in nearly every cellular process and play a regulatory role in central nervous system (CNS) associated diseases. Accordingly, exosomal miRNAs could be ideal biomarkers

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41

Zhang, Xiaochun. "Involvement of neuroinflammation in models of neurodegeneration." Laramie, Wyo. : University of Wyoming, 2008. http://proquest.umi.com/pqdweb?did=1663059561&sid=3&Fmt=2&clientId=18949&RQT=309&VName=PQD.

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42

Eckert, Bodil. "Hypoglycaemia studies on central and peripheral nerve function /." Lund : Dept. of Internal Medicine, University of Lund, 1998. http://catalog.hathitrust.org/api/volumes/oclc/57426099.html.

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43

Foster, Michelle Tranace. "Central nervous system regulation of fat cell lipid mobilization the role of the sympathetic nervous system /." restricted, 2005. http://etd.gsu.edu/theses/available/etd-11162005-154631/.

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Thesis (Ph. D.)--Georgia State University, 2005.<br>Timothy Bartness, committee chair; Elliott Albers, Ruth Harris , Sarah Pallas, committee members. Electronic text (181 p. : ill.)) : digital, PDF file. Description based on contents viewed July 17, 2007. Includes bibliographical references (p. 148-181).

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Foster, Michelle Tranace. "Central Nervous System Regulation of Fat Cell Lipid Mobilization: The Role of the Sympathetic Nervous System." Digital Archive @ GSU, 2006. http://digitalarchive.gsu.edu/biology_diss/2.

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Obesity is a growing disorder in the United States, affecting over 60% of the population. We previously defined sympathetic nervous system (SNS) outflow from brain to white adipose tissue (WAT) using a viral transneuronal tract tracer. SNS innervation of WAT is the principle initiator of lipolysis, whereas decreases in sympathetic drive promote lipid accumulation. Which of the many origins of SNS outflow from brain to WAT results in SNS-mediated changes in lipid mobilization (increases in drive) or accumulation (decrease in drive) is unknown. Previous research indicates that sympathetic denerv

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45

Tep-Cullison, Chhavy R. "Distinct roles of p75 regulation on myelination in the peripheral nervous system and central nervous system." The Ohio State University, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=osu1299179635.

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46

Akers, Stephen Matthew. "Modeling central nervous system involvement in acute lymphoblastic leukemia." Morgantown, W. Va. : [West Virginia University Libraries], 2010. http://hdl.handle.net/10450/11227.

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Thesis (Ph. D.)--West Virginia University, 2010.<br>Title from document title page. Document formatted into pages; contains x, 102 p. : ill. (some col.). Includes abstract. Includes bibliographical references.

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47

Zhang, Fan. "Modulation of genomic expression in the central nervous system." Doctoral thesis, Universite Libre de Bruxelles, 1997. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/212219.

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48

Mabon, Joy. "Strategies to reduce inflammation in the central nervous system." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp03/MQ39851.pdf.

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49

Lyng, Eric E. Bottiglieri Teodoro. "Gamma Hydroxybutyrate (GHB) : mechanisms of central nervous system toxicity /." Waco, Tex. : Baylor University, 2006. http://hdl.handle.net/2104/4211.

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50

Stromnes, Ingunn Margarete. "T cell determinants of central nervous system autoimmune disease /." Thesis, Connect to this title online; UW restricted, 2007. http://hdl.handle.net/1773/8333.

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