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Dissertations / Theses on the topic 'Cocaïne – pharmacologie'

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Published: 4 June 2021

Last updated: 4 February 2022

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1

Garin, Emmanuelle. "Pharmacologie des psychostimulants : cocai͏̈ne, amphétamines, haschich." Paris 5, 1995. http://www.theses.fr/1995PA05P273.

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2

Pol, Bodetto Sarah. "Rôle de la protéine phosphatase 1 dans les mécanismes d’action de la cocaïne et implication des modifications épigénétiques dans sa régulation." Thesis, Strasbourg, 2012. http://www.theses.fr/2012STRAJ101/document.

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La consommation répétée de drogues induit une plasticité cérébrale, qui pourrait sous-tendre le développement de la dépendance. La protéine phosphatase de type 1 (PP1) étant un acteur majeur de ces processus, nous nous sommes intéressés à sa régulation par la cocaïne. Nous avons montré qu’un traitement chronique par la cocaïne induit la répression du gène codant la sous-unitécatalytique β de PP1 (PP1Cβ), via l’hyperméthylation de sa région promotrice et le recrutement de la protéine de liaison à l’ADN méthylé, Mecp2. Cette répression, observée dans les principales structures du système de réco

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3

Karila, Laurent. "Le modèle CAIMAN (Cocaine Addiction Imaging Medications And Neurotransmitters study) : un modèle d'étude clinique, pharmacologique et d'imagerie cérébrale dans l'addiction à la cocaïne." Paris 6, 2012. http://www.theses.fr/2012PA066406.

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L’addiction à la cocaïne est une pathologie multifactorielle d’installation progressive avec de nombreuses conséquences. Aucune pharmacothérapie n’est actuellement validée pour son traitement. La synthèse récente des données pharmacologiques suggère que le modafinil, agissant sur de nombreux systèmes neurobiologiques, pourrait jouer un rôle dans le sevrage et dans la prévention de la rechute et ainsi améliorer le pronostic des patients dépendants. De nombreux essais cliniques ont été menés avec cette molécule. Il n’existe aucune donnée sur les effets sur le transporteur de la dopamine (DAT), r

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4

Javanmard, Sahar. "Synthesis and pharmacology of site-specific cocaine abuse treatment agents." Diss., Georgia Institute of Technology, 2002. http://hdl.handle.net/1853/30952.

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5

Wetzel, Hanna N. "Preclinical Development of the Anti-cocaine Monoclonal Antibody h2E2 for the Treatment of Cocaine Addiction." University of Cincinnati / OhioLINK, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1529333855259163.

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6

Craige, Caryne. "Regulation of Cocaine-induced Behaviors and Anxiety Produced by Cocaine Withdrawal through the Serotonin(2C) Receptor." Diss., Temple University Libraries, 2013. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/239587.

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Pharmacology<br>Ph.D.<br>Cocaine is a powerfully active psychostimulant which exerts its effects through blockade of dopamine, serotonin and norepinephrine transporters and resultant increases in extracellular levels of these neurotransmitters. Much of the focus on cocaine abuse in the literature has been directed towards study of the dopamine system; however, several studies have identified a role for the serotonin system in regulating the rewarding effects of cocaine as well. Specifically, the serotonin 2C (5-HT2C) receptor regulates cocaine-induced alterations in serotonin and dopamine leve

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7

Moore, Susanna. "Synthesis and Pharmacology of Potential Site-Specific Therapeutic Agents for Cocaine Abuse." Diss., Georgia Institute of Technology, 2004. http://hdl.handle.net/1853/5010.

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Synthesis and Pharmacology of Potential Site-Directed Therapeutic Agents for Cocaine Abuse Susanna Moore 235 Pages Directed by Dr. David M. Collard and Dr. Howard M. Deutsch Stimulants such as cocaine continue to dominate the nations illicit drug problem. An effective medication for any aspect of cocaine addiction has not been developed. Cocaine binds, although not selectively, to the dopamine transporter (DAT) and disrupts normal dopamine (DA) neurotransmission between neurons. While the dopamine hypothesis for the mechanism of action of cocaine has been widely accepted, cocaine also p

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8

Zhang, Ting. "DEVELOPMENT AND PRECLINICAL EVALUATION OF LONG-LASTING COCAINE HYDROLASES FOR COCAINE OVERDOSE AND COCAINE USE DISORDER TREATMENT." UKnowledge, 2018. https://uknowledge.uky.edu/pharmacy_etds/93.

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Cocaine is a plant-based illicit drug commonly involved in substance use disorder. Although cocaine overdose and cocaine use disorders cause adverse health consequences to individuals and the economic burden on their family and society, there are no FDA (Food and Drug Administration) approved medications for treatment. Recently, it has been recognized that delivery of cocaine hydrolase (CocH) is a promising therapeutic strategy. Human butyrylcholinesterase (hBChE), the primary enzyme involved in cocaine metabolism in human, have advantages over other candidates for the development of CocH. Pre

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9

Johnson, Amy. "The Pharmacology of an Agonist Medication to Treat Stimulant Use Disorder." VCU Scholars Compass, 2017. https://scholarscompass.vcu.edu/etd/5177.

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Cocaine use disorder is a serious public health issue for which no approved pharmacotherapies exist. The development of a pharmacotherapy for cocaine use disorder is a priority for the National Institute on Drug Abuse. Amphetamine maintenance has been shown to be effective to reduce cocaine use in double-blind placebo controlled clinical trials, but has not been approved due to concerns over safety and abuse liability. Development of new pharmacotherapies is facilitated by preclinical testing for effectiveness and identification of new targets for medication development. The first part of this

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10

Costa, Campos Renan. "Striatum, Dopamine et Automatisation dans l’Addiction à la Cocaïne et dans la Rechute : Investigation Pharmacologique et Comportementale." Thesis, Bordeaux, 2017. http://www.theses.fr/2017BORD0934/document.

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L'un des aspects les plus problématiques de l’addiction est la vulnérabilité à la rechute qui persiste même longtemps après la disparition des symptômes de sevrage. Les modèles rongeurs d'auto-administration (AA) démontrent que la réexposition à la drogue, les stimuli associés à la drogue ou le stress sont des déclencheurs majeurs de la rechute. Bien que les différentes catégories de drogues varient dans leurs mécanismes pharmacologiques primaires, elles partagent toutes un effet aigu d'augmentation des niveaux de dopamine (DA) dans le striatum. Après une utilisation répétée, les propriétés ad

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11

Kim, Shinja Rhea. "Pharmacokinectic and pharmacodynamic aspects of cocaine and its interaction with ethanol." Diss., The University of Arizona, 1997. http://hdl.handle.net/10150/289511.

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The main purpose of the research described in this dissertation was to evaluate various aspects of cocaine in pharmacokinetics and pharmacodynamics including: physiologically based-pharmacokinetics modeling; the influence of ethanol on cocaine disposition. Further, cocaine and cocaethylene (CE) were compared using pharmacokinetic-pharmacodynamic (PK-PD) models. Lastly, PK-PD models after cocaine and a combination of cocaine and ethanol dose were developed. Cocaine was administered by iv with or without ethanol in rats. CE was formed only in the group of rats given cocaine in the presence of et

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12

Marckel, Jordan A. "The in-vivo Preclinical Development of a Humanized Anti-cocaine Monoclonal Antibody and its Fab Fragment for the Treatment of Cocaine Abuse." University of Cincinnati / OhioLINK, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1613745458699203.

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13

Zhang, Liang. "Synthesis and pharmacology of site-specific cocaine abuse treatment agents : 2-(aminomethyl)-3-phenylbicyclo[221] and [221]-alkane dopamine uptake inhibitors." Thesis, Georgia Institute of Technology, 1999. http://hdl.handle.net/1853/26015.

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14

Miller, Jonathan S. "GSK3: A Neuromodulator of Cocaine-Induced Behavioral Responses." Diss., Temple University Libraries, 2009. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/40192.

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Pharmacology<br>Ph.D.<br>Cocaine is a highly abused psychostimulant with repeated use potential culminating in addiction, a disease associated with compulsive drug seeking, use and high rates of relapse despite adverse consequences. It is well established that cocaine acts by binding to and blocking monoamine transporters therefore increasing synaptic extracellular monoamine concentrations. Cocaine also increases extracellular levels of the excitatory amino acid glutamate within the neural circuitry comprising the ascending dopamine system. Cocaine induces a number of behavioral and neurochemi

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15

Wood, Douglas M. (Douglas Michael). "Discriminative Stimulus Properties of Cocaine: Tolerance and Cross-Tolerance Characteristics." Thesis, North Texas State University, 1985. https://digital.library.unt.edu/ark:/67531/metadc500536/.

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Rats were trained to discriminate an injection of cocaine, 5.0 mg/kg, from an injection of saline, using a two-lever choice paradigm: one lever was correct after cocaine injection, the other lever was correct after a saline injection. After training, cocaine and methamphetamine were generalized to the cocaine lever, but phenethylamine (PEA) was only partially generalized. Cocaine was injected every 8 hrs, 20.0 mg/kg, and the discriminability of 5.0 mg/kg was tested every other day. Redetermination of the cocaine generalization curve after 6 days of chronic administration showed a shift to the

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16

Brownell, Arnold S. "Synthesis and pharmacology of 2-substituted-6-(N,N-dimethylamino)-5-phenylbicyclo[222]octanes as dopamine uptake inhibitors : 2-phenyl and 2-benzyl analogs as potential cocaine abuse treatment agents." Thesis, Georgia Institute of Technology, 2003. http://hdl.handle.net/1853/27590.

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17

Kim, Jae Kyun. "CXCL12/CXCR4 signaling in mesocorticolimbic reward pathways: relevance to cocaine reinforcement and relapse." Diss., Temple University Libraries, 2016. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/399036.

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Pharmacology<br>Ph.D.<br>The role of chemokines as chemotactic cytokines and their functions in the immune system and related pathologies are well defined. Recently, strong evidence supporting the hypothesis that chemokines can act as modulators of neuronal activity and influence neurotransmission has been reported. The chemokine CXCL12 is constitutively expressed in adult brain and expression of CXCL12 and its cognate receptor CXCR4 have been reported in regions of rat brain that construct dopamine (DA) and glutamate (GLU) pathways such as ventral tegmental area (VTA), substantia nigra (SN),

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18

Coons, Susanna. "Synthesis and pharmacology of site-specific cocaine abuse treatment agents : 6-(N,N-Dimethylamino)-5-(4-chlorophenyl)bicyclo[222]octan-2-yl benzoate." Thesis, Georgia Institute of Technology, 2000. http://hdl.handle.net/1853/27609.

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19

Chaves, Alysia Anne. "Mechanisms of AIDS and cocaine related cardiovascular disease." Columbus, Ohio Ohio State University, 2003. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1056031201.

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Thesis (Ph.D.)--Ohio State University, 2003.<br>Title from first page of PDF file. Document formatted into pages; contains xx, 401 p.; also includes graphics (some col.). Includes abstract and vita. Advisor: John A. Bauer, Dept.of Pharmacy. Includes bibliographical references (p. 387-391).

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20

Penney, Christine. "Determining dopamine D1 receptor changes in cocaine abusers using positron emission tomography and SCH 23390." Thesis, McGill University, 2000. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=30828.

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An underlying mechanism of cocaine is its ability to bind to the dopamine transporter thus preventing dopamine (DA) reuptake, and leading to an increase of endogenous DA in the synapse. Excessive synaptic DA may lead to neuroadaptions of the DA receptors. In vitro animal studies have demonstrated a cocaine-induced down-regulation of D1 receptors in limbic regions of the brain. PET studies in rats have also noted a decrease in D1 receptor numbers in the striatum. In humans, D1 receptors have not been examined using either in vitro or PET techniques. The present investigation was conducted to de

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21

Hagi-Pavli, Eleni. "Synthesis of transition state analogues designed to generate antibodies that catalyse the hydrolysis of cocaine." Thesis, Queen Mary, University of London, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.338895.

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22

Xie, Xiaohu. "Role of medial prefrontal cortical group II metabotropic glutamate receptor in the development of cocaine sensitization." View the abstract Download the full-text PDF version, 2007. http://etd.utmem.edu/World-Access/Xie/2007-023-Xie.pdf.

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Thesis (Ph.D.)--University of Tennessee Health Science Center, 2007.<br>Title from title page screen (viewed on June 20, 2008). Research advisor: Jeffery D.Steketee, Ph.D. Document formatted into pages (xi, 89 p. : ill.). Vita. Abstract. Includes bibliographical references (p. 71-89).

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23

Han, Bing. "Mechanistic Consequences of Cardiac Oxidative Stress." The Ohio State University, 2008. http://rave.ohiolink.edu/etdc/view?acc_num=osu1203478009.

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24

Lamarre, Neil Stanley. "Utilizing novel dose equivalence methodologies to examine cocaine's effects on the vasculature." Diss., Temple University Libraries, 2013. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/221180.

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Pharmacology<br>Ph.D.<br>ABSTRACT: UTILIZING NOVEL DOSE EQUIVALENCE METHODOLOGIES TO EXAMINE COCAINE'S EFFECTS ON THE VASCULATURE Neil S. Lamarre Doctor of Philosophy Temple University School of Medicine, 2013 Doctoral Advisory Committee Chair: Ronald J. Tallarida, Ph.D. Cocaine abuse and addiction is a serious health problem, resulting in thousands of emergency room visits and deaths each year in the United States. It is particularly toxic to the cardiovascular system, including deleterious effects on the peripheral vasculature. These effects are not well understood, but evidence suggests chr

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25

O'Neill, Brian. "Anatomy and Pharmacology of Dopamine Transporter-Mediated Reward and Locomotor Responses to Psychostimulants." The Ohio State University, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=osu1352859081.

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26

Soderman, Avery Rune. "The Role of Mu Opioid Receptors in the Behavioral Effects of Cocaine." Diss., Temple University Libraries, 2008. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/22825.

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Pharmacology<br>Ph.D.<br>Animal models have proven to be useful tools for modeling human neurochemical and behavioral responses to drugs of abuse, including cocaine. Cocaine is a psychomotor stimulant that facilitates monoaminergic neurotransmission by binding to transporters and inhibiting the reuptake of dopamine, serotonin and norepinephrine into presynaptic neurons. Many of the behavioral effects of cocaine, including its locomotor-activating and reinforcing properties, have been attributed to the ability of cocaine to enhance dopaminergic activity. In addition to its direct effects on mon

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27

Enman, Nicole Marie. "Dopamine reward dysfunction and cocaine-seeking in a rat model of PTSD." Diss., Temple University Libraries, 2014. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/259963.

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Pharmacology<br>Ph.D.<br>Posttraumatic stress disorder (PTSD) co-occurs with substance use disorders at high rates, but the neurobiological basis of this relationship remains largely unknown. Identifying mechanisms that underlie this association is necessary, and recognizing pathologies shared by these disorders may provide pertinent information in understanding their functional relationship. Separate lines of evidence suggest that PTSD and drug addiction may share a common feature, that is, dysregulation of the brain's reward circuitry. We hypothesize that PTSD results in reduced dopaminergic

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28

Simms, Debra Kay 1959. "The effects of serotonergic disruption on the locomotor response induced by cocaine, phencyclidine, and a phencyclidine analog." Thesis, The University of Arizona, 1990. http://hdl.handle.net/10150/278216.

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This study assessed the involvement of serotonergic systems in the locomotor-stimulating effects of cocaine, phencyclidine (PCP), and the PCP analog, N- (1-(2-benzo(b)thiophenyl)cyclohexyl) piperidine (BTCP). Central serotonin (5-HT) activity was disrupted in rats with para-chloroamphetamine (p-CA), or ritanserin pretreatment, and by lesioning of the medial raphe (MR) and dorsal raphe (DR) nuclei. P-CA potentiated cocaine- and PCP- but not BTCP-induced hyperactivity. Ritanserin enhanced PCP hyperlocomotion and attenuated caffeine hyperactivity, but failed to alter cocaine and BTCP hyperlocomot

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29

ALAJAJI, MAI. "EARLY ADOLESCENT NICOTINE EXPOSURE HAS LONG-LASTING EFFECTS ON COCAINE-INDUCED BEHAVIORS IN MICE." VCU Scholars Compass, 2013. http://scholarscompass.vcu.edu/etd/492.

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Nicotine is one of the most commonly used drugs among adolescent populations. Given the fact that adolescence is a unique developmental stage, during which nicotine has long-term effects on future drug-taking behavior, it is essential to understand how early exposure to nicotine during adolescence may affect the abuse liability of other drugs. We hypothesize that repeated exposure to low doses of nicotine in adolescence induce age-specific enhancement of the rewarding effects of several drugs of abuse in the conditioned place preference (CPP) test. Furthermore, we predict that these changes in

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30

Hill, Erik R. "Cocaine Binding Site from the Structure Function Analysis of the Neurotransmitter Reuptake Transporters." The Ohio State University, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=osu1273590773.

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31

Teran, Angie. "AGE-DEPENDENT EFFECTS OF EEDQ ON COCAINE-INDUCED LOCOMOTOR ACTIVITY AND D2 RECEPTOR SUPERSENSITIVITY." CSUSB ScholarWorks, 2019. https://scholarworks.lib.csusb.edu/etd/934.

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The neurochemical changes occurring between the preweanling period and adolescence could be crucial for understanding the role development plays in the manifestation of psychotic behaviors. N-ethoxycarbonyl-2-ethoxy-1,2-dihydroquinoline (EEDQ) fully attenuates the DA agonist-induced behaviors of adult rats, while potentiating the DA agonist-induced locomotor activity of preweanling rats. My specific hypotheses were as follows: (1) Systemically administered EEDQ would block the cocaine-induced locomotor activity of adult rats. (2) Systemically administered EEDQ would potentiate the cocaine-indu

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32

Khalid, Helene. "S-Mephedrone: preclinical investigation of a synthetic cathinone against behavioral and neurochemical effects of cocaine and MDPV." Diss., Temple University Libraries, 2017. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/434922.

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Pharmacology<br>Ph.D.<br>Synthetic cathinones are an emerging class of novel psychoactive substances whose rising rates of abuse have made them a significant public health issue. Recently, synthetic cathinones have emerged as popular drugs of abuse in the United States and Europe. Illicit drug dealers have synthesized stable analogues of cathinones and marketed them via the Internet as “legal high” alternatives to commonly abused psychostimulants. Some adverse effects of synthetic cathinone intoxication include depression, anxiety, myocardial infarction, cardiac dysrhythmias, pulmonary edema,

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33

Hendrick, Elizabeth S. "The Effects of Footshock on the Reinforcing Efficacy of Cocaine in Male Long-Evans Rats." VCU Scholars Compass, 2005. http://scholarscompass.vcu.edu/etd/1540.

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Many links exist between cocaine abuse and stress. The literature and laboratory studies in rats suggest that this could be because stress increases the reinforcing efficacy of cocaine. Using male Long-Evans rats, experiments in this thesis tested effects of footshock on the reinforcing efficacy of cocaine using a progressive ratio schedule of reinforcement. They also examined effects of footshock on the reinforcing efficacy of a half-maximal dose of cocaine. Finally, they tested the effects of footshock on cocaine self-administration in rats initially resistant to acquisition of cocaine self-

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34

Gentile, Taylor Arthur. "Investigations into the Role of Orexin (Hypocretin) and Dynorphin in Drug Seeking, Reinforcement, and Withdrawal." Diss., Temple University Libraries, 2018. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/507530.

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Biomedical Sciences<br>Ph.D.<br>Psychostimulant dependence remains a major health and economic problem, leading to premature death and costing $181 billion annually in health care, crime, and lost productivity costs. Currently, no pharmacotherapies are available to effectively treat psychostimulant dependence. Psychostimulants cause changes in neural circuits involved in reward and affect, but addiction neurocircuitry is incompletely understood and new targets for therapeutic intervention are needed. Lateral hypothalamic orexins (hypocretins) have been shown to have functional roles in arousal

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35

Rudberg, Krista N. "THE IMPORTANCE OF SEROTONERGIC AND ADRENERGIC RECEPTORS FOR THE INDUCTION AND EXPRESSION OF ONE-TRIAL COCAINE-INDUCED BEHAVIORAL SENSITIZATION." CSUSB ScholarWorks, 2016. https://scholarworks.lib.csusb.edu/etd/420.

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Addiction is a complex process in which behavioral sensitization may be an important component. While the behavioral effects of sensitization are well established, the intricate neurobiology of the phenomenon is still largely unknown. Dopamine systems mediate the induction of behavioral sensitization in adult rats, but there is a large amount of evidence showing that other neurotransmitter systems also modulate the induction process. For example, the α1b-adrenergic and 5-HT2A receptor systems are known to modulate the sensitized responding of adult rats, but the roles that these receptor syste

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36

Nwaneshiudu, Chinwe A. "Characterization of a functional role of the neurokinin-3 receptor in behavioral effects of cocaine." Diss., Temple University Libraries, 2011. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/62614.

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Pharmacology<br>Ph.D.<br>The tachykinin NK-3 receptor is a G-protein coupled receptor activated by mammalian tachykinin neuropeptides, which can modulate dopaminergic neurotransmission, and alter dopamine-mediated behaviors. The NK-3 receptor is currently under investigation as a novel therapeutic target for cocaine addiction. Our studies, as outlined in this dissertation, sought to determine if NK-3 receptors have a functional role in the acute as well as long-term behavioral effects of cocaine. Administration of NK-3 receptor agonists or antagonists potentiates or attenuates dopamine-med

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37

Simmons, Steven James. "HYPOCRETIN/OREXIN AND THE VENTRAL MIDBRAIN: TOPOGRAPHY AND FUNCTION ASSOCIATED WITH PSYCHOSTIMULANT-TAKING AND AFFECT." Diss., Temple University Libraries, 2018. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/507835.

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Biomedical Sciences<br>Ph.D.<br>Abuse of psychostimulants including cocaine and new synthetic formulations remains an international public health problem and economic burden. Addiction develops consequential to positive and negative drives that underlie “getting” and “staying” high. Dopamine (DA), arising from ventral tegmental area (VTA), projects to ventral striatal targets to encode reward signals and reward prediction. Mesolimbic DA is implicated in both the immediate rewarding effects of psychostimulants, and its hypoactivity underlies negative affect as drug levels decline. Accordingly,

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38

Moyer, Robert A. "Exploration of Functional Genetic Variants in Candidate Genes for Psychiatric Disorders." The Ohio State University, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=osu1283184584.

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39

Alajaji, Mai. "THE IMPACT OF ADOLESCENT NICOTINE EXPOSURE ON DRUG DEPENDENCE IN ADULTHOOD." VCU Scholars Compass, 2010. http://scholarscompass.vcu.edu/etd/127.

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Nicotine is one of the first and most commonly abused drugs in adolescence. According to The Center for Disease Control, every day more than 6000 adolescents try their first cigarette and over 3000 of them become daily smokers. Smoking among adolescents is a strong predictor of future drug abuse and dependence in adulthood. A number of studies has suggests that adolescents pre-exposed to nicotine may suffer permanent disruption of the brain’s reward systems through changes in dopamine receptor function. We hypothesize that nicotine exposure during adolescence causes long lasting neurobiologica

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40

Trecki, Jordan. "THE MODULATION OF THE MESOLIMBIC AND NIGROSTRIATAL DOPAMINE PATHWAYS BY CXCL12 AND CXCR4." Diss., Temple University Libraries, 2009. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/57720.

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Pharmacology<br>Ph.D.<br>The role of chemokines in immune function is clearly established. Recent evidence suggests that these molecules also play an important role in the CNS as modulators of neuronal activity. The chemokine CXCL12 has been identified in several regions of the adult rat brain including the substantia nigra, ventral tegmental area and caudate putamen. CXCR4, a receptor activated by CXCL12, is expressed by dopaminergic neurons in the substantia nigra. The research presented herein explored the behavioral modulation of CXCL12, expression of the CXCR4 receptor in the forebrain of

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41

Wei, Hua. "Screening of Functional Norepinephrine Transporter Insensitive to Cocaine Inhibition and Generation of Knock-In Mouse." The Ohio State University, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=osu1230840494.

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42

Sanjakdar, Sarah. "INVESTIGATING THE ROLE OF α6 and α4 CONTAINING NEURONAL NICOTINIC ACETYLCHOLINE RECEPTORS IN NICOTINE AND COCAINE CONDITIONED PLACE PREFERENCE TESTS IN MICE". VCU Scholars Compass, 2012. http://scholarscompass.vcu.edu/etd/346.

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Neuronal nicotinic acetylcholine receptors modulate both cholinergic and non-cholinergic synaptic transmission. Our research concerns α6 and α4 neuronal nicotinic subunits because they often co-assemble with the β2 subunit, which has abundant expression in the CNS and previous work has demonstrated that β2* nAChRs are involved in nicotine and cocaine reward. α6β2* and α4β2* nAChRs are highly expressed in midbrain, which is known to be critical for the incentive salience associated with natural and artificial (drug) reward. Our goal was to assess the role of α6β2* and α4β2* nAChRs in nicotine a

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Braun, Ivan Mario. "Potencial de abuso do midazolam intranasal em usuários de cocaína aspirada e voluntários normais." Universidade de São Paulo, 2012. http://www.teses.usp.br/teses/disponiveis/5/5142/tde-28112012-124456/.

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INTRODUÇÃO: O midazolam é uma imidazobenzodiazepina usada para induzir o sono, produzir sedação antes de procedimentos dolorosos e no tratamento do estado de mal epiléptico. Seu uso pela via intranasal proporciona um rápido início de ação e esta via, em muitos casos, pode substituir as vias endovenosa e intramuscular, mais invasivas. Assim, o midazolam intranasal tem sido sugerido no tratamento extra-hospitalar de crises epilépticas e ataques de pânico. Por outro lado, os benzodiazepínicos possuem um potencial para serem abusados, principalmente em usuários de outras drogas. OBJETIVO: o presen

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Somkuwar, Sucharita S. "METHYLPHENIDATE AND ATOMOXETINE TREATMENT DURING ADOLESCENCE IN THE SPONTANEOUSLY HYPERTENSIVE RAT: MECHANISMS UNDERLYING HIGH COCAINE ABUSE LIABILITY IN ATTENTION DEFICIT/HYPERACTIVITY DISORDER." UKnowledge, 2013. http://uknowledge.uky.edu/pharmacy_etds/27.

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Effects of pharmacotherapies for Attention Deficit/Hyperactivity Disorder (ADHD) on cocaine abuse liability in ADHD are not understood. Spontaneously Hypertensive Rats (SHR), an ADHD model, exhibited greater cocaine self-administration than control Wistar-Kyoto and Wistar rats. Methylphenidate, but not atomoxetine during adolescence enhanced cocaine self-administration in adult SHRs compared to controls. The mesocortical dopaminergic system, including medial prefrontal (mPFC) and orbitofrontal (OFC) cortices, is important for ADHD and cocaine addiction. Dopamine and norepinephrine transporter

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Batman, Angela. "MODULATION OF COCAINE-LIKE BEHAVIOURAL ACTIVITY BY SEROTONIN UPTAKE INHIBITION RELATIVE TO THE EFFECTS OF THE NOVEL AND SELECTIVE DOPAMINE TRANSPORTER INHIBITOR, D-84." VCU Scholars Compass, 2010. http://scholarscompass.vcu.edu/etd/2181.

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Cocaine dependence is a major health concern worldwide, but despite this high rate of abuse there are currently no approved therapies for cocaine dependence. Replacement pharmacotherapies are one possible approach for treating cocaine dependence, and identification of such therapeutics for cocaine abuse is the long-term goal of this research. Cocaine binds to, and inhibits uptake at the dopamine (DAT), serotonergic (SERT) and noradrenaline (NET) uptake transporters, but studies have shown that cocaine produces its strong behavioural and positive reinforcing effects through inhibition of the D

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Greenwood, Maria A. "Differential behavioral effects of ketamine between adolescent and adult Sprague-Dawley rats." VCU Scholars Compass, 2013. http://scholarscompass.vcu.edu/etd/3045.

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The dissociative anesthetic ketamine has been subject to growing abuse worldwide, particularly in adolescents. This project compared the effects of ketamine in conditioned place preference and intravenous self-administration in adolescent (PND 28-50) and adult (>PND70) Sprague-Dawley rats. Cocaine served as a positive control. In CPP, adolescents demonstrated preferences for ketamine, while adults developed an aversion. In the self-administration procedure, adults acquired the behavior more rapidly, but there was no difference in the percentage of subjects reaching acquisition nor in respondin

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Naughton, Bartholomew J. IV. "Brain Region and Cell Type Specific Approaches to Study Drug Abuse." The Ohio State University, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=osu1314715486.

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Allain, Florence. "Manipuler la pharmacocinétique de la cocaïne chez le rat pour comprendre et traiter un phénotype toxicomane." Thèse, 2017. http://hdl.handle.net/1866/21596.

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Hodebourg, Ritchy. "L’influence d’un traitement à la N-Acétylcystéine sur la motivation à s’auto-administrer de la cocaïne chez le rat." Thèse, 2018. http://hdl.handle.net/1866/21857.

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Minogianis, Ellie-Anna. "Augmenter la vitesse d’injection de la cocaïne favorise l’apparition de comportements de consommation caractéristiques de la toxicomanie." Thèse, 2012. http://hdl.handle.net/1866/8613.

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Nombreux individus vont expérimenter avec les drogues d’abus, mais peu vont devenir toxicomanes. Plusieurs facteurs sont impliqués dans la transition d’un usage récréatif à l’addiction. Les drogues, les conditionnements et les voies d’administration qui mènent à l’augmentation rapide du taux drogue dans le cerveau favorisent cette évolution. La raison est méconnue. Nous avons émis l’hypothèse que l’injection rapide de drogue promeut des changements dans le cerveau qui mènent à l’augmentation de la consommation et de la motivation à obtenir la drogue. Nous avons comparé la consommation lors de

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