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Books on the topic 'Dopaminergic mechanisms'

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Published: 4 June 2021
Last updated: 30 July 2024

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1

1937-, Bodis-Wollner Ivan, Piccolino Marco, and International Brain Research Organization. Congress, eds. Dopaminergic mechanisms in vision. New York: Liss, 1988.

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2

R, Ashby Charles, ed. The modulation of dopaminergic neurotransmission by other neurotransmitters. Boca Raton: CRC Press, 1996.

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3

Kujacic, Mirjana. Dopaminergic control of adrenomedullary function in the rat. Göteberg [Sweden]: Dept. of Pharmacology, University of Göteberg, 1994.

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4

P, Riederer, ed. The Role of brain dopamine. Berlin: Springer-Verlag, 1989.

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5

Paul, Willner, Scheel-Krüger Jørgen, and European Behavioral Pharmacology Society, eds. The mesolimbic dopamine system: From motivation to action. Chichester: Wiley, 1991.

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6

Miller, Robert, 1943 Aug. 29- and Wickens J, eds. Brain dynamics and the striatal complex. Amsterdam, Netherlands: Harwood Academic, 2000.

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7

Anton, Reiner, ed. Phylogeny and development of catecholamine systems in the CNS of vertebrates. Cambridge: University of Cambridge Press, 1994.

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8

Kjell, Fuxe, and Wenner-Grenska samfundet, eds. Trophic regulation of the basal ganglia: Focus on dopamine neurons. Oxford, OX, UK: Pergamon, 1994.

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9

W, Stone T., ed. CNS neurotransmitters and neuromodulators: Glutamate. Boca Raton: CRC Press, 1995.

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10

C, Baron J., and European Economic Community, eds. Brain dopaminergic systems: Imaging with positron tomography : proceedings of a workshop held in Caen, France, within the framework of the European Community medical and public health research. Dordrecht: Kluwer Academic Publishers, 1991.

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11

P, Soares-da-Silva, ed. Cardiovascular and renal actions of Dopamine: Proceedings of the IVth International Conference on Peripheral Dopamine held in Porto, Portugal on 18-20 June 1992. Oxford, England: Pergamon Press, 1993.

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12

Soares, Barbara Domingos. Modulation of Dopaminergic System Ontogeny by Low-Level Lead Exposure: A Potential Underlying Mechanism for the Onset of Drug Sensitization. [New York, N.Y.?]: [publisher not identified], 2016.

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13

Masaya, Segawa, and Nomura Y. 1940-, eds. Age-related dopamine-dependent disorders. Basel: Karger, 1995.

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14

Mechanisms of Degeneration and Protection of the Dopaminergic System. F P Graham Company, 2001.

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15

McElvain, James Scott. In vitro studies of the kinetics of endogenous dopamine release and reuptake into rat striatal suspensions using rotating disk electrode voltammetry. 1992.

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16

(Editor), Liana Bolis, Luca Pani (Editor), Julio Licinio (Editor), and C. Liana Bolis (Editor), eds. Dopaminergic System: Evolution from Biological to Clinical Aspects. Lippincott Williams & Wilkins, 2001.

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17

Dilts, Roger P. Autoradiographic localization of mu and delta opioid receptors in the mesocorticolimbic dopamine system. 1989.

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18

The dopaminergic mind in human history and evolution. Cambridge [England]: Cambridge University Press, 2009.

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19

Meiergerd, Susan Marie. Kinetic investigation of the dopamine transport system. 1994.

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20

Sofic, E., C. Konradi, J. Kornhuber, P. Riederer, and Jack Haley. Role of Brain Dopamine. Springer London, Limited, 2012.

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21

Geracioti, Thomas D., Jeffrey R. Strawn, and Matthew D. Wortman. Mechanisms of Action in the Pharmacology of PTSD. Edited by Israel Liberzon and Kerry J. Ressler. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190215422.003.0020.

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This chapter reviews medications currently available for PTSD in the context of their mechanisms of action, pathophysiological relevance, and clinical efficacy data. It systematically reviews aminergic mechanisms in PTSD pharmacology, including commonly used serotonin and norepinephrine agents, selective reuptake inhibitors and receptors drugs, as well as dopaminergic agents and psychostimulants. It also discusses the use of anticonvusants and antianxiety agents that modulate GABAergic and glutamatergic signaling, such as carbamazepine, VPA, benzodiazepines, gabapentine, and others. It also reviews other clinically available agents as well as HPA axis-modulating compounds, both for treatment and secondary prevention of PTSD. It concludes with the suggestion that clinical selection of one or more of these medications for PTSD should be based on individual patient considerations, including target symptoms, PTSD subtype, post-traumatic interval, comorbidities, genotypes for CYP450 enzymes, and genetic polymorphisms of clinical relevance.
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22

Povlock, Sue Laura. Cocaine and the kinetics of the transport of dopamine in the striatum and nucleus accumbens. 1995.

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23

Chiara, Gaetano Di. Dopamine in the CNS I. Springer London, Limited, 2012.

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24

Chiara, Gaetano Di. Dopamine in the CNS I. Springer Berlin / Heidelberg, 2012.

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25

Dopamine in the CNS I. Springer, 2002.

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26

Dopamine in the CNS I. Springer, 2011.

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27

Willner, Paul. Mesolimbic Dopamine System: From Motivation to Action. John Wiley & Sons Ltd (Import), 1991.

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28

Calne, Donald B., and Kjell Fuxe. Dopaminergic Ergot Derivatives and Motor Function: Proceedings of an International Symposium Held in the Wenner-Gren Center, Stockholm, July 24-25 1978. Elsevier Science & Technology Books, 2013.

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29

Robert, Miller, and Jeffrey Wickens. Brain Dynamics and the Striatal Complex. Taylor & Francis Group, 2000.

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30

Robert, Miller, and Jeffrey Wickens. Brain Dynamics and the Striatal Complex. Taylor & Francis Group, 2000.

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31

Robert, Miller, and Jeffrey Wickens. Brain Dynamics and the Striatal Complex. Taylor & Francis Group, 2000.

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32

Robert, Miller, and Jeffrey Wickens. Brain Dynamics and the Striatal Complex. Taylor & Francis Group, 2000.

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33

Vernier, Philippe, Anita Sidhu, and Marc Laruelle. Dopamine Receptors and Transporters: Function, Imaging and Clinical Implication, Second Edition. Taylor & Francis Group, 2003.

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34

Chapman, Mary Ann. Differential effects of unique profile antipsychotic drugs and neurotensin on extracellular amino acids in basal ganglia regions of the rat brain. 1994.

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35

Vernier, Philippe, Anita Sidhu, and Marc Laruelle. Dopamine Receptors and Transporters: Function, Imaging and Clinical Implication, Second Edition. Taylor & Francis Group, 2003.

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36

Mahon, Katie, Manuela Russo, and M. Mercedes Perez-Rodriguez. Cognitive Enhancement in Bipolar Disorder. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190214401.003.0011.

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Neurocognitive deficits are acknowledged as integral features of bipolar disorder (BD) and are known to contribute to the compromised level of functioning in individuals with BD. This chapter provides an overview of the current state of cognitive enhancement in BD. Few pharmacological agents have been investigated with regard to their potential for pro-cognitive effects in BD. Dopaminergic agents (pramipexole) and stimulants (modafinil, armodafinil, and amphetamine) as adjunctive treatment in BD appear to be promising cognitive enhancers, and there are few ongoing randomized clinical trials targeting both cognitive dysfunctions and clinical symptomatology in BD. Glutamatergic agents (d-cycloserine) may hold promise as potential cognitive enhancing agents in BD; however, as for dopaminergic agents and stimulants, no conclusive data exist. Larger samples and longer follow-up are needed to obtain a deep understanding of the efficacy and safety of these compounds and their role in the neurobiological mechanisms underpinning cognition in BD.
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37

Stone, Trevor W. CNS Neurotransmitters and Neuromodulators: Acetylcholine. Taylor & Francis Group, 2020.

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38

Stone, Trevor W. CNS Neurotransmitters and Neuromodulators: Acetylcholine. Taylor & Francis Group, 2020.

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39

Stone, Trevor W. CNS Neurotransmitters and Neuromodulators: Neuroactive Steroids (CNS Neurotransmitters & Neuromodulators). CRC, 1996.

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40

Stone, Trevor W. CNS Neurotransmitters and Neuromodulators: Dopamine. CRC-Press, 1996.

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41

Stone, Trevor W. CNS Neurotransmitters and Neuromodulators: Acetylcholine. Taylor & Francis Group, 2020.

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42

Stone, Trevor W. CNS Neurotransmitters and Neuromodulators: Acetylcholine. CRC, 1994.

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43

Stone, Trevor W. CNS Neurotransmitters and Neuromodulators: Glutamate. CRC, 1995.

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44

Stone, Trevor W. CNS Neurotransmitters and Neuromodulators: Acetylcholine. Taylor & Francis Group, 2020.

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45

Plasma HVA levels and contrived leisure experiences of female college students. 1989.

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46

Plasma HVA levels and contrived leisure experiences of female college students. 1991.

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47

Plasma HVA levels and contrived leisure experiences of female college students. 1991.

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48

Crosson, Bruce A., Anastasia Ford, and Anastasia M. Raymer. Transcortical Motor Aphasia. Edited by Anastasia M. Raymer and Leslie J. Gonzalez Rothi. Oxford University Press, 2015. http://dx.doi.org/10.1093/oxfordhb/9780199772391.013.11.

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The defining symptoms of transcortical motor aphasia (TCMA) are nonfluent verbal output with relatively preserved repetition. Other symptoms, such as naming difficulties, agrammatic output, or even some paraphasias, may occur, but these are not cardinal symptoms defining TCMA and are not necessary for the diagnosis. The core anatomy involved in TCMA is a lesion of the medial frontal cortex, especially the left presupplementary motor area (pre-SMA) and adjacent Brodmann’s area 32; a lesion of the left posterior inferior frontal cortex, especially pars opercularis and ventral lateral premotor cortex; or a lesion of the pathways between these frontal structures. TCMA occasionally has been reported with a lesion of the left basal ganglia, the left thalamus, or the ascending dopaminergic pathways. From a cognitive standpoint, TCMA can be conceptualized as a disorder of intention, in other words, as a disorder of initiation and continuation of spoken language that is internally motivated. The medial frontal cortex provides the impetus to speak; this impetus to speak is conveyed to lateral frontal structures through frontal–subcortical pathways where it activates various language production mechanisms. The influence of the ascending dopaminergic pathways may occur either through their heavy connections with the pre-SMA region or through their influence on the basal ganglia. The influence of the basal ganglia and thalamus probably occurs through their connections with the medial frontal cortex. Assessments for TCMA should involve a thorough evaluation of conversational or narrative language output and repetition. New treatments are available that attempt to engage right-hemisphere intention mechanisms with left-hand movements and may be effective in TCMA. Although dopamine agonists have also shown some positive effects in increasing verbal output in TCMA, trials have been small, and some caution must be exercised in interpreting these findings.
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49

Faraone, Stephen V., Pradeep G. Bhide, and Joseph Biederman. Neurobiology of Attention Deficit Hyperactivity Disorder. Edited by Dennis S. Charney, Eric J. Nestler, Pamela Sklar, and Joseph D. Buxbaum. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190681425.003.0064.

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Attention deficit hyperactivity disorder (ADHD) is a prevalent, early-onset and persistent disorder of inattention, hyperactivity, and impulsivity. The mechanisms of action of ADHD medications, neuroimaging studies, and studies of monoamine systems and animal models suggest that dysregulation of catecholaminergic neurotransmission in cerebellar-corticostriatal circuits plays a key role in the pathophysiology of ADHD. The efficacy of ADHD medications likely arises from their differing profile of effects on (a) dopaminergic and noradrenergic systems and (b) the localization of these effects in prefrontal cortex and striatum. ADHD has a very high heritability, and although molecular genetic studies have found no causal common DNA variants yet, they have found strong evidence that rare duplications and deletions are risk factors for ADHD. Environmental risk factors, especially those that impact early neurodevelopment (i.e., exposure to cigarette smoking and alcohol during pregnancy), also influence susceptibility to ADHD.
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50

Kaar, Stephen J., Steven Potkin, and Oliver Howes. The neurobiology of antipsychotic treatment response and resistance. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198828761.003.0005.

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Dopamine D2/3 receptor occupancy by antipsychotic drugs is central to clinical response and many of their side effects. Yet the locus of dopaminergic alterations in the majority of patients with schizophrenia is not the D2/3 receptor but, instead, presynaptic, comprising elevated striatal dopamine synthesis and release capacity. However, whilst this explains why dopamine D2/3 receptor blockade is effective in many patients, a proportion of patients does not respond. In some this is because of inadequate antipsychotic blockade of dopamine receptors, but there are others who do not respond to antipsychotic treatment despite substantial dopamine D2/3 receptor blockade. The neurobiology of treatment resistance does not seem to involve the presynaptic dopamine dysfunction typically seen in patients, suggesting that it needs different treatments. Disruptions to the glutamatergic system, and to dopamine D1 and D2/3 receptors and serotonin 2A receptors have all been proposed as potential mechanisms underlying treatment resistance and as targets for novel treatments.
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