Libros: "Dopamine and serotonin"

1

Serotonin-dopamine interaction: Experimental evidence and therapeutic relevance. Amsterdam: Elsevier, 2008.

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2

Thompson, Miles. Mutation screening of dopamine and serotonin candidate genes in Tourette's syndrome and alcohol-dependent patients. Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1999.

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3

Bailey, Matthew Richard. An Examination of Goal-Directed Motivation in Mice: The Role of Dopamine D2 and Serotonin 2C Receptors. [New York, N.Y.?]: [publisher not identified], 2017.

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4

Ruden, Ronald A. The craving brain: The biobalance approach to controlling addictions. New York: HarperCollins Publishers, 1997.

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5

1947-, Byalick Marcia, ed. The craving brain: A bold new approach to breaking free from drug addiction, overeating, alcoholism, gambling. 2^a ed. New York: Perennial/an imprint of HarperCollins Publishers, 2000.

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6

Hennes, Rebekah. Bite Size Pieces, Create a Foundation. Lulu Press, Inc., 2009.

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7

Munoz, Monica y Marshall McKinney. Serotonin and Dopamine Receptors: Functions, Synthesis and Health Effects. Nova Science Publishers, Incorporated, 2018.

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8

Giovanni, Giuseppe Di, Ennio Esposito y Vincenzo Di Matteo. Serotonin-Dopamine Interaction: Experimental Evidence and Therapeutic Relevance. Elsevier Science & Technology Books, 2008.

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9

Iem, Goshua. Smoothies and Sweet-Food for Happiness: Serotonin, Dopamine, and Oxytocin. Independently Published, 2019.

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10

Torres-Malaga, Dr Marianne Sierra. The Interactions of Serotonin and Dopamine in Obsessive Compulsive Disorder. Createspace Independent Publishing Platform, 2018.

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11

adam, sareena. AthshlánúDO BRAIN: Treisiú Do Leibhéil Serotonin, Dopamine, Oxytocin, Agus Endorphin. Independently Published, 2022.

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12

García-Cazorla, Angels y Rafael Artuch. Brain Serotonin Deficiency. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0032.

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Brain serotonin deficiency is a heterogeneous condition whose etiology remains unknown in the majority of cases. Strong evidence supports a major role for brain serotonin deficiency in common conditions such as depression and other psychiatric and cognitive disorders, which are probably due to interactions between genetic and environmental factors. Mendelian monogenic conditions leading to brain serotonin deficiency have also been identified, but they are rare. These diseases are associated with defects in other neurotransmitters (primarily dopamine), and it is difficult to link serotonin deficiency with specific neurological syndromes. Secondary serotonin deficiency is also common. In adults, when serotonin deficiency is thought to contribute to neurological symptoms such as sleep disturbance and alterations in behavior, treatment with serotonin precursors may be useful.

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13

Iem, Goshua. Be Happy: The Food Made Me Joyful. Serotonin, Dopamine, and Oxytocin. Independently Published, 2019.

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14

ORTEGA, Margot. Simplified Handbook of Serotonin and Dopamine: A Quintessential Guide for Beginners. Independently Published, 2022.

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15

(Editor), Ronald J. Bradley, Adron R. Harris (Editor), Peter Jenner (Editor) y John Smythies (Editor), eds. The Neuromodulators (International Review of Neurobiology) (International Review of Neurobiology). Academic Press, 2005.

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16

Happiness Hormones: How Accustom Brain Work Out Serotonin, Dopamine, Endorphin and Oxytocin. Independently Published, 2022.

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17

Publishing, Modern Psychology. Happiness: Habits to Increase Serotonin, Dopamine, Oxytocin and Endorphins and Naturally Improve Brain Chemistry. Independently Published, 2018.

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18

Iem, Goshua. Be Happy : The Food Made Me Joyful. the Best Recipes: Serotonin, Dopamine, and Oxytocin. Independently Published, 2019.

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19

Baek, Jae-Kyeong. Behavioral studies of dopa-decarboxylase mutant Drosophila lacking serotonin and dopamine in central nervous system. 1987.

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20

Habits of a happy brain: Retrain your brain to boost your serotonin, dopamine, oxytocin, & endorphin levels. Adams Media, 2016.

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21

Davis, Margaret A. Adrenal Fatigue Diet: Reset your Energy, Balance your Hormones and Boost your Serotonin, Dopamine and Oxytocin. HMPL Publishing, 2017.

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22

Breuning, Loretta Graziano. Habits of a Happy Brain: Retrain Your Brain to Boost Your Serotonin, Dopamine, Oxytocin, & Endorphin Levels. Simon & Schuster Audio and Blackstone Audio, 2019.

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23

James, Lee. Your Brain Electric: Everything you need to know about optimising neurotransmitters including serotonin, dopamine and noradrenaline. CreateSpace Independent Publishing Platform, 2014.

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24

Breuning, Loretta Graziano. Habits of a Happy Brain: Retrain Your Brain to Boost Your Serotonin, Dopamine, Oxytocin, and Endorphin Levels. Adams Media Corporation, 2015.

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25

Noot, V. Happy Brain : 35 Tips to a Happy Brain: How to Boost Your Oxytocin, Dopamine, Endorphins, and Serotonin. Independently Published, 2015.

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26

James, Lee. Better Living through Neurochemistry: A guide to the optimization of serotonin, dopamine and the neurotransmitters that color your world. CreateSpace Independent Publishing Platform, 2014.

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27

Kaar, Stephen J., Steven Potkin y 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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28

Heales, Simon, Simon Pope, Viruna Neergheen y Manju Kurian. Abnormalities of CSF Neurotransmitters/Folates. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0082.

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The term Neurotansmitter disorder, in the area of metabolic disease, focuses particularly on inborn errors affecting monoamine (dopamine & serotonin), pyridoxal phosphate (B6) and folate metabolism. Whilst there has been considerable focus on these disorders with regards to the paediatric population, it is clear that an increasing number of adult patients are being identified. Adult neurologists need to be aware of the clinical presentation of such patients and the appropriate tests that need to be requested to ensure a correct diagnosis is achieved. CSF profiling, by a specialist laboratory, is often required. This has the ability to very often identify the nature of a primary defect with regards to implementation of appropriate treatment. For some of these disorders, treatment can be effective. This may be in the form of monoamine/vitamin replacement. However there are exceptions, e.g. aromatic amino acid decarboxylase and dopamine transporter deficiencies. There also needs also to be an awareness of the growing list of secondary factors that can cause impaired dopamine and serotonin metabolism.

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29

Colors, Loraine. Funny and Sarcastic Quotes Coloring Book: With Stress Relieving and Relaxing Designs to Make You Smile Releasing Dopamine and Serotonin. Independently Published, 2022.

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30

Smythies, John R. The neuromodulators. vii, 285 p, 2005.

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31

(Editor), Ronald J. Bradley, Adron R. Harris (Editor), Peter Jenner (Editor) y John Smythies (Editor), eds. The Neuromodulators (International Review of Neurobiology) (International Review of Neurobiology). Academic Press, 2005.

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32

Nageshwaran, Sathiji, Heather C. Wilson, Anthony Dickenson y David Ledingham. Parkinson’s disease and parkinsonism. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199664368.003.0009.

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This chapter discusses the evidence-based pharmacological management of motor and non-motor (autonomic disease, dementia, psychosis, depression, and sleep disorder) Parkinson’s disease (PD) and Parkinson’s plus syndromes (progressive supranuclear palsy (PSP), multiple system atrophy (MSA), and corticobasal degeneration (CBD)). Drugs to use with caution in parkinsonism are highlighted. Clinical features and evidence-based management of impulse control disorders (ICDs), serotonin syndrome, dopamine agonist withdrawal syndrome (DAWS), and neuroleptic malignant syndrome (NMS)/Parkinson’s hyperpyrexia syndrome (PHS) are also reviewed.

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33

Friedel, Robert O. y Stephen M. Stahl. The Fundamentals of Brain Neurotransmission. Editado por Christian Schmahl, K. Luan Phan, Robert O. Friedel y Larry J. Siever. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199362318.003.0002.

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This chapter outlines the fundamental principles underlying neuroscience, particularly as it relates to neurotransmission and neuropharmacology. It then reviews and synthesizes of the role of different neurochemical and neurotransmitter systems that underlie brain function and synaptic transmission, including GABA, glutamate, serotonin, dopamine, norepinephrine, acetylcholine, and histamine. In addition, it describes various psychoactive medications are used in the treatment of personality disorders, such as mood stabilizers and antipsychotics. Moreover, it describes how these agents target these systems by describing their different mechanisms of action. It provides a primer to better understand the pathophysiology and pharmacological treatment of personality disorders discussed in the book.

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34

Narayana, Shalini, Andrew B. Newberg y Abass Alavi. Positron Emission Tomography. Editado por Andrew C. Papanicolaou. Oxford University Press, 2014. http://dx.doi.org/10.1093/oxfordhb/9780199764228.013.9.

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This chapter describes the application of positron emission tomography (PET) technology to study neurotransmitter systems. The process of developing radiotracers to study the neurotransmitter systems, namely radioligands and the technical aspects of utilizing these radiotracers in PET imaging, is discussed. Normal distribution of neurotransmitters including dopamine, serotonin, opioids, and γ-aminobutyric acid (GABA), as well as abnormalities of these systems in various neurological and psychiatric disorders, are highlighted. The chapter provides evidence that radioligand imaging has been useful not only in delineating pathophysiological processes in psychiatric disorders, but also in contributing to the diagnosis, prognosis, and disease course, and in assessing drug effects. Recent advances in receptor imaging that are rapidly gaining clinical relevance are also discussed.

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35

Graat, Ilse, Martijn Figee y Damiaan Denys. Neurotransmitter Dysregulation in OCD. Editado por Christopher Pittenger. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190228163.003.0025.

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Obsessive-compulsive disorder (OCD) is associated with abnormalities in the cortico-striatal–thalamic–cortical (CSTC) circuitry, and may be associated with dysregulation of neurotransmitters within this network. The major neurotransmitters of the CSTC are serotonin, dopamine, glutamate and γ‎-aminobutyric acid (GABA. This chapter reviews evidence of the involvement of these neurotransmitters in OCD from pharmaocological, genetic, and imaging studies. yielding an integrated neurotransmitter model of OCD. It concludes that the neurotransmitter model of OCD involves dopaminergic and glutamatergic overactivity in frontostriatal pathways, along with diminished serotonergic and GABAergic neurotransmission in frontolimbic systems. These neurotransmitter imbalances may explain frontostriatal hyperactivity and impaired frontolimbic emotion regulation. Advancing our understanding of neurotransmitter abnormalities in OCD, and how abnormalities in different transmitter systems relate to one another, holds promise for the development of new pharmacotherapies.

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36

Lee, Royce, Jennifer R. Fanning y Emil F. Coccaro. The Clinical Neuroscience of Impulsive Aggression. Editado por Christian Schmahl, K. Luan Phan, Robert O. Friedel y Larry J. Siever. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199362318.003.0008.

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Aggression can be categorized into three subtypes: premeditated aggression, frustration-related aggression, and impulsive aggression (IA), which is the focus of this chapter. It first delineates the social information processing model of IA and its neurobiological underpinnings, with a special focus on ventral prefrontal-amygdala, frontostriatal, and frontoparietal circuits. In these circuits, structural as well as functional alterations have been associated with IA. A large body of basic and clinical research has examined the role of neurotransmitters (glutamate, GABA) and neuromodulators (monoamines and neuropeptides) in mediating IA. The important role of the monoamines dopamine, serotonin, norepinephrine, and acetylcholine in the mediation of different aspects of IA and the pharmacological potential resulting from these alterations are depicted in the second half of the chapter. The chapter concludes with an overview of the most important etiological factors.

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37

Nielsen, David A., Dmitri Proudnikov y Mary Jeanne Kreek. The Genetics of Impulsivity. Editado por Jon E. Grant y Marc N. Potenza. Oxford University Press, 2012. http://dx.doi.org/10.1093/oxfordhb/9780195389715.013.0080.

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Impulsivity is a complex trait that varies across healthy individuals, although when excessive, it is generally regarded as dysfunctional. Impulsive behavior may lead to initiation of drug addiction that interferes with inhibitory controls, which may in turn result in facilitation of the individual’s impulsive acts. Although environmental factors play a considerable role in impulsive behavior, a body of evidence collected in twin studies suggests that about 45% of the variance in impulsivity is accounted for by genetic factors. Genetic variants studied in association with impulsivity include those fortryptophan hydroxylase 1 and 2 (TPH1 and TPH2), the serotonintransporter (SERT), serotonin receptors, and genes of the monoamine metabolism pathway (e.g., monoamine oxidase A, MAOA). Other systems may also play a role in these behaviors, such as the dopaminergic system (the dopamine receptors DRD2, DRD3, and DRD4, and the dopamine transporter, DAT), the catecholaminergic system (catechol-O-methyltransferase, COMT), and the GABAergic system (GABAreceptor subunit alpha-1, GABRA1; GABA receptor subunit alpha-6, GABRA6; and GABA receptor subunit beta-1, GABRB1). Taking into account involvement of the hypothalamic-pituitary-adrenal (HPA) axis, the number of candidate genes implicated in impulsivity may be increased significantly and, therefore, may go far beyond those of serotonergic and dopaminergic systems. For a number of years, our group has conducted studies of the association of genes involved in the modulation of the stress-responsive HPA axis and several neurotransmitter systems, all involved in the pathophysiology of anxiety and depressive disorders, impulse control and compulsive disorders, with drug addiction. These genes include those of the opioid system: the mu- and kappa-opioid receptors (OPRM1 and OPRK1) and the nociceptin/orphaninFQ receptor (OPRL1); the serotonergic system: TPH1 and TPH2 and the serotonin receptor 1B (5THR1B); the catecholamine system: COMT; the HPA axis: themelanocortin receptor type 2 (MC2R or adrenocorticotropic hormone, ACTHR); and the cannabinoid system: the cannabinoid receptor type 1 (CNR1). In this chapter we will focus on these findings.

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38

Roze, Emmanuel y Nenad Blau. Biogenic Monoamine Disorders. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0031.

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Biogenic monoamine disorders are a group of inherited diseases characterized by a defect in the synthesis, transport, or degradation of catecholamines and serotonin. The phenotype mostly reflects the pattern and severity of the monoamine deficiency. Movement disorders due to cerebral dopamine deficiency are almost always prominent, mostly in the form of dystonia and/or parkinsonism. These disorders are potentially devastating yet treatable. Early diagnosis and treatment are crucial to prevent ongoing brain dysfunction. Detection of hyperphenylalaninemia in a neonate could be a good clue to the diagnosis. Final diagnosis is often based on a detailed biochemical investigation of the cerebrospinal fluid and can be confirmed by molecular analysis. Treatment is aimed at restoring neurotransmitter homeostasis using monoamine precursors, monoamine agonists, and inhibitors of monoamine degradation. It also comprises the control of hyperphenylalaninemia and the prevention of cerebral folate deficiency, when applicable.

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39

Pittenger, Christopher. The Pharmacological Treatment of Refractory OCD. Editado por Christopher Pittenger. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190228163.003.0041.

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Evidence-based interventions for OCD, both psychotherapeutic and pharmacological, are of benefit to many. However, even when optimally deployed, first- and second-line treatments leave a substantial fraction of patients—perhaps as many as 20% to 25%—without meaningful improvement. Furthermore, many who are classified as “responders” to first- and second-line treatments continue to have substantial residual symptoms and attendant morbidity. This chapter reviews various pharmacological strategies that have been used for the treatment of refractory OCD, including agents targeting serotonin, dopamine, and glutamate neurotransmission. Although the evidence base supporting the use of these agents is not as robust as it is for first-line interventions, many have shown promise in some studies. The prevalence of refractory OCD symptoms means that such pharmacological strategies must frequently be considered in clinical practice, despite the lack of definitive guidance from controlled studies.

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40

Mason, Peggy. Synthesis, Packaging, and Termination of Neurotransmitters. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190237493.003.0012.

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The synthesis, packaging, and termination of action of neurotransmitters are detailed. There are far more varieties of peptide neurotransmitters than there are of low-molecular-weight neurotransmitters. Yet low-molecular-weight neurotransmitters are the ubiquitous workhorses of the nervous system. Acetylcholine, the catecholamines norepinephrine and dopamine, serotonin, glutamate, and GABA are examined in some depth. The vesicular transporters that carry low-molecular-weight neurotransmitters from the cytoplasm into synaptic vesicles are covered. The role of monoamines in affect and mood and the psychotropic effects of monoaminergic drugs are discussed. Principles of catecholamine synthesis are applied to understand phenylketonuria. Uptake of monoamines into neurons is discussed in the context of amphetamine, cocaine, and other drugs of abuse. Stiff-person syndrome, which results from an impairment of GABA synthesis, is introduced. The modes of action for peptide and gaseous neurotransmitters are briefly covered.

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41

Chen, Michael C. y Ian H. Gotlib. Molecular Foundations of the Symptoms of Major Depressive Disorder. Editado por Turhan Canli. Oxford University Press, 2013. http://dx.doi.org/10.1093/oxfordhb/9780199753888.013.002.

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Major Depressive Disorder (MDD) is a prevalent and costly disorder with a broad range of cognitive, affective, and behavioral symptoms. Despite the absence of a clear final common molecular pathway in depression, many molecular systems have been implicated in MDD. In particular, disruptions in molecular systems like serotonin, dopamine, glutamate, and other neurotransmitters, as well as in stress hormones, cytokines, neurotrophins, and neuropeptides, may contribute to MDD. To link the symptoms of MDD with molecular dysfunction, this article examines these molecules in the context of three symptom clusters of MDD: cognitive/affective symptoms, volitional/behavioral symptoms, and homeostatic/vegetative symptoms. It examines how these molecules and their receptor, transport, and regulatory systems contribute to MDD and to the development of specific symptom clusters. It presents two possible frameworks of molecular dysfunction in MDD that encompass the interactions between vulnerability phenotypes and biochemical perturbations that may lead to the heterogeneous symptoms of this disorder.

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42

Alavi, Abass y Andrew B. Newberg. Functional Neuroimaging: A Transformative Tool for Integrative Psychiatry. Editado por Anthony J. Bazzan y Daniel A. Monti. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190690557.003.0014.

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Functional neuroimaging with positron emission tomography (PET), single photon emission computed tomography (SPECT), and functional magnetic resonance imaging (fMRI) can be highly useful in the evaluation and management of patients with psychiatric disorders. PET and SPECT imaging typically evaluate cerebral metabolism and blood flow, respectively, and can determine patterns associated with different disorders such as depression or schizophrenia. PET and SPECT imaging can also evaluate neurotransmitter changes such as dopamine or serotonin associated with different psychiatric disorders. fMRI is an excellent tool for studying the effects of psychiatric disorders on specific brain processes related to cognition and mood. fMRI activations studies allow researchers to present various stimuli to a subject in order to determine how the brain reacts and whether psychiatric disorders are associated with different brain reactivity patterns. Functional neuroimaging with PET, SPECT, and fMRI can be highly useful in the investigation of the mechanism of action of integrative therapies for psychiatric disorders.

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43

Robbins, Trevor. The Neuropsycho–Pharmacology of Attention. Editado por Anna C. (Kia) Nobre y Sabine Kastner. Oxford University Press, 2014. http://dx.doi.org/10.1093/oxfordhb/9780199675111.013.028.

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Pharmacological influences on cognition and behaviour are often accompanied by effects on different aspects of attention. The actions of many psychoactive drugs (often used in the treatment of psychiatric disorders) depend on effects exerted on the classical chemical modulatory neurotransmitter systems including acetylcholine, and the monoamines, dopamine, noradrenaline and serotonin (or 5-hydroxytryptamine, 5-HT). These chemical systems originate in the reticular core of the brain and modulate attention by actions on forebrain structures including the thalamus, striatum, and the neocortex (especially the prefrontal cortex). Current research is attempting to dissect separable functions of these chemical neurotransmitters in mediating attention in relation to states of arousal and stress in comparable test paradigms in experimental animals and humans. New directions in research in this area are also identified, including the functions of the novel neurotransmitter orexin, and the role of GABA and glutamate in gamma oscillations and the network properties of the neocortex.

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44

Oliván Roldán, Carlos. Genética de la esquizofrenia: serotonina, dopamina e interleukinas. Editorial científica 3Ciencias, 2016. http://dx.doi.org/10.17993/med.2016.23.

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45

Glückshormone: Wie Gewöhnen Gehirn Trainieren Serotonin, Dopamin, Endorphin und Oxytocin. Independently Published, 2022.

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46

Toohey, Peter. Hold On. Oxford University Press, 2020. http://dx.doi.org/10.1093/oso/9780190083618.001.0001.

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What do you do when you’re not asleep and when you’re not eating? You’re most likely waiting—to finish work, to get home, to finish your chores. This book is not really about how to manage all that waiting—“an action,” according to the OED, “of staying where one is until a particular time or event.” It’s a book describing how many people experience waiting. Waiting, which is sculpted by the passing of time, is an experience just as much as it is a situation. In this book I’ll be focusing on the experience, on how it feels to wait. This experience can encompass such things as hesitation and curiosity, dithering and procrastination, hunting and being hunted, fearing and being feared, dread and illness, courting and parenting, anticipation and excitement, listening to and even performing music, being religious, being happy or unhappy, being bored and being boring, doing business and making decisions (all of which I’ll discuss). Waiting is also characterized by such brain chemicals as serotonin and dopamine. They enable the experience of waiting and they can even change the way that waiting’s basis, the passing of time, is registered. Waiting, probably the most commonly experienced situation that humans and animals encounter apart from sleep, is the experience that may characterize most interpersonal relations.

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47

Ormoni Della Felicità: Come Abituare Cervello Allenarsi Serotonina, Dopamina, Endorfina e Ossitocina. Independently Published, 2022.

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48

Hormonas de la Felicidad: Cómo Acostumbrar Cerebro Elaborar Serotonina, Dopamina, Endorfina y Oxitocina. Independently Published, 2022.

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49

JEFFERY. Treine Seu Cérebro Com Hormônios de Alegria: O Método Mais Eficaz para Preparar Sua Mente para Criar Serotonina, Dopamina, Endorfina e Oxitocina. Independently Published, 2021.

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50

JEFFERY. Entrena Tu Cerebro con Hormonas de la Alegría: El Método Más Eficaz para Preparar Su Mente para Crear Serotonina, Dopamina, Endorfina y Oxitocina. Independently Published, 2021.

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Libros sobre el tema "Dopamine and serotonin"

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