Academic literature on the topic 'Psychopharmacology; Neuroscience'

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Journal articles on the topic "Psychopharmacology; Neuroscience"

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Birnbaum, Robert J. "Neuroscience and Psychopharmacology into the Next Millennium." CNS Spectrums 4, no. 7 (July 1999): 36–52. http://dx.doi.org/10.1017/s1092852900012001.

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AbstractThe end of the millennium provides an opportunity to review some of the common practices that were present in psychopharmacology during the 20th century. The author focuses on two approaches that have dominated research and guided the clinical application of psychopharmacologic therapeutics: the unitary clinically-based and single-lesion perspectives. The author expands upon these older formulations of neuropsychiatric disease pathogenesis and describes how the approach to psychopharmacologic research and therapeutics has changed in light of advances in the basic neurosciences. Relevant recent advances in the basic neurosciences that shed light on the pathophysiology of neuropsychiatric disease states and that guide psychopharmacologic practices are described. The use of atypical antipsychotic agents to treat schizophrenia is given as one example of the clinical applications of the approach to psychopharmacology in the next century.
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Uchida, Hiroyuki, Shigeto Yamawaki, Won-Myong Bahk, and Duk-In Jon. "Neuroscience-based Nomenclature (NbN) for Clinical Psychopharmacology and Neuroscience." Clinical Psychopharmacology and Neuroscience 14, no. 2 (May 31, 2016): 115–16. http://dx.doi.org/10.9758/cpn.2016.14.2.115.

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Minchin, M. C. W. "Psychopharmacology." Neuropharmacology 25, no. 1 (January 1986): 109. http://dx.doi.org/10.1016/0028-3908(86)90066-3.

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Nutt, David J., and Pierre Blier. "Neuroscience-based Nomenclature (NbN) for Journal of Psychopharmacology." Journal of Psychopharmacology 30, no. 5 (April 19, 2016): 413–15. http://dx.doi.org/10.1177/0269881116642903.

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Gorman, Adrienne M., and Karen M. Doyle. "Considerations and recent advances in neuroscience." Biochemical Society Transactions 37, no. 1 (January 20, 2009): 299–302. http://dx.doi.org/10.1042/bst0370299.

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Neuroscience is a rapidly developing area of science which has benefitted from the blurring of interdisciplinary boundaries. This was apparent in the range of papers presented at this year's Neuroscience Ireland Conference, held in Galway during August 2008. The event was attended by academics, postdoctoral and postgraduate researchers, scientists from industry and clinicians. The themes of this year's conference, neurodegeneration, neuroregeneration, pain, glial cell biology and psychopharmacology, were chosen for their reflection of areas of strength in neuroscience within Ireland. In addition to basic science, translational research also featured strongly.
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Vrecko, Scott. "Neuroscience, power and culture: an introduction." History of the Human Sciences 23, no. 1 (February 2010): 1–10. http://dx.doi.org/10.1177/0952695109354395.

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In line with their vast expansion over the last few decades, the brain sciences — including neurobiology, psychopharmacology, biological psychiatry, and brain imaging — are becoming increasingly prominent in a variety of cultural formations, from self-help guides and the arts to advertising and public health programmes. This article, which introduces the special issue of History of the Human Science on ‘Neuroscience, Power and Culture’, considers the ways that social and historical research can, through empirical investigations grounded in the observation of what is actually happening and has already happened in the sciences of mind and brain, complement speculative discussions of the possible social implications of neuroscience that now appear regularly in the media and in philosophical bioethics. It suggests that the neurosciences are best understood in terms of their lineage within the ‘psy’-disciplines, and that, accordingly, our analyses of them will be strengthened by drawing on existing literatures on the history and politics of psychology — particularly those that analyze formations of knowledge, power and subjectivity associated with the discipline and its practical applications. Additionally, it argues against taking today’s neuroscientific facts and brain-targetting technologies as starting points for analysis, and for greater recognition of the ways that these are shaped by historical, cultural and political-economic forces.
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Marsden, Charles A., and André Rex. "Transgenics and Psychopharmacology Introduction." Reviews in the Neurosciences 11, no. 1 (January 2000): 1–2. http://dx.doi.org/10.1515/revneuro.2000.11.1.1.

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Lehmann, Heinz E., and Thomas A. Ban. "The History of the Psychopharmacology of Schizophrenia." Canadian Journal of Psychiatry 42, no. 2 (March 1997): 152–62. http://dx.doi.org/10.1177/070674379704200205.

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Objective: To review the historical development of the psychopharmacological treatment of schizophrenia. Method: A chronological literature review of the clinical practices and theoretical models that have controlled drug treatment of schizophrenia at different times. Results: Effective treatment of schizophrenia was achieved only after the introduction of antipsychotic drugs, in the 1950s, and is still progressing. Conclusion: Close collaboration between basic neuroscience and careful and informed clinical practice are likely to lead to continued progress.
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Leccese, Arthur. "Pharmacophobic psychopharmacology." Pharmacology Biochemistry and Behavior 46, no. 2 (October 1993): 497. http://dx.doi.org/10.1016/0091-3057(93)90396-b.

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Hynie, S. "Psychopharmacology: An Introduction." Neuropharmacology 25, no. 12 (December 1986): 1408. http://dx.doi.org/10.1016/0028-3908(86)90124-3.

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Dissertations / Theses on the topic "Psychopharmacology; Neuroscience"

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Hall, Frank Scott. "The behavioural and neurochemical effects of social separation on the rat." Thesis, University of Cambridge, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.320115.

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Terbeck, Sylvia. "Psychopharmacology of moral and social judgments." Thesis, University of Oxford, 2012. http://ora.ox.ac.uk/objects/uuid:cf403fa5-4499-4e8f-b5f6-73efa256dcba.

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This thesis is an interdisciplinary project in experimental social psychology, psychopharmacology, neuroscience, and neuroethics. The role of emotion in higher order psychological processes – social and moral judgments – was investigated. Specifically the role of noradrenergic mediated emotional arousal was researched. Behavioural studies demonstrated that acute beta adrenergic blockade with propranolol led to a reduction in negative implicit racial associations and also a modification of moral decision making. These findings suggest that basic affective processes might be causally relevant for higher order evaluations. However, enhancement with the noradrenergic potentiating agent reboxetine did not show effects opposite to those of propranolol on racial attitudes or moral judgments, which might indicate that emotional arousal, specific to beta-adrenoceptors might be involved in the effects of propranolol. Further a pharmacological fMRI study demonstrated that the activation pattern in brain regions commonly associated with intergroup bias -- such as the amygdala, insula, dorsolateral prefrontal cortex, and fusiform gyrus -- was affected by propranolol, and that the effect in the amygdala was correlated with implicit racial bias. Taken together the research suggests that automatic emotional arousal plays a role in higher order psychological processes, such as moral and social judgments, which aids the understanding of the underlying neurobiology of such processes. Finally, the ethical implications – such as the prospect of pharmacological moral enhancement – are discussed. The findings also suggest that the moral and social effects of already widely used psychotropic medications should be subject to further empirical and ethical investigation.
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Salvador, Alexandre. "Modulation pharmacologique du raisonnement et de la prise de décision : apports pour la psychiatrie." Thesis, Sorbonne Paris Cité, 2017. http://www.theses.fr/2017USPCB007/document.

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L’innovation thérapeutique est limitée en psychiatrie. De nombreux médicaments sélectionnés sur la base de résultats encourageants dans les essais chez l’animal se révèlent décevants lors des essais cliniques. La validité limitée des modèles animaux, et leur utilisation pour tenter de mimer des pathologies définies de façon catégorielle sur la base de regroupement de symptômes de surface sans lien clair avec les processus cérébraux, les mécanismes biologiques ou la génétique, participent à ces difficultés. Une branche des neurosciences cognitives, l’étude de l’apprentissage par renforcement, associée à l’utilisation d’interventions pharmacologiques ciblées chez le sujet malade ou le sujet sain, représente une opportunité de mieux caractériser les processus cérébraux sous-tendant certaines dimensions cardinales des pathologies psychiatriques. Nous illustrons l’utilisation de l’étude de l’apprentissage par renforcement avec intervention pharmacologique dans deux études expérimentales. La première cherche à caractériser l’effet de l’aripiprazole, un antipsychotique atypique, chez des patients atteints du syndrome Gilles de la Tourette, en utilisant une tâche d’apprentissage contrefactuel, évaluant la capacité à apprendre non seulement des conséquences de ses actions, mais également des conséquences hypothétiques d’actions alternatives possibles. La seconde étude, randomisée contrôlée et en double aveugle, étudie l’effet de deux classes différentes d’antidépresseurs, l’escitalopram et l’agomélatine, chez le sujet sain. L’effet de leur administration est évalué à court terme (3 jours) et à long terme (8 semaines) dans deux tâches probabilistes de sélection de stimulus, l’une simple, l’autre avec renversements occasionnels. L’utilisation de cette approche pourrait participer à la définition d’endophénotypes et, en collaboration avec la recherche préclinique, aider à la création de nouveaux modèles animaux pour en améliorer la valeur prédictive
Successful new drug development has declined in psychiatry in the last decades. This is in part the resut of a high failure rate in translating positive preclinical efficacy results to positive clinical trials. Limitations in the validity of animal models and shortcomings in the usefullnes of the current categorical diagnostic system. Cognitive neurosciences and particularly reinforcement learning and its computational analysis might provide biomarkers required to develop new ways of classifying mental disorders on the basis of both observable behaviour and neurobiological measues. Used in conjunction with pharmacological challenges, it may bring new insights into the physiopahtology and brain mechanisms underlying psychiatric disorders. It may also help design new animal models with imporved predictive validity for the develoment of medications relying on innovative mechanisms of action. We illustrate the use of reinforcement learning and pharmacological challenge in two experimental studies. In the first experiment, we administered a reinforcement learning task that involves both direct learning from obtained outcomes and indirect learning from forgone outcomes to two groups of Gilles de la Tourette patients, one receiving aripiprazole, one unmedicated and to a group of healty subjects. In the second experiment, we administered two probabilistic stimulus selection learning tasks (one simple, one with occasional reversals) to healthy subjects randomly and blindly allocated to either escitalopram, a typical serotonin reuptake inhibitor, agomelatine, an antidepressant with a different mechanism of action, or placebo. The experiment compard the effect of these two classes of antidepressants to placebo after both short term (3 days) and long term (8 weeks) treatment. These experiments bring insights into the understanding of the clinical condition studied, and the effects of the drugs tested. Implications of this approach for the translational approach to drug development is discussed
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Capitao, Liliana. "Early effects of fluoxetine on emotional processing : implications for adolescent depression." Thesis, University of Oxford, 2014. http://ora.ox.ac.uk/objects/uuid:c713518b-97bd-4692-99ba-288f37c97ddd.

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Depression in adolescence is a major health problem, associated with poor psychological function and key risk factors both for later illness and suicidal behaviours. The antidepressant fluoxetine is commonly used in this population and it is shown to have a favourable benefit-to-risk profile. However, controversy still exists about the use of antidepressants in young people and there is little research focusing on underlying mechanisms of wanted and unwanted actions in this group. This doctoral thesis aims to investigate, for the first time, the acute effects of fluoxetine on emotional processing, using a combination of behavioural and neuroimaging techniques. The aim is to achieve a greater understanding of the mechanisms underlying fluoxetine use in depressed adolescents, in light of differences seen in their clinical presentation and response to antidepressant drugs. In the first study (Chapter Two), a single dose of fluoxetine was shown to decrease the recognition of anger in a sample of young adult volunteers, an effect not previously seen in acute studies of older participants. This effect may be particularly relevant for the treatment of adolescent depression, in which symptoms of anger and irritability are often prominent. Beyond this, fluoxetine was shown to increase the recognition of positive vs. negative facial information, and also exerted an anxiolytic-like influence, eliminating the emotion-potentiated startle effect. However, no influence was seen in measures of attentional vigilance to threat. In an attempt to overcome methodological limitations of this study, a paradigm was developed that is particularly sensitive to the detection of automatic biases towards threatening information (Chapter Three). Chapter Four describes a neuroimaging study with depressed adolescents, in which a single dose of fluoxetine was found to reduce amygdala activity in response to anger. Early changes in amygdala activity to fear correlated with decreased symptoms of anxiety and depression in the first 7-10 days of treatment. Chapter Five explores the effects of acute fluoxetine in a sample of high trait anger males. This study replicated the finding that fluoxetine acts to increase the recognition of positive information, whilst showing preliminary evidence for a reduction in attentional vigilance to angry faces. Overall, fluoxetine was found to decrease the processing of anger across studies. This effect was seen alongside a broader influence on positive vs. negative information and anxiolytic-like properties. Together, these results indicate that fluoxetine has direct effects on processes that are especially relevant to adolescent depression and suggest a potential cognitive mechanism for the efficacy of this particular antidepressant in adolescent patients.
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Schmidt, Kristin. "Manipulating the hypothalamic-pituitary-adrenal axis : effects on cognitive and emotional information processing and neural connectivity." Thesis, University of Oxford, 2016. https://ora.ox.ac.uk/objects/uuid:c0475a98-e070-4446-9179-eb87047cb854.

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Despite extensive evidence documenting abnormal hypothalamic-pituitary-adrenal (HPA) axis functioning as a risk factor for the development of depression and other psychiatric disorders, and experimental evidence from acute stress manipulations, the effects of sustained cortisol alterations on clinically relevant cognitive-behavioural and neural processing remain poorly understood. The aim of this thesis was to characterise how non-acute changes in cortisol levels modify behavioural and neural biases implicated in stress-related disorders by following two complementary lines of evidence: firstly, by increasing cortisol via a direct pharmacological intervention; and secondly, by testing the ability of gut microbiota manipulations to alter cortisol reactivity. The first study found that sustained increases in cortisol following 10-day administration of hydrocortisone were associated with altered memory and emotional processing in healthy volunteers. Specifically, participants receiving hydrocortisone showed enhanced recognition of emotional words, while their neutral memory performance was unaffected despite lower parahippocampal and occipital activation during viewing and encoding of neutral pictures. Furthermore, we found that resting-state functional connectivity between limbic-temporal regions of interest (amygdala and hippocampus) and the striatum (head of the caudate), as well as frontal and prelimbic cortices was decreased. In contrast, hippocampal and visual processing during negative facial expressions, and functional connectivity between the amygdala and the brainstem at rest, were increased in the hydrocortisone versus placebo groups. Overall, these findings suggest that non-acute increases in glucocorticoids enhance processing of emotionally salient information in limbic-temporal regions, which may modulate further neural mechanisms of sensory and homeostatic relevance. Enhancements in declarative emotional memory following hydrocortisone also implicate the modulation of amygdalar-hippocampal interactions by cortisol. Conversely, neutral stimulus processing was found to be either reduced or unaffected across a number of cognitive and memory domains. A specific increase for negative processing was further supported by poorer self-reported well-being at the mid-point of the study in participants receiving hydrocortisone. In a separate study exploring the ability of prebiotic supplements to affect cortisol reactivity and emotional processing, a Bimuno-galactooligosaccharide prebiotic was found to reduce the waking cortisol response and increase positive versus negative attentional processing in healthy volunteers. While these effects were not found to be associated, they provide initial promising evidence of the ability to target the HPA axis and emotional processing via the gut microbiota in humans. Overall, this thesis supports the idea that stress-induced physiological changes after prolonged or repeated cortisol exposure are associated with neural and behavioural alterations, which in turn have been crucial in understanding neuropsychological mechanisms underlying psychiatric disease. A better stratification of the effects of sustained HPA axis alterations on psychiatrically relevant cognitive-emotional domains and neural mechanisms thus remains of high priority.
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Tziortzi, Andri. "Quantitative dopamine imaging in humans using magnetic resonance and positron emission tomography." Thesis, University of Oxford, 2014. http://ora.ox.ac.uk/objects/uuid:26b8b4c2-0237-4c40-8c84-9ae818a0dabf.

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Dopamine is an important neurotransmitter that is involved in several human functions such as reward, cognition, emotions and movement. Abnormalities of the neurotransmitter itself, or the dopamine receptors through which it exerts its actions, contribute to a wide range of psychiatric and neurological disorders such as Parkinson’s disease and schizophrenia. Thus far, despite the great interest and extensive research, the exact role of dopamine and the causalities of dopamine related disorders are not fully understood. Here we have developed multimodal imaging methods, to investigate the release of dopamine and the distribution of the dopamine D2-like receptor family in-vivo in healthy humans. We use the [11C]PHNO PET ligand, which enables exploration of dopamine-related parameters in striatal regions, and for the first time in extrastriatal regions, that are known to be associated with distinctive functions and disorders. Our methods involve robust approaches for the manual and automated delineation of these brain regions, in terms of structural and functional organisation, using information from structural and diffusion MRI images. These data have been combined with [11C]PHNO PET data for quantitative dopamine imaging. Our investigation has revealed the distribution and the relative density of the D3R and D2R sites of the dopamine D2-like receptor family, in healthy humans. In addition, we have demonstrated that the release of dopamine has a functional rather than a structural specificity and that the relative densities of the D3R and D2R sites do not drive this specificity. We have also shown that the dopamine D3R receptor is primarily distributed in regions that have a central role in reward and addiction. A finding that supports theories that assigns a primarily limbic role to the D3R.
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Laatikainen, Linda Maria. "The role of catechol-O-methyltransferase (COMT) in hippocampal function." Thesis, University of Oxford, 2010. http://ora.ox.ac.uk/objects/uuid:d0c9e1fa-a052-4af7-aaff-00548365e024.

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Catechol-O-methyltransferase (COMT) metabolises catechol-containing compounds, including dopamine. The aim of this thesis was to investigate whether COMT is involved in hippocampal function. This thesis also explored the role of functional polymorphisms within the COMT gene in the pathogenesis of schizophrenia and schizophrenia-related phenotypes. First, as part of a study investigating the role of COMT in schizophrenia, human hippocampal COMT mRNA levels were shown to be neither altered in schizophrenia or bipolar disease, nor affected by COMT genotype. Hence, functional COMT polymorphisms do not appear to operate by altering gross COMT mRNA expression. Importantly, this study showed that COMT is expressed in the human hippocampus. Second, the role of COMT in hippocampal neurochemistry was explored by studying the effect of pharmacological COMT inhibition on catecholamines and metabolites in rat hippocampal homogenates, and extracellularly, using microdialysis. Both demonstrated that COMT modulates hippocampal dopamine metabolism. Thus, hippocampal COMT is of functional significance with respect to dopamine. Third, the effect of COMT inhibition on hippocampus-dependent behaviour was investigated. The results suggested a memory-enhancing effect of pharmacological COMT inhibition on hippocampus-dependent associative and non-associative forms of short-term memory in rats. In contrast, acute COMT inhibition appeared to have no effect on behavioural correlates of ventral hippocampal function i.e. anxiety-like behaviour. In summary, the expression of COMT mRNA in the human hippocampus, as well as the effect of COMT inhibition on rat hippocampal neurochemistry and hippocampus-dependent behaviour provide evidence for a functional role of COMT in the hippocampus. Moreover, changes in COMT activity alter hippocampal dopamine metabolism, which could be a potential mechanism for the role of COMT in hippocampus-dependent short-term memory.
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Betts, Jill Frances. "D-amino acid oxidase, D-serine and the dopamine system : their interactions and implications for schizophrenia." Thesis, University of Oxford, 2012. http://ora.ox.ac.uk/objects/uuid:de02286f-3e33-4e3e-bc5b-222b62a28ba5.

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D-amino acid oxidase (DAO) is a flavin-dependent enzyme that is expressed in the mammalian brain. It is the metabolising enzyme of several D-amino acids, including D serine, which is an endogenous agonist at the glycine co-agonist site of the glutamatergic NMDA receptor. As such, regulation of D serine levels in the brain by DAO may indirectly modulate the activity of NMDA receptors. The expression and activity of DAO have been reported to be increased in schizophrenia. It has been identified as a putative susceptibility gene for the disorder, and as a potential therapeutic target. This thesis explored three aspects of the interface between DAO and the DA system. First, the expression of DA was investigated in the ventral tegmental area (VTA), the source of the dopaminergic mesocortical pathway. Traditionally, DAO was considered to be an enzyme confined to the hindbrain and to glia, but more recent studies have reported its expression in additional brain regions, and also in neurons. DAO mRNA and protein was found to be expressed in the VTA, and was present in both neurons and glia in this region, whereas in the cerebellum, DAO expression appeared solely glial. DA output from the VTA is regulated by NMDA receptors, and hence expression of DAO in the VTA suggests that it may serve a role in modulating cortical DA via regulation of D serine levels and NMDA receptor function. The second part of this thesis investigated the effects of DAO inhibition and D serine administration on DA levels in the prefrontal cortex (PFC) using in vivo microdialysis. Systemic DAO inhibition and D serine administration resulted in increases in extracellular levels of DA metabolites in the PFC, despite no detectable change in DA. Similarly, DA metabolites in the PFC increased after local application of D serine to the VTA, but no change was detected in DA. However, local DAO inhibition in the VTA resulted in increased levels of both DA and its metabolites, and DAO inhibition combined with D serine administration also produced increases in DA. This suggested that DAO and its regulation of D-serine levels may serve to indirectly modulate mesocortical DA function, and this may be mediated via the VTA. This notion was supported in the final section of this thesis, in which the expression of three DA genes was measured in the PFC of a novel line of DAO knockout mice. In this pilot study, there was evidence for an increase in Comt and Drd2 mRNAs in the knockout mice. As such, constitutive abolition of DAO activity may also alter mesocortical DA function. These studies provide new insights into the presence and role of DAO beyond the hindbrain, and point to a potentially important physiological function in modulating the activity of the mesocortical DA system via the VTA. This could be therapeutically relevant in the context of elevating cortical DA in the treatment of schizophrenia, and may provide supporting evidence for the clinical use of DAO inhibitors.
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Ashirova, Margarita Olegovna. "Utilization of Placebo Response in Double-Blind Psychopharmacological Studies, Contextual Perspective." Antioch University / OhioLINK, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=antioch1445977459.

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Browne, James Donald Caleb. "Acquisition and Responding for Conditioned Reinforcement in the Mouse: Effects of Methylphenidate, and the Role of the Dopamine Transporter." Thesis, 2012. http://hdl.handle.net/1807/33367.

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This work characterized the ability of mice to respond for conditioned reinforcement, a phenomenon that can be used to investigate neural substrates of incentive learning. In both C57Bl/6 and CD1 mice, a reward-associated stimulus acted as a conditioned reinforcer (CR). Responding was stable over multiple test days, enhanced in CD1 mice by the dopamine transporter (DAT) blocker methylphenidate, and was extinguished when responding no longer produced the CR. However, transgenic C57Bl/6 mice overexpressing DAT, which decreased striatal dopamine by 40% responded normally for CR. Therefore, these results suggest that mice can be used to study brain mechanisms of incentive motivation. However, the choice of mouse strain in this paradigm is important as outbred CD1 mice appeared more susceptible to a DAT blocker compared to the inbred C57Bl/6 strain. These results also suggest that selective responding for a CR remains intact in a chronically hypodopaminergic state.
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Books on the topic "Psychopharmacology; Neuroscience"

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Behavioral neuroscience of drug addiction. Heidelberg: Springer, 2010.

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An introduction to drugs and the neuroscience of behavior. Australia: Wadsworth Cengage Learning, 2014.

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Ingram, Rick E. Vulnerability to depression: From cognitive neuroscience to prevention and treatment. New York: Guilford Press, 2011.

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Your brain on food: How chemicals control your thoughts and feelings. New York: Oxford University Press, 2010.

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Hofmann, F. B. Nicotine Psychopharmacology. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009.

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service), SpringerLink (Online, ed. Cannabinoids and the Brain. Boston, MA: Springer Science + Business Media, LLC, 2008.

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Neill, Jo C. Biological Basis of Sex Differences in Psychopharmacology. Berlin, Heidelberg: Springer-Verlag Berlin Heidelberg, 2011.

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Instant psychopharmacology: A guide for the nonmedical mental health professional. New York: Norton, 1998.

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Carlos, Zarate Juan, and SpringerLink (Online service), eds. Behavioral Neurobiology of Bipolar Disorder and its Treatment. Berlin, Heidelberg: Springer-Verlag Berlin Heidelberg, 2011.

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Diamond, Ronald J. Instant psychopharmacology: Up-to-date information about the most commonly prescribed drugs for emotional health. 2nd ed. New York: Norton, 2002.

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Book chapters on the topic "Psychopharmacology; Neuroscience"

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Hoyer, Daniel, Eric P. Zorrilla, Pietro Cottone, Sarah Parylak, Micaela Morelli, Nicola Simola, Nicola Simola, et al. "Cognitive Neuroscience." In Encyclopedia of Psychopharmacology, 323. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-540-68706-1_1345.

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Hoyer, Daniel, Eric P. Zorrilla, Pietro Cottone, Sarah Parylak, Micaela Morelli, Nicola Simola, Nicola Simola, et al. "Cognitive Enhancers: Neuroscience and Society." In Encyclopedia of Psychopharmacology, 314–17. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-540-68706-1_169.

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Terbeck, Sylvia. "Psychopharmacology and Prejudice." In The Social Neuroscience of Intergroup Relations:, 51–67. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-46338-4_4.

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Morein-Zamir, Sharon, and Barbara Jacquelyn Sahakian. "Pharmaceutical Cognitive Enhancers: Neuroscience and Society." In Encyclopedia of Psychopharmacology, 1–5. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-27772-6_169-2.

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Morein-Zamir, Sharon, and Barbara Jacquelyn Sahakian. "Pharmaceutical Cognitive Enhancers: Neuroscience and Society." In Encyclopedia of Psychopharmacology, 1267–71. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-36172-2_169.

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Lowe, Nicole Gellings, Maria Paola Rapagnani, Chiara Mattei, and Stephen M. Stahl. "The Psychopharmacology of Hallucinations: Ironic Insights into Mechanisms of Action." In The Neuroscience of Hallucinations, 471–92. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-4121-2_24.

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Bunney, W. E., and B. G. Bunney. "A View of Psychopharmacology, Neuroscience, and the Major Psychoses." In Neuropsychopharmacology, 11–26. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-74034-3_2.

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Haralanov, Svetlozar, Evelina Haralanova, Emil Milushev, and Diana Shkodrova. "Locomotor Movement-Pattern Analysis as an Individualized Objective and Quantitative Approach in Psychiatry and Psychopharmacology: Clinical and Theoretical Implications." In Psychiatry and Neuroscience Update, 387–416. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-95360-1_32.

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Echarte, Luis E. "Cosmetic Psychopharmacology, Inauthentic Experiences, and the Instrumentalization of Human Faculties: Beyond Post-emotional Society." In Psychiatry and Neuroscience Update - Vol. II, 77–103. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-53126-7_8.

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Light, Gregory A., and Neal R. Swerdlow. "Neurophysiological Biomarkers Informing the Clinical Neuroscience of Schizophrenia: Mismatch Negativity and Prepulse Inhibition of Startle." In Electrophysiology and Psychophysiology in Psychiatry and Psychopharmacology, 293–314. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/7854_2014_316.

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