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Добірка наукової літератури з теми "Dopamine and serotonin"

Автор: Grafiati
Опубліковано: 11 березня 2023

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Статті в журналах з теми "Dopamine and serotonin"

1

Wardhana, Made, Martina Windari, Nila Puspasari, and Nyoman Suryawati. "Role of Serotonin and Dopamine in Psoriasis: A Case-Control Study." Open Access Macedonian Journal of Medical Sciences 7, no. 7 (April 14, 2019): 1138–42. http://dx.doi.org/10.3889/oamjms.2019.267.

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BACKGROUND: Psoriasis is a chronic inflammatory disease mediated by the immune system with increased proliferation of keratinocytes. The exact cause is unknown but as a multifactor, such as infection, trauma and psychological stress have been thought to play a role in its pathophysiology. Dopamine and serotonin are believed to have a strong role in stress conditions and also directly play a role in psoriasis. AIM: This study aimed to evaluate the role of dopamine, serotonin, and psychological stress in psoriasis. METHODS: This study used a case-control design involving 30 patients with psoriasis (as a case group) and 30 healthy controls in the Dermatology and Venereology Polyclinic of Sanglah General Hospital Denpasar during the period December 2016 to February 2017. All samples were taken for venous blood examination serum dopamine and serotonin and analysed using the ELISA method. Statistical analysis using an independent t-test, partial correlation, receiver operator characteristic (ROC) curve, and logistic regression model. RESULT: There were significant differences in serotonin, dopamine, and stress index levels between groups with psoriasis and non-psoriasis (102.68 ± 25.44 Vs. 154.17 ± 20.90; p < 0.001), (437.13 ± 164.83 Vs. 138.11 ± 89.51; p < 0.001), and (138.5 ± 27.80 Vs. 92.55 ± 42.97; p < 0.001). Significant negative correlation was found between serotonin level and stress index (r = -0.366; p = 0.016) and between serotonin and dopamine (r = -0.634; p < 0.001) but a positive correlation was found between dopamine and stress index (r = 0.459; p = 0.042). Serotonin and dopamine showed that it could be used as a biochemical predictive model for psoriasis (AUC > 0.7). Multivariable risk analysis model high serum dopamine was the most important risk factor for the occurrence of psoriasis (adjusted OR: 7.8; 95% CI: 3.45-15.57; p = 0.024) CONCLUSION: Serotonin and dopamine have a significant role in the pathophysiology of the occurrence of psoriasis, and psychological stress can affect psoriasis through its influence on serotonin and dopamine.
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2

Penington, Nicholas J., and R. J. Reiffenstein. "Possible involvement of serotonin receptors in the facilitatory effect of a hallucinogenic phenethylamine on single facial motoneurons." Canadian Journal of Physiology and Pharmacology 64, no. 10 (October 1, 1986): 1302–9. http://dx.doi.org/10.1139/y86-220.

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2,5-Dimemoxy-4-methylamphetamine (DOM, "STP") is a potent hallucinogen, proposed to be a serotonin receptor agonist. Its effects have not previously been tested upon central neurons where serotonin is excitatory and serotonin antagonists are effective. Extracellular single unit recordings were obtained from facial motoneurons in anaesthetized rats, and drugs were applied from five-barrelled micropipettes by iontophoresis. Facial motoneurons were commonly silent. During subthreshold application of glutamate, firing could be induced by dopamine and DOM. As reported by others, serotonin and noradrenaline also excited facial motoneurons under these conditions. Methysergide antagonized responses to serotonin and DOM but not those to noradrenaline; methysergide could not usually discriminate between responses to serotonin and dopamine. Ketanserin reversibly antagonized (but could not discriminate between) responses to serotonin, dopamine, and noradrenaline. Chlorpromazine antagonized responses to dopamine at doses that did not alter serotonin-induced excitation, and responses to DOM were not reduced by doses of chlorpromazine, that had no local anaesthetic effect on action potentials elicited by DOM and serotonin. These results suggest that DOM is an agonist on at least one type of central serotonin receptor. This receptor may also be a ketanserin (5-HT2) binding site.
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3

Millichap, J. Gordon. "Dopamine-Serotonin Transporter Disease." Pediatric Neurology Briefs 27, no. 4 (April 1, 2013): 25. http://dx.doi.org/10.15844/pedneurbriefs-27-4-1.

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4

Dalley, J. W., and J. P. Roiser. "Dopamine, serotonin and impulsivity." Neuroscience 215 (July 2012): 42–58. http://dx.doi.org/10.1016/j.neuroscience.2012.03.065.

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5

García, Néstor H., Theresa J. Berndt, Gertrude M. Tyce, and Franklyn G. Knox. "Chronic oral l-DOPA increases dopamine and decreases serotonin excretions." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 277, no. 5 (November 1, 1999): R1476—R1480. http://dx.doi.org/10.1152/ajpregu.1999.277.5.r1476.

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Given the common pathways for uptake and synthesis for dopamine and serotonin, enhanced renal dopamine synthesis in response to increased substrate 3,4-dihydroxyphenylalanine (l-DOPA) is postulated to decrease renal serotonin synthesis. The present study compared the effects of chronic oral administration ofl-DOPA on dopamine and serotonin excretion in vivo, with the effects of enhanced dopamine synthesis per nephron due to adaptation to reduced renal mass (RRM). Four groups of rats were studied: sham-operated rats and rats with RRM in the absence and presence of chronic orall-DOPA.l-DOPA (2 mg ⋅ 100 g body wt−1 ⋅ day−1) for 6–14 days increased calculated dopamine synthesis per nephron in sham-operated rats from 2.0 ± 0.3 ( n = 7) to 13.6 ± 1.8 pg ⋅ day−1 ⋅ nephron−1( n = 7, P < 0.05) and in rats with RRM from 6.1 ± 1.3 ( n = 7) to 39.3 ± 5.2 pg ⋅ day−1 ⋅ nephron−1( n = 7, P < 0.05). Chronic orall-DOPA concomitantly decreased serotonin synthesis per nephron in sham-operated rats (1.6 ± 0.1 to 1.0 ± 0.1 pg ⋅ day−1 ⋅ nephron−1, n = 7, P < 0.05) and in rats with RRM (5.6 ± 0.9 to 2.6 ± 0.4 pg ⋅ day−1 ⋅ nephron−1, n = 7, P < 0.05). Both serotonin and dopamine synthesis per nephron were increased in rats with RRM. In conclusion, chronic oral administration ofl-DOPA enhances dopamine excretion and decreases serotonin excretion in normal rats and in rats with reduced renal mass. Both dopamine and serotonin excretions per nephron were elevated by renal mass reduction.
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6

Garattini, Silvio, and Rosario Samanin. "Biochemical hypotheses on antidepressant drugs: a guide for clinicians or a toy for pharmacologists?" Psychological Medicine 18, no. 2 (May 1988): 287–304. http://dx.doi.org/10.1017/s0033291700007844.

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SynopsisThe development of knowledge about the mechanism of action of tricyclic and the so-called ‘atypical’ antidepressants (AD) is reviewed. The discovery of clinically active antidepressants with little or no effect on noradrenaline or serotonin uptake has disproved the widely accepted concept that inhibition of monoamine uptake is a prerequisite for antidepressant activity. Another serious objection to this hypothesis is that blockade of monoamine uptake occurs in a matter of minutes after administration while 2–3 weeks of repeated treatment are necessary for the clinical AD effect. Nevertheless, the effect of repeated treatment with AD is compatible with the hypothesis that changes in central monoamine transmission are involved in the clinical activity of these drugs. Major changes in monoamine function after repeated treatment with AD include: desensitization and reduced density of noradrenaline receptors coupled to the adenylcyclase system, opposite changes in the sensitivity of α1 (increased) and α2-adrenoreceptors (decreased), down regulation of serotonin2 receptors and complex changes in the behavioural and electrophysiological responsiveness to serotonin agonists, subsensitivity of presynaptic dopamine receptors and enhanced activity of the mesolimbic dopamine system, decreased and increased density of GABA-A and GABA-B receptors respectively and down regulation of [3H]benzodiazepine binding.It remains to be clarified whether some of these changes have larger roles than others or whether they all contribute to the AD activity. An important role of dopamine in the activity of AD drugs is suggested by findings in the forced swimming test, whereas both catecholamines seem to be involved in the attenuation of escape deficit provoked by inescapable shock (learned helplessness). No clear evidence for a role of serotonin (with the possible exception of serotonin1A receptors) or GABA has been obtained in these experimental models of depression. The general validity of these findings obviously rests on the assumption that these models represent significant aspects of human depression.
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7

Ali, D. W., and I. Orchard. "The uptake and release of serotonin and dopamine associated with locust (Locusta migratoria) salivary glands." Journal of Experimental Biology 199, no. 3 (March 1, 1996): 699–709. http://dx.doi.org/10.1242/jeb.199.3.699.

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The uptake and release characteristics of dopamine and serotonin in the salivary glands of the locust Locusta migratoria were examined. Cyclic AMP levels were determined in salivary glands in which the salivary nerve was stimulated under different experimental paradigms. Stimulation of the salivary nerve leads to time- and frequency-dependent elevations of cyclic AMP levels in the glands. The potent and specific D1 receptor antagonist SCH-23390 is capable of partially inhibiting the electrophysiologically induced elevations of cyclic AMP levels. The salivary glands appear to possess uptake transporters for serotonin and dopamine. [3H]serotonin uptake is Na+-dependent and is composed of high- and low-affinity components. [3H]dopamine uptake is Na+-independent and can be partially reduced by a challenge with high-K+ saline and by a challenge with ice-cold saline. Uptake inhibitors are capable of blocking the uptake of radiolabelled serotonin and dopamine. There is a Ca2+-dependent efflux of [3H]serotonin and [3H]dopamine from previously loaded salivary glands in response to stimulation of the salivary nerve and to treatment with a high-K+ saline.
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8

Just, F., and B. Walz. "The effects of serotonin and dopamine on salivary secretion by isolated cockroach salivary glands." Journal of Experimental Biology 199, no. 2 (February 1, 1996): 407–13. http://dx.doi.org/10.1242/jeb.199.2.407.

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We have studied the effects of 3-hydroxytyramine (dopamine) and 5-hydroxytryptamine (serotonin) on (1) the rates of salivation from isolated salivary glands of the cockroach Periplaneta americana, (2) the protein content of the saliva, and (3) the ultrastructure of the salivary gland epithelium. The rates of neurotransmitter-induced salivation varied in a dose-dependent manner within the concentration range 10(-9) to 10(-4) mol l-1. Half-maximal secretory rates were induced by 6x10(-7) mol l-1 serotonin and 1.1x10(-7) mol l-1 dopamine. Stimulation of the glands by serotonin resulted in the production of a protein-rich saliva, whereas saliva was protein-free after stimulation by dopamine. Electron microscopic studies revealed that the central cells, which are believed to produce the proteinaceous components of the saliva, secrete their vesicular content after stimulation by 10(-6) mol l-1 serotonin for 20 min. In contrast, no morphological changes could be detected after stimulation by 10(-6) mol l-1 dopamine. These data indicate that dopamine stimulates only the secretion of the fluid component of the saliva, whereas serotonin is necessary to stimulate secretion of the proteinaceous components.
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9

Cox, Sylvia M. L., Chawki Benkelfat, Alain Dagher, J. Scott Delaney, France Durand, Theodore Kolivakis, Kevin F. Casey, and Marco Leyton. "Effects of lowered serotonin transmission on cocaine-induced striatal dopamine response: PET [11C]raclopride study in humans." British Journal of Psychiatry 199, no. 5 (November 2011): 391–97. http://dx.doi.org/10.1192/bjp.bp.110.084178.

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BackgroundLow serotonin transmission is thought to increase susceptibility to a wide range of substance use disorders and impulsive traits.AimsTo investigate the effects of lowered serotonin on cocaine-induced (1.0 mg/kg cocaine, self-administered intranasally) dopamine responses and drug craving.MethodIn non-dependent cocaine users, serotonin transmission was reduced using the acute tryptophan depletion method. Striatal dopamine responses were measured using positron emission tomography with [11C]raclopride.ResultsAcute tryptophan depletion increased drug craving and striatal dopamine responses to cocaine. These acute tryptophan depletion-induced increases did not occur in the absence of cocaine.ConclusionsThe results suggest that low serotonin transmission can increase dopaminergic and appetitive responses to cocaine. These findings might identify a mechanism by which individuals with low serotonin are at elevated risk for both substance use disorders and comorbid conditions.
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10

Sershen, Henry, Audrey Hashim, and Abel Lajtha. "Serotonin-mediated striatal dopamine release involves the dopamine uptake site and the serotonin receptor." Brain Research Bulletin 53, no. 3 (October 2000): 353–57. http://dx.doi.org/10.1016/s0361-9230(00)00358-0.

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Дисертації з теми "Dopamine and serotonin"

1

De, La Fuente Barrigon C. "Dopamine and serotonin metabolism in Parkinsonian models." Thesis, University College London (University of London), 2018. http://discovery.ucl.ac.uk/10054116/.

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Parkinson’s disease (PD) is a neurodegenerative disorder caused by loss of dopaminergic neurons in the substantia nigra. Different pathogenic mechanisms have been implicated, including loss of mitochondrial complex I function and dysfunction of lysosomal glucocerebrosidase (GBA1) (Neumann et al., 2009; Schapira et al., 1990). Also, it has been hypothesised that serotonin metabolism could be affected in these patients due to the number of enzymes shared by both pathways (Albizu et al., 2011). This thesis considers the potential involvement of complex I and GBA1 in PD using HPLC analysis of changes in the extracellular levels of the metabolites of dopamine and serotonin, and the expression and activity of the enzymes of the dopamine pathway. Using SH-SY5Y cells, complex I deficiency was modelled using rotenone, and GBA1 deficiency was modelled using conduritol B epoxide (CBE). Inhibition of mitochondrial complex I or GBA1 significantly increased extracellular concentrations of 3,4-dihydroxyphenylacetic acid (DOPAC) and 5-hydroxyindoleacetic acid (5-HIAA), direct products of the degradation by monoamine oxidase (MAO) of dopamine and serotonin respectively. These results suggest increased MAO activity, providing evidence for the involvement of impaired complex I or GBA1 activity in the dopamine deficiency seen in PD. As MAO produces hydrogen peroxide as a side-product, its increased activity could enhance the oxidative stress present in PD (Dias et al., 2013). Therefore, intracellular GSH levels were quantified to determine whether the antioxidant mechanisms were affected, but no changes were observed. In addition to the main project, I collaborated with a number of groups to study monoamine metabolism in parkinsonian models. Also, the glycoprofile of cerebrospinal fluid (CSF) of patients with and without impaired dopamine metabolism was studied to explore the possibility of using glycans as pathologic biomarkers.
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2

Manrique, Muñante Rubén. "Love: there is (bio)chemistry between us." Revista de Química, 2014. http://repositorio.pucp.edu.pe/index/handle/123456789/99292.

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El enamoramiento implica procesos bioquímicos en los que sustancias como neurotransmisores, neuromoduladores y hormonas  interaccionan con células nerviosas u otros órganos. Al estar enamorados, los niveles de dopamina aumentan generando atención, deseo y motivación en todo lo relacionado al ser amado. La serotonina, por el contrario, se presenta en concentraciones bajas en este estado. La oxitocina, por su parte, entra en juego cuando la demanda de dopamina no se logra suplir y es crucial al entablar relaciones de largo plazo. El entendimiento del mecanismo de la oxitocina en el ser humano es crucial no solo para el conocimiento académico sino también porque brinda luces para el tratamiento de algunos desórdenes psicológicos.
Romantic love involves biochemical processes in which substances such as neurotransmitters, neuromodulators and hormones interact with other nerve cells or organs. When being in love, dopamine levels increases, generating attention, desire and motivation in everything related to the beloved person. Serotonin, however, is present in low levels in this state. When the body does not supply the necessary amount of dopamine, oxytocin is released. Oxytocin is vital in long term relationships. Understanding the mechanism of oxytocin in humans is crucial not only for academic knowledge of the chemistry of love but also because it provides new lights for the treatment of some psychological disorders.
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3

Burke, Mark 1975. "Factors that influence the dopamine neuron as revealed by dopamine transporter expression." Thesis, McGill University, 2005. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=85892.

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The primary focus of the present thesis is the exploration of factors that influence the dopamine (DA) neuron by examining the expression of the dopamine transporter (DAT), a marker of the DA neuron. The secondary focus of this thesis is on the serotonin neuron and in particular the serotonin transporter (SERT), a marker of the serotonin neuron. To this end three distinct and separate models have been employed. The goals of this thesis were: (1) to test the hypothesis that monoamine oxidase inhibition during development alters serotonergic innervation in the cortex and raphe, while not affecting relative DA innervation of nigrostriatal pathway, (2) to test the hypothesis that elevated brain levels of hypoxanthine (Hx) deleteriously affect the DA neuron, and (3) to test the hypothesis that densities of DAT and SERT in brainstem cell body regions distinguish alcohol-preferring vervet monkeys with different behavioral patterns of ethanol consumption.
Alterations in the activity of monoamine oxidase (MAO), a degradative enzyme that plays an important role in regulating levels of monoamine transmitters, may have a profound effect on brain development. The present study investigates relative DA and serotonin innervation of cortical and subcortical areas, measured by DAT and SERT densities, following MAO inhibition (A or B or A+B) in mice throughout gestation and early post-natal development. DAT binding was unaltered within the nigrostriatal pathway. The most significant finding reported here is that the combined MAO-A+B inhibition significantly reduced SERT binding by 25% in both the cortex and raphe nucleus. Lower levels of SERT binding were apparent during the early post-natal period (PND 14), a period during which pups were still exposed to MAO inhibitors in the dam's milk, but also persisted into later life (PND's 35 and 90) after inhibitors were no longer being administered. Persistent effects were restricted to cortex and raphe, suggesting a relative vulnerability of these regions to alterations in monoamine transmitter levels during development.
The second study presents data demonstrating that Hx delivered intracerebroventricularly significantly reduces the number of tyrosine hydroxylase immunoreactive cells (TH-ir) in the substantia nigra by 22% and 30%, at 7 and 21 days, respectively. After 3 days of Hx administration, striatal DA and serotonin were elevated over control levels by 22% and 25%, respectively, but returned to control levels by 7 days. The serotonin metabolite 5-HIAA was elevated after 3 days of Hx, but levels of DA metabolites were not different from control. Locomotion, a behavior thought to be related to DA transmission, was elevated following Hx treatment, as were presynaptic markers of the DA system such as DAT and TH protein levels. The persistent reduction in TH positive cell numbers suggests that Hx damages or kills DA neurons. The increase in intracellular DA at early time points suggests that Hx might interfere with DA release, possibly by temporarily inactivating DA neurons. These findings are consistent with the hypothesis that Hx, a purine significantly elevated in blood and CSF of Lesch-Nyhan patients, maybe involved in DA dysfunction.
Studies on alcohol abuse have focused on the mesolimbic DA pathway and the serotonergic influence within this pathway. Here we report that abstinent binge-drinking monkeys have significant reductions of SERT binding, and to a lesser extent, DAT binding in the midbrain region, while abstinent heavy-drinking subjects have elevated levels of DAT binding, as compared to controls. Both mesolimbic and nigrostriatal pathways are affected. CSF levels of both HVA and 5-HIAA substantiate the neuroanatomical differences between binge- and heavy-drinking vervets. Taken together, these findings provide a neurochemical profile with which to further distinguish subtypes of alcohol-preferring vervet monkeys.
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4

Dassanayake, Ashlea Fiona. "Dual dopamine/serotonin treatment approach for addictive behaviour." Thesis, University of Canterbury. Department of Psychology, 2013. http://hdl.handle.net/10092/7945.

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Illicit drug abuse and addiction is a major problem in New Zealand and worldwide with approximately 12% of illicit drug users classified as having drug dependence or drug-use disorders. The chronically relapsing nature of drug addiction is a prominent feature of this disorder and a significant barrier to treating addiction. Amphetamine-type drugs, more than any other class of drugs, have seen an increase in global usage since the early 1990's. The lack of approved medications for the treatment of stimulant addiction together with an increasing treatment demand drives the need for pharmaceutical intervention. Substitute treatment approaches primarily focus on the dopamine (DA) system. However, several lines of research implicate a dual role for serotonin (5-HT). Using a benztropine (BZT) analogue, JHW 007 (JHW), and an atypical antidepressant, trazodone (TRAZ), we sought to test whether the combined modulation of DA and 5-HT during a period of extinction produced greater attenuation to drug-induced reinstatement compared to either DA or 5-HT alone. One hundred and two (102) male Long Evans rats were tested using an extinction-reinstatement model of methamphetamine (MA) addiction in conditioned place preference (CPP) (n=72) and self-administration (n=30) experimental designs. We hypothesised that a combined DA/5-HT treatment would further attenuate MA-induced reinstatement. Findings showed that JHW significantly attenuated MA-induced reinstatement in our self-administration model but not CPP, while TRAZ failed to significantly attenuate reinstatement in both experiments. The combination treatment group showed a mild attenuation to drug seeking with CPP, but this finding was not significant. Due to time restrictions, we did not test the combination group using a self-administration procedure. Unfortunately we were unable to fully address our initially proposed hypothesis, but our results with JHW add further support to this BZT analogue as a promising stimulant abuse medication.
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Teles, Rita Tique Arriaga. "Efeito do treino na neurobioquímica cerebral do cão." Master's thesis, Universidade de Évora, 2018. http://hdl.handle.net/10174/23173.

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Com o objetivo de perceber de se o treino afeta a comunicação química do cérebro canino de uma forma permanente, estudaram-se dois grupos de cães: um grupo de cães treinado com marcadores e outro grupo sem contacto com nenhum tipo de treino. Foram recolhidas amostras sanguíneas dos dois grupos e medidas as concentrações de serotonina e dopamina. Os valores médios encontrados para a serotonina e dopamina para o grupo de controlo foram de 269.66 μg/l 56,97 ng/l respetivamente. Para a serotonina, a comparação das médias revelou diferenças entre os grupos (p=0,087), havendo uma diminuição no grupo de cães treinados. Já a dopamina não se verificou ser diferente entres os dois grupos estudados (p=0,2). As vias dopaminérgicas ativadas em situações de compulsão/adição são as mesmas que se ativam no circuito do reforço. Também os valores de serotonina estão diminuídos nesses casos, sugerindo que poderá haver uma componente compulsiva/aditiva em cães treinados; ABSTRACT: The effect of training markers in the cerebral neurochemistry of the dog To understand if dog training affects permanently the chemical communication of canine brain, two groups of dogs were studied: one group had dogs trained with markers and the other one had dogs without any type of training. Blood samples were collected from both groups and concentrations of serotonin and dopamine were measured. The mean values found for serotonin and dopamine for the control group were 269.66 μg/l and 56.93 ng/l respectively. Comparison of means of the groups revealed different values of serotonin between the two groups (p-value= 0,087) having a decrease in serotonin in the trained dog group. As for dopamine, it was not found to be different between the two groups studied (p-value=0,2). The dopaminergic pathways activated in compulsion/addition situations are the same ones that activate in the reinforcement circuit. Also, serotonin levels are decreased in these cases, suggesting that there may be a compulsive/additive component in trained dogs.
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Garcila-Argulello, Segundo Francisco. "Development of dopamine and serotonin agonist radioligands for PET studies." Thesis, Imperial College London, 2007. http://hdl.handle.net/10044/1/8377.

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7

Servidio, Susan. "Serotonergic modulation of a dopaminergic \"model\" of parkinsonism in the rat : neurochemical and clinical considerations /." The Ohio State University, 1985. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487260859496757.

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8

Chernoloz, Olga. "Reciprocal Interactions Between Monoamines as a Basis for the Antidepressant Response Potential." Thesis, Université d'Ottawa / University of Ottawa, 2012. http://hdl.handle.net/10393/22663.

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Despite substantial progress in the area of depression research, the current treatments for Major Depressive Disorder (MDD) remain suboptimal. Therefore, various medications are often used as augmenting agents in pharmacotherapy of treatment-resistant MDD. Despite the relative clinical success, little is known about the precise mechanisms of their antidepressant action. The present work was focused on describing the effects of three drugs with distinctive pharmacological properties (pramipexole, aripiprazole, and quetiapine) on function of the monoaminergic systems involved in the pathophysiology and treatment of MDD. Reciprocal interactions between the monoamines serotonin, norepinephrine, and dopamine systems allow the drugs targeting one neuronal entity to modify the function of the other two chemospecific entities. Electrophysiological experiments were carried out in anaesthetized rats after 2 and 14 days of drug administration to determine their immediate and the clinically-relevant long-term effects upon monoaminergic systems. Pramipexole is a selective D2-like agonist with no affinity for any other types of receptors. It is currently approved for use in Parkinson’s disorder and the restless leg syndrome. Long-term pramipexole administration resulted in a net increase in function of both dopamine and serotonin systems. Aripiprazole is a unique antipsychotic medication. Unlike all other representatives of this pharmacological class that antagonize D2 receptor, this drug acts as a partial agonist at this site. Chronic administration of aripiprazole elevated the discharge rate of the serotonin neurons, presumably increasing the overall serotonergic neurotransmission. Like aripiprazole, quetiapine is one of three atypical antypsicotic drugs approved for use in MDD. Prolonged administration of quetiapine led to a significant increase in both noradrenergic and serotonergic neurotransmission. Importantly, the clinically counter-productive decrease in the spontaneous firing of catecholaminergic neurons, induced by SSRIs, was overturned by the concomitant administration of both aripiprazole and quetiapine. The increase in serotonergic neurotransmission was a consistent finding between all three drugs studied herein. In every case this enhancement was attained in a distinctive manner. Understanding of the precise mechanisms leading to the amplification/normalization of function of monoamines enables potential construction of optimal treatment strategies thereby allowing clinicians greater pharmacological flexibility in the management of depressive symptoms.
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Herman, Anna. "Alteration of Monoaminergic Neuronal Firing by Acute Administration of Cariprazine: An In Vivo Electrophysiological Study." Thesis, Université d'Ottawa / University of Ottawa, 2017. http://hdl.handle.net/10393/36713.

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Cariprazine is a novel dopamine (DA) and serotonin (5-HT) partial agonist with an in vitro receptor affinity profile that endows it with the potential to be used successfully in the treatment of both unipolar and bipolar disorders. The objective of this study was to determine whether in vitro findings with cariprazine lead to functional alterations of monoamine systems in the intact rat brain. In vivo electrophysiological recordings were carried out in male Sprague-Dawley rats under chloral hydrate anesthesia. Dorsal raphé nucleus (DRN), locus coeruleus (LC), and hippocampus cornu ammonis region 3 (CA3) pyramidal neurons were recorded and cariprazine was administered systemically by intravenous injection or locally through iontophoresis. In the DRN, cariprazine induced a complete inhibition of the firing of 5-HT neurons, which was fully reversed by the selective 5-HT1A antagonist WAY100.635. In the LC, the inhibitory effect of the preferential 5-HT2A agonist 2,5-dimethoxy-4-iodoamphetamine (DOI) was reversed by cariprazine with an ED50 value of 67 µg/kg, i.v., and it did not block the inhibitory effect of the α2-adrenergic agonist clonidine. In the hippocampus, when cariprazine was administered by iontophoresis, it inhibited the firing of pyramidal neurons, but it did not dampen the suppressant effect of 5-HT. These results indicate that, in vivo, cariprazine acts as a 5-HT1A agonist in the DRN, as an antagonist on 5-HT2A receptors controlling the firing of NE neurons, and is a full agonist at 5-HT1A receptors located on pyramidal neurons of the hippocampus. The modulatory actions of cariprazine on the 5-HT and NE systems may contribute to its reported effectiveness in depressive episodes.
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Gill, Mark D. "Aminergic modulation of spontaneous and reflexly generated motor output of crayfish walking leg motor neurons." Thesis, University of Bristol, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.262842.

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Книги з теми "Dopamine and serotonin"

1

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

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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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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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1947-, Byalick Marcia, ed. The craving brain: A bold new approach to breaking free from drug addiction, overeating, alcoholism, gambling. 2nd 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, and 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, and 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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Torres-Malaga, Dr Marianne Sierra. The Interactions of Serotonin and Dopamine in Obsessive Compulsive Disorder. Createspace Independent Publishing Platform, 2018.

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Частини книг з теми "Dopamine and serotonin"

1

Ellenbroek, Bart A., and Andrea M. Cesura. "Antipsychotics and the Dopamine–Serotonin Connection." In Small Molecule Therapeutics for Schizophrenia, 1–49. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/7355_2014_51.

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2

Kintscher, Ulrich. "Reuptake Inhibitors of Dopamine, Noradrenaline, and Serotonin." In Handbook of Experimental Pharmacology, 339–47. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-24716-3_15.

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3

Feuerstein, Thomas J. "Presynaptic Receptors for Dopamine, Histamine, and Serotonin." In Handbook of Experimental Pharmacology, 289–338. Berlin, Heidelberg: Springer Berlin Heidelberg, 2008. http://dx.doi.org/10.1007/978-3-540-74805-2_10.

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4

Ahonen, A., M. Dahlström, I. Moilanen, P. Torniainen, and J. Heikkilä. "Brain Serotonin and Dopamine Transporters in Depressive Children." In Radioactive Isotopes in Clinical Medicine and Research XXIII, 31–36. Basel: Birkhäuser Basel, 1999. http://dx.doi.org/10.1007/978-3-0348-8782-3_4.

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5

Borison, Richard L., and Bruce I. Diamond. "Combined Serotonin 5-HT2and Dopamine Da2Antagonist Treatments in Chronic Schizophrenia." In Medical Science Symposia Series, 271–76. Dordrecht: Springer Netherlands, 1993. http://dx.doi.org/10.1007/978-94-011-1920-7_32.

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6

Zhou, Fu-Ming, and John A. Dani. "Dopamine and Serotonin Crosstalk Within the Dopaminergic and Serotonergic Systems." In Co-Existence and Co-Release of Classical Neurotransmitters, 1–36. Boston, MA: Springer US, 2008. http://dx.doi.org/10.1007/978-0-387-09622-3_9.

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7

Povlock, Sue L., and Susan G. Amara. "The Structure and Function of Norepinephrine, Dopamine, and Serotonin Transporters." In Neurotransmitter Transporters, 1–28. Totowa, NJ: Humana Press, 1997. http://dx.doi.org/10.1007/978-1-59259-470-2_1.

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Nummenmaa, Lauri, Kerttu Seppälä, and Vesa Putkinen. "Molecular Imaging of the Human Emotion Circuit." In Social and Affective Neuroscience of Everyday Human Interaction, 3–21. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-031-08651-9_1.

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AbstractEmotions modulate behavioral priorities via central and peripheral nervous systems. Understanding emotions from the perspective of specific neurotransmitter systems is critical, because of the central role of affect in multiple psychopathologies and the role of specific neuroreceptor systems as corresponding drug targets. Here, we provide an integrative overview of molecular imaging studies that have targeted the human emotion circuit at the level of specific neuroreceptors and transmitters. We focus specifically on opioid, dopamine, and serotonin systems, given their key role in modulating motivation and emotions, and discuss how they contribute to both healthy and pathological emotions.
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Rothman, Richard B., Bruce E. Blough, and Michael H. Baumann. "Dual Dopamine/Serotonin Releasers as Potential Medications for Stimulant and Alcohol Addictions." In Drug Addiction, 311–26. New York, NY: Springer New York, 2008. http://dx.doi.org/10.1007/978-0-387-76678-2_19.

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Cathala, Adeline, and Umberto Spampinato. "Serotonin 2B Receptor Interactions with Dopamine Network: Implications for Therapeutics in Schizophrenia." In 5-HT2B Receptors, 323–33. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-55920-5_19.

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Тези доповідей конференцій з теми "Dopamine and serotonin"

1

Wang, Dongshu, Yihai Duan, and Juyang Weng. "Serotonin and dopamine systems: Internal areas and sequential tasks." In 2014 International Joint Conference on Neural Networks (IJCNN). IEEE, 2014. http://dx.doi.org/10.1109/ijcnn.2014.6889957.

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Singh, Vipin. "SPECTROSCOPY AND BRAIN CHEMISTRY Of SEROTONIN AND DOPAMINE CONFORMERS." In 2022 International Symposium on Molecular Spectroscopy. Urbana, Illinois: University of Illinois at Urbana-Champaign, 2022. http://dx.doi.org/10.15278/isms.2022.tf09.

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DE SMEDT, G. "THE INTERACTION OF DOPAMINE AND SEROTONIN IN DEVELOPING PSYCHOPHARMACOLOGICAL MODELS." In IX World Congress of Psychiatry. WORLD SCIENTIFIC, 1994. http://dx.doi.org/10.1142/9789814440912_0022.

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Paslaski, Stephen, Courtland VanDam, and Juyang Weng. "Modeling dopamine and serotonin systems in a visual recognition network." In 2011 International Joint Conference on Neural Networks (IJCNN 2011 - San Jose). IEEE, 2011. http://dx.doi.org/10.1109/ijcnn.2011.6033618.

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Zheng, Zejia, Kui Qian, Juyang Weng, and Zhengyou Zhang. "Modeling the effects of neuromodulation on internal brain areas: Serotonin and dopamine." In 2013 International Joint Conference on Neural Networks (IJCNN 2013 - Dallas). IEEE, 2013. http://dx.doi.org/10.1109/ijcnn.2013.6706905.

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Krishnan, Rajasree G., Beena Saraswathyamma, T. Anjana Raj, and M. G. Gopika. "Poly (riboflavin) modified pencil graphite for the simultaneous electrochemical determination of serotonin and dopamine." In INTERNATIONAL CONFERENCE ON TRENDS IN MATERIAL SCIENCE AND INVENTIVE MATERIALS: ICTMIM 2020. AIP Publishing, 2020. http://dx.doi.org/10.1063/5.0015807.

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Stupin, Victor, Evgeniya Kuryanova, Andrey Tryasuchev, and David Teply. "INFLUENCE OF SEROTONIN AND DOPAMINE ON HEART RATE VARIABILITY OF RATS IN THE STATE OF NARCOSIS SLEEP." In XVI International interdisciplinary congress "Neuroscience for Medicine and Psychology". LLC MAKS Press, 2020. http://dx.doi.org/10.29003/m1269.sudak.ns2020-16/440-441.

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Lu, Jianqing, Feiyi Sun, Hong Ma, Hong Qing, and Yulin Deng. "Quantitative detection of dopamine, serotonin and their metabolites in rat model of Parkinson's disease using HPLC-MS/MS." In 2015 IEEE International Conference on Mechatronics and Automation (ICMA). IEEE, 2015. http://dx.doi.org/10.1109/icma.2015.7237700.

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Hidayah, A. S. Nurul, O. Nurul Wahida, M. N. Norefrina Shafinaz, and A. G. Idris. "Morphology of salivary gland and distribution of dopamine and serotonin on red palm weevil (RPW), Rhynchophorus ferrugineus (Coleoptera: Curculionidae)." In THE 2013 UKM FST POSTGRADUATE COLLOQUIUM: Proceedings of the Universiti Kebangsaan Malaysia, Faculty of Science and Technology 2013 Postgraduate Colloquium. AIP Publishing LLC, 2013. http://dx.doi.org/10.1063/1.4858680.

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"Effects of central administration of Cerebral dopamine neurotrophic factor (CDNF) on the behavior and serotonin system in the mouse brain." In Bioinformatics of Genome Regulation and Structure/Systems Biology (BGRS/SB-2022) :. Institute of Cytology and Genetics, the Siberian Branch of the Russian Academy of Sciences, 2022. http://dx.doi.org/10.18699/sbb-2022-546.

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Звіти організацій з теми "Dopamine and serotonin"

1

Yan, Qingshan. Ethanol and Mesolimbic Serotonin/Dopamine Interactions via 5HT-1B. Fort Belvoir, VA: Defense Technical Information Center, March 2004. http://dx.doi.org/10.21236/ada426009.

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Yan, Qingshan. Ethanol and Mesolimbic Serotonin/Dopamine Interactions Via 5-HT1B Receptors. Fort Belvoir, VA: Defense Technical Information Center, March 2006. http://dx.doi.org/10.21236/ada455523.

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Yan, Qingshan. Ethanol and Mesolimbic Serotonin/Dopamine Interactions via 5HT-1B Receptors. Fort Belvoir, VA: Defense Technical Information Center, March 2003. http://dx.doi.org/10.21236/ada416991.

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Yan, Qingshan. Ethanol and Mesolimbic Serotonin/Dopamine Interactions via 5-HT-1B Receptors. Fort Belvoir, VA: Defense Technical Information Center, March 2005. http://dx.doi.org/10.21236/ada443060.

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5

Mainen, Zachary F. Electrophysiological Monitoring of the Interactions Between the Serotonin and Dopamine Systems During Goal Directed Behaviors. Fort Belvoir, VA: Defense Technical Information Center, April 2006. http://dx.doi.org/10.21236/ada450259.

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Mainen, Zachary F. Electrophysiological Monitoring of the Interactions between the Serotonin and Dopamine Systems during the Initiation of Goal Directed Behaviors. Fort Belvoir, VA: Defense Technical Information Center, April 2005. http://dx.doi.org/10.21236/ada435440.

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