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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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11

Seyedi, Marzieh, Fatemeh Gholami, Mahsa Samadi, Mahmoud Djalali, Mohammad Effatpanah, Mir Saeed Yekaninejad, Rezvan Hashemi, Mina Abdolahi, Maryam Chamari, and Niyaz Mohammadzadeh Honarvar. "The Effect of Vitamin D3 Supplementation on Serum BDNF, Dopamine, and Serotonin in Children with Attention-Deficit/Hyperactivity Disorder." CNS & Neurological Disorders - Drug Targets 18, no. 6 (August 30, 2019): 496–501. http://dx.doi.org/10.2174/1871527318666190703103709.

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Background & Objective: Attention-Deficit/Hyperactivity Disorder (ADHD) is one of the most common psychiatric disorders in childhood. The exact etiology of this disease is unknown, but it is believed to be related to the disorder of catecholaminergic and serotonergic systems. Also, serum vitamin D levels in patients with ADHD is lower. Several studies have also shown the effect of vitamin D on the synthesis pathways of dopamine, serotonin, and a number of neurotrophic factors. Therefore, this study aimed to investigate the effect of vitamin D3 supplementation on serum levels of Brain-Derived Neurotrophic Factor (BDNF), dopamine, and serotonin in school-aged children with ADHD. Methods: Eighty-six children with ADHD were divided into two groups, based on randomized permuted blocks. Patients received 2000 IU vitamin D/day or a placebo for 12 weeks. Serum levels of BDNF, dopamine, serotonin, and 25-hydroxyvitamin D [25(OH)D] were measured at baseline and at the end of the study. Results: Serum levels of 25(OH)D and dopamine significantly increased in the vitamin D group, compared to the placebo group (p < 0.05). However, serum BDNF and serotonin levels did not change significantly. Conclusion: Vitamin D3 supplementation in children with ADHD can increase serum dopamine levels, but further studies are needed to determine the effects of vitamin D on neurotrophic factors and serotonin.
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12

Ball, Alexander K., William H. Baldridge, and Timothy C. Fernback. "Neuromodulation of pigment movement in the RPE of normal and 6-OHDA-lesioned goldfish retinas." Visual Neuroscience 10, no. 3 (May 1993): 529–40. http://dx.doi.org/10.1017/s0952523800004740.

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AbstractThe role of dopamine as the endogenous signal-initiating light-dependent changes in the distribution of pigment granules in goldfish retinal pigment epithelium was investigated. In normal retinas, light adaptation resulted in the dispersion of pigment granules. This effect of light was mimicked by the intraocular injection of dopamine or serotonin, which is thought to increase endogenous dopamine release, into dark-adapted eyes. The effect of light, dopamine, or serotonin on dark-adapted retinas was blocked by the dopamine receptor antagonists haloperidol and sulpiride. However, lesioning the endogenous source of retinal dopamine, by prior intraocular injection of 6-hydroxydopamine (6-OHDA), did not block the dispersion of pigment granules in light-adapted retinas. No significant differences in pigment dispersion were noted between unlesioned and lesioned light- or dark-adapted retinas. However, the effect of light on pigment dispersion was no longer blocked by haloperidol or sulpiride in 6-OHDA lesioned animals. Dopamine and serotonin mimicked the effect of light when injected into lesioned dark-adapted eyes, but their effects were also not blocked by haloperidol or sulpiride. These results suggest that dopamine, acting on D2 receptors, is sufficient to induce pigment migration in unlesioned animals. In 6-OHDA-lesioned animals, however, pigment migration is mediated by a receptor mechanism other than D2.
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13

Ase, A. R., F. Amdiss, C. Hébert, N. Huang, N. M. van Gelder, and T. A. Reader. "Effects of antipsychotic drugs on dopamine and serotonin contents and metabolites, dopamine and serotonin transporters, and serotonin 1A receptors." Journal of Neural Transmission 106, no. 1 (February 15, 1999): 75–105. http://dx.doi.org/10.1007/s007020050142.

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14

Zhou, Fu-Ming, Yong Liang, Ramiro Salas, Lifen Zhang, Mariella De Biasi, and John A. Dani. "Corelease of Dopamine and Serotonin from Striatal Dopamine Terminals." Neuron 46, no. 1 (April 2005): 65–74. http://dx.doi.org/10.1016/j.neuron.2005.02.010.

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15

Müller, Hans-Wilhelm, Hubertus Hautzel, and Susanne Nikolaus. "Different patterns of dopaminergic and serotonergic dysfunction in manic, depressive and euthymic phases of bipolar disorder." Nuklearmedizin 56, no. 05 (2017): 191–200. http://dx.doi.org/10.3413/nukmed-0893-17-04.

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SummaryA variety of alterations in brain neurotransmitter systems has been proposed as the cause of bipolar disorder (BD). We conducted a PUBMED search, which provided a total of 45 in vivo investigations with PET and SPECT, in which binding to serotonin transporter (SERT), 5-HT1A receptor (R), 5-HT2AR, dopamine transporter (DAT), vesicular monoamine transporter (VMAT2), D1R, D2R, muscarinic M2R and nicotinic ß2-nAChR as well as dopamine synthesis and/or dopamine release were assessed in BD patients in the manic (6 studies, 39 patients, 77 controls), depressive (15 studies, 248 patients, 488 controls) or eu- thymic condition (18 studies, 265 patients, 293 controls) and in mixed collectives of BD patients (6 studies, 55 patients, 80 controls). The retrospective analysis revealed a complex pattern of dysregulations within and between neurotransmitter systems, which is causally linked to the acute and euthymic states of BD. While increased mesencephalic, limbic and parietotemporoccipital serotonin and increased frontal dopamine underlie mania, the depressive state is characterized by decreased frontal and limbic serotonin, increased frontal and limbic acetylcholine and increased frontal dopamine. Also in euthymia, no normalization of receptor and transporter densities was observed. Alterations of regulation states of bindings sites, however, act together to achieve a normalization of mesencephalic, limbic and cortical serotonin.
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16

Boyer, Bancel, Perray, Pouderoux, Balmes, and Bali. "Effect of Champagne Compared to Still White Wine on Peripheral Neurotransmitter Concentrations." International Journal for Vitamin and Nutrition Research 74, no. 5 (September 1, 2004): 321–28. http://dx.doi.org/10.1024/0300-9831.74.5.321.

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To evaluate how the peripheral release of neurotransmitters such as serotonin, dopamine, cholecystokinin, and beta-endorphin is involved in drinking behavior, blood concentrations of these neurotransmitters were followed in 40 healthy young volunteers during the first hour after ingestion of a moderate dose of some common alcoholic beverages (champagne, still white wine) as compared to water. Concerning serotonin levels, two groups of subjects are statistically distinct: one with low basal serotonin levels (< 620 nmol/L) which responded with an increase in serotonin (52% in 10 minutes), and a second group with higher basal serotonin levels (> 620 nmol/L) which responded with a decrease (190% in 60 minutes). Variations in serotonin concentrations appear to depend upon the alcoholic content of the beverage. A rapid increase in plasma dopamine concentrations after consumption of champagne seems to be due to the nonalcoholic content of the beverage. Cholecystokinin values were not significantly different between the three beverages: the observed increase can be explained by a moderate gastric distention. Beta-endorphin levels didn't change significantly after drinking. In conclusion, some significant blood variations of serotonin and dopamine appeared even after moderately dose of champagne or still white wine. These changes might be partially responsible for the different drinking behavior.
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17

Wood, Jesse, Zoe LaPalombara, and Susanne E. Ahmari. "Monoamine abnormalities in the SAPAP3 knockout model of obsessive-compulsive disorder-related behaviour." Philosophical Transactions of the Royal Society B: Biological Sciences 373, no. 1742 (January 29, 2018): 20170023. http://dx.doi.org/10.1098/rstb.2017.0023.

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Obsessive-compulsive disorder (OCD) is a leading cause of illness-related disability, but the neural mechanisms underlying OCD symptoms are unclear. One potential mechanism of OCD pathology is monoamine dysregulation. Because of the difficulty of studying monoamine signalling in patients, animal models offer a viable alternative to understanding this aspect of OCD pathophysiology. We used HPLC to characterize post-mortem monoamine levels in lateral orbitofrontal cortex (OFC), medial OFC, medial prefrontal cortex and dorsal and ventral striatum of SAPAP-3 knockout (KO) mice, a well-validated model of compulsive-like behaviours in OCD. As predicted from previous studies, excessive grooming was significantly increased in SAPAP-3 KO mice. Overall levels of the serotonin metabolite 5-hydroxyindoleacetic acid (HIAA) and the ratio of 5HIAA/serotonin (serotonin turnover) were increased in all cortical and striatal regions examined. In addition, dihydroxyphenylacetic acid/dopamine ratio was increased in lateral OFC, and HVA/dopamine ratio was increased in lateral and medial OFC. No baseline differences in serotonin or dopamine tissue content were observed. These data provide evidence of monoaminergic dysregulation in a translational model of OCD symptoms and are consistent with aberrant cortical and striatal serotonin and dopamine release/metabolism in SAPAP-3 KO mice. These results are guiding ongoing experiments using circuit and cell-type specific manipulations of dopamine and serotonin to determine the contributions of these monoaminergic systems to compulsive behaviours, and serve here as a touchstone for an expanded discussion of these techniques for precise circuit dissection. This article is part of the discussion meeting issue ‘Of mice and mental health: facilitating dialogue between basic and clinical neuroscientists'.
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18

Rodríguez, Marcela C., María D. Rubianes, and Gustavo A. Rivas. "Highly Selective Determination of Dopamine in the Presence of Ascorbic Acid and Serotonin at Glassy Carbon Electrodes Modified with Carbon Nanotubes Dispersed in Polyethylenimine." Journal of Nanoscience and Nanotechnology 8, no. 11 (November 1, 2008): 6003–9. http://dx.doi.org/10.1166/jnn.2008.466.

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We report the highly selective and sensitive voltammetric dopamine quantification in the presence of ascorbic acid and serotonin by using glassy carbon electrodes modified with a dispersion of multi-wall carbon nanotubes (MWCNT) in polyethylenimine, PEI (GCE/MWCNT-PEI). The electrocatalytic activity of the MWCNT deposited on the glassy carbon electrode has allowed an important decrease in the overvoltages for the oxidation of ascorbic acid and dopamine, making possible a clear definition of dopamine, serotonin and ascorbic acid oxidation processes. The sensitivities for dopamine in the presence and absence of 1.0 mM ascorbic acid and serotonin were (2.18±0.03 × 105 μAM−1 (r = 0.9998); and (2.10±0.07 × 105 μAM−1 (r = 0.9985), respectively, demonstrating the excellent performance of the GCE/MWCNT-PEI. The detection limit for dopamine in the mixture was 9.2 × 10−7 M. The R. S. D. for the determination of 50 μM dopamine using four different electrodes was 3.9% when modified with the same MWCNT/PEI dispersion, and 4.6% when using four different dispersions. The modified electrode has been successfully applied for recovery assays of dopamine in human blood serum. Therefore, the new sensor represents an interesting and promising alternative for the electrochemical quantification of neurotransmitters and other analytes of clinical interest.
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19

Karpova, I. V., V. V. Mikheev, V. V. Marysheva, E. R. Bychkov, and P. D. Shabanov. "Effect of acute hypoxia with hypercapnia on the content of monoamines in symmetrical brain structures of the BALB/c male mice." Biomeditsinskaya Khimiya 60, no. 2 (2014): 258–63. http://dx.doi.org/10.18097/pbmc20146002258.

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The changes in activity of monoaminergic systems of both the right and the left brain hemispheres of the BALB/c male mice after an acute hypoxia with hypercapnia were studied. The concentrations of dopamine, serotonin and their metabolites dihydroxyphenylacetic, homovanilic and 5-hydroxyindolacetic acids were measured by HPLC in the brain cortex, hippocampus and striatum of the right and the left hemispheres. The more high concentration of serotonin was revealed only in the cortex of the left hemisphere in control mice without hypoxia with hypercapnia. The asymmetry in dopamine level was not registered in all structures studied. Acute hypoxia with hypercapnia decreased the dopamine level in the striatum and the serotonin level both in the hippocampus and the brain cortex. The dopamine metabolites level was reduced in the striatum and in the brain cortex of hypoxed mice: both metabolites in the right brain cortex and only dihydroxyphenylacetic acid in the left brain cortex. Serotonin metabolism was decreased in all brain structures studied after hypoxia with hypercapnia in mice. Therefore, serotoninergic system of the brain is more sensitive to acute hypoxia with hypercapnia than dopaminergic system.
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20

Houpert, P., P. Lestaevel, C. Amourette, B. Dhieux, C. Bussy, and F. Paquet. "Effect of U and 137Cs chronic contamination on dopamine and serotonin metabolism in the central nervous system of the rat." Canadian Journal of Physiology and Pharmacology 82, no. 2 (February 1, 2004): 161–66. http://dx.doi.org/10.1139/y04-012.

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Following the Chernobyl accident, the most significant problem for the population of the former Soviet Union for the next 50-70 years will be chronic internal contamination by radionuclides. One of the few experiments carried out in this field reported that neurotransmitter metabolism in the central nervous system of the rat was disturbed after feeding with oats contaminated by 137Cs for 1 month. The present study assessed the effect of chronic contamination by depleted U or 137Cs on the metabolism of two neurotransmitters in cerebral areas of rats. Dopamine and serotonin were chosen because their metabolism has been shown to be disturbed after external irradiation, even at moderate doses. Dopamine, serotonin, and some of their catabolites were measured by high-pressure liquid chromatography coupled with an electrochemical detector in five cerebral structures of rats contaminated over a 1-month period by drinking water (40 mg U·L–1 or 6500 Bq 137Cs·L–1). In the striatum, hippocampus, cerebral cortex, thalamus, and cerebellum, the dopamine, serotonin, and catabolite levels were not significantly different between the control rats and rats contaminated by U or 137Cs. These results are not in accordance with those previously described.Key words: uranium, caesium, dopamine, serotonin, HPLC.
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21

Ago, Yukio, Wataru Tanabe, Momoko Higuchi, Shinji Tsukada, Tatsunori Tanaka, Takumi Yamaguchi, Hisato Igarashi, et al. "(R)-Ketamine Induces a Greater Increase in Prefrontal 5-HT Release Than (S)-Ketamine and Ketamine Metabolites via an AMPA Receptor-Independent Mechanism." International Journal of Neuropsychopharmacology 22, no. 10 (July 21, 2019): 665–74. http://dx.doi.org/10.1093/ijnp/pyz041.

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Abstract Background Although recent studies provide insight into the molecular mechanisms of the effects of ketamine, the antidepressant mechanism of ketamine enantiomers and their metabolites is not fully understood. In view of the involvement of mechanisms other than the N-methyl-D-aspartate receptor in ketamine’s action, we investigated the effects of (R)-ketamine, (S)-ketamine, (R)-norketamine [(R)-NK], (S)-NK, (2R,6R)-hydroxynorketamine [(2R,6R)-HNK], and (2S,6S)-HNK on monoaminergic neurotransmission in the prefrontal cortex of mice. Methods The extracellular monoamine levels in the prefrontal cortex were measured by in vivo microdialysis. Results (R)-Ketamine and (S)-ketamine acutely increased serotonin release in a dose-dependent manner, and the effect of (R)-ketamine was greater than that of (S)-ketamine. In contrast, (S)-ketamine caused a robust increase in dopamine release compared with (R)-ketamine. Both ketamine enantiomers increased noradrenaline release, but these effects did not differ. (2R,6R)-HNK caused a slight but significant increase in serotonin and noradrenaline but not dopamine release. (S)-NK increased dopamine and noradrenaline but not serotonin release. Differential effects between (R)-ketamine and (S)-ketamine were also observed in a lipopolysaccharide-induced model of depression. An α-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid (AMPA) receptor antagonist, 2,3-dioxo-6-nitro-1,2,3,4- tetrahydrobenzo[f]quinoxaline-7-sulfonamide (NBQX), attenuated (S)-ketamine-induced, but not (R)-ketamine-induced serotonin release, whereas NBQX blocked dopamine release induced by both enantiomers. Local application of (R)-ketamine into the prefrontal cortex caused a greater increase in prefrontal serotonin release than that of (S)-ketamine. Conclusions (R)-Ketamine strongly activates the prefrontal serotonergic system through an AMPA receptor-independent mechanism. (S)-Ketamine-induced serotonin and dopamine release was AMPA receptor-dependent. These findings provide a neurochemical basis for the underlying pharmacological differences between ketamine enantiomers and their metabolites.
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22

Morissette, Marc, Daniel Lévesque, Alain Bélanger, and Thérèse Di Paolo. "A physiological dose of estradiol with progesterone affects striatum biogenic amines." Canadian Journal of Physiology and Pharmacology 68, no. 12 (December 1, 1990): 1520–26. http://dx.doi.org/10.1139/y90-231.

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The acute effect of estradiol and progesterone on dopamine and serotonin metabolism in rat striatum was studied. One subcutaneous injection of 17β-estradiol (300 ng) and progesterone (150 μg) into intact male rats increased plasma levels of these steroids, while testosterone, corticosterone, and estrone remained unchanged. Dehydroepiandrosterone, androstane-3β, 17β-diol and dihydrotestosterone remained undetectably low. Prolactin decreased and androstane-3α,17β-diol, and 17-OH progesterone increased, but less than estradiol and progesterone. Peak levels of striatal dopamine, dihydroxyphenylacetic acid, and homovanillic acid were observed 15–45 min after steroid injection with a return to control values after 45–60 min, while serotonin and 5-hydroxyindoleacetic acid levels were slightly decreased. An injection of estradiol (70 ng) with progesterone (70μg) to ovariectomized female rats left plasma prolactin levels unchanged, while striatum dopamine and serotonin as well as their metabolite concentrations peaked 15–60 min after steroid injection and returned to control values after 45–75 min. To allow for a better comparison of the action of these steroids, the effect of estradiol or progesterone alone and in combination on the brain of ovariectomized rats was compared in the same experiment. A similar increase in metabolites of dopamine levels was observed after these steroids alone or in combination, while dopamine levels were increased only after progesterone alone or in combination with estradiol. An injection of estradiol or progesterone to ovariectomized rats led to peak steroid concentrations at approximately the same time in the brain and plasma. In addition, plasma and brain steroid levels were significantly correlated. Thus, levels of estradiol and progesterone that occur during the estrous cycle can rapidly increase striatum dopaminergic activity in rats of both sexes, while serotonin activity is increased only in female rats.Key words: estradiol, progesterone, striatum, dopamine, serotonin.
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23

Gopal, Navya, and Arath Raghavan Sudha Devi. "Effect of administration of neurotransmitters: Serotonin and dopamine on testicular maturation in the freshwater crab Travancoriana schirnerae Bott, 1969 (Crustacea: Gecarcinucidae)." Brazilian Journal of Biological Sciences 6, no. 13 (2019): 413–28. http://dx.doi.org/10.21472/bjbs.061309.

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The current investigation aimed at the effect of administration of the neurotransmitters, serotonin and dopamine, on testicular maturation in the freshwater crab Travancoriana schirnerae Bott, 1969 (Crustacea: Gecarcinucidae). Adult males in active, inactive and revival phases of spermatogenesis were injected with serotonin and dopamine in multiple doses and their dissected testes were submitted to histomorphological examinations. Though serotonin treatment during active phase showed increased values for testicular index, acinar diameter and proportion of mature spermatozoa, only the testicular index values differed statistically from that of controls. Serotonin administration during inactive phase caused an increase in testicular index and acinar diameter, reduction in intra and interacinar spaces and pycnosis of germ cells and detection of division stages. A notable increase in the testicular index, acinar diameter and fresh batches of spermatozoa was perceptible in crabs injected with serotonin during revival phase. In contrast, dopamine injection showed a decline in testicular activity irrespective of the phase of spermatogenesis, as evinced from low testicular index, acinar diameter, presence of small, irregularly shaped acini with indistinct acinar boundaries, reduction in the number of mature spermatozoa and absence of division stages. To conclude, the stimulatory neurotransmittant, serotonin can be used to induce testicular maturation in species of aquaculture potential.
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24

Bakoyiannis, Ioannis. "New insights into dopamine-serotonin coupling." Lab Animal 51, no. 5 (May 2022): 129. http://dx.doi.org/10.1038/s41684-022-00971-8.

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25

Balcioglu, Aygul, and Richard J. Wurtman. "Striatal Serotonin Receptors and Dopamine Release." Journal of Neurochemistry 75, no. 2 (January 4, 2002): 886. http://dx.doi.org/10.1046/j.1471-4159.2000.0750886.x.

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26

Stier, C. T. "Serotonin and Dopamine in Essential Hypertension." American Journal of Hypertension 26, no. 2 (December 28, 2012): 151. http://dx.doi.org/10.1093/ajh/hps085.

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27

Byars, A., K. Burris, S. Jordan, K. Tottori, T. Kikuchi, and R. McQuade. "Aripiprazole: A dopamine-serotonin system stabilizer." European Neuropsychopharmacology 12 (October 2002): 290–91. http://dx.doi.org/10.1016/s0924-977x(02)80412-6.

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28

NISHAWALA, MELISSA A., MARIAN CALLAGHAN, J. JEFFREY MALATACK, BETH MOUGHAN, PAUL J. AMBROSINI, BERNADETTE PRICE, and JOSEPHINE ELIA. "Pancreatitis Associated with Serotonin-Dopamine Antagonists." Journal of Child and Adolescent Psychopharmacology 7, no. 3 (January 1997): 211–13. http://dx.doi.org/10.1089/cap.1997.7.211.

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29

Kurahashi, N., R. McQuade, K. D. Burris, S. Jordan, K. Tottori, and T. Kikuchi. "Aripiprazole: A dopamine-serotonin system stabilizer." Schizophrenia Research 60, no. 1 (March 2003): 312–13. http://dx.doi.org/10.1016/s0920-9964(03)80255-4.

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30

Kilcuchi, T., K. D. Burris, S. Jordan, and R. D. McQuade. "Aripiprazole: a dopamine-serotonin system stabilizer." European Psychiatry 17 (May 2002): 103. http://dx.doi.org/10.1016/s0924-9338(02)80467-9.

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31

Daw, Nathaniel D., Sham Kakade, and Peter Dayan. "Opponent interactions between serotonin and dopamine." Neural Networks 15, no. 4-6 (June 2002): 603–16. http://dx.doi.org/10.1016/s0893-6080(02)00052-7.

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32

Lee, S. "Oligomerization of Dopamine and Serotonin Receptors." Neuropsychopharmacology 23, no. 4 (October 2000): S32—S40. http://dx.doi.org/10.1016/s0893-133x(00)00155-x.

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33

卿, 若婷. "Serotonin and Dopamine Modulate Maternal Behavior." Advances in Psychology 10, no. 02 (2020): 145–55. http://dx.doi.org/10.12677/ap.2020.102019.

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34

Yamawaki, S., T. Hayashi, N. Yokota, T. Takahashi, G. Sato, and Y. Tahara. "Serotonin-dopamine antagonists in elderly schizophrenics." European Neuropsychopharmacology 6 (June 1996): 28. http://dx.doi.org/10.1016/0924-977x(96)87427-x.

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35

Algül, Şermin. "Psychiatric disorders and Nesfatin-1Psikiyatrik hastalıklar ve Nesfatin-1." International Journal of Human Sciences 12, no. 1 (April 30, 2015): 1397. http://dx.doi.org/10.14687/ijhs.v12i1.3149.

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<p>Nowadays psychiatric disorders is complex group of diseases that many factors play a role in the etiology and prevalence of it's very higher. Neurotransmitters levels such as serotonin norepinefrin and dopamine in the brain is changed in case of illness. For instance Neurotransmitters such as serotonin, norepinefrin and dopamine is decreased in depression and dopamine is increased in schizophrenia. Many of the antidepressants drugs that used in the treatment of depression leads to weight gain in patients. Nesfatin-1 is expressed that recently discovered, being an anorexigenic peptid and derived NEFA / nukleobindin2 (NUCB2) in the brain's stress-related field. Plasma nesfatin-1 levels were found to be very high psychiatric patients than normal people with. Peptids' brings to mind the idea that may be important in the prognosis of the disease which the decreased of the level of hormone following treatment process and high in case of illness. It's will provide a better understanding of the prognosis of the disease that can also be explained the effect of these hormones under stress in this disease. In future studies, to understand the antidepressants effect of nesfatin-1 the important molecular mechanisms related with the nesfatin-1 receptor should be necessary to define. In light of recent studies, it is thought that nesfatin-1 could be a important antidepressant drug in the near future.</p><p><strong>Özet </strong><br />Psikiyatrik hastalıklar günümüzde prevalansı çok yüksek olan etiyolojisinde birçok faktörün rol oynadığı yaygın ve kompleks bir hastalık grubudur. Hastalık durumunda beyinde serotonin, norepinefrin, dopamin gibi nörotransmitterlerin düzeyleri değişmektedir. Örneğin depresyonda serotonin, norepinefrin ve dopamin azalmaktayken; şizofrenide ise dopamin artmaktadır. Major depresyon tedavisinde kullanılan antidepresan ilaçların çoğu hastalarda kilo alımına yol açmaktadır. NEFA/nukleobindin2 (NUKB2)'den kaynaklanan son yıllarda keşfedilen anoreksijenik bir peptid olan nesfatin-1, beynin stresle alakalı alanlarında bulunmaktadır. Psikiyatrik hastalarda normal insanlara kıyasla plazma nesfatin-1 düzeyi çok yüksek bulunmuştur. Hastalık durumunda yüksek iken, tedavi sürecini takiben hormon seviyesinin düşmesi peptidin hastalığın prognozunda önemli olabileceği fikrini akla getirmektedir. Bu rahatsızlıklarda stres altında bu gibi hormonların etkilerinin açıklanması hastalığın prognozunun daha iyi anlaşılmasını sağlayacaktır. Gelecek çalışmalarda, nesfatin-1'in antidepresif etkisini anlamak için; nesfatin-1 reseptörleri ile ilgili önemli moleküler mekanizmaların tanımlanması gerekmektedir. Son yapılan çalışmaların ışığında, nesfatin-1'in yakın gelecekte önemli bir antidepresan ilacı olabileceği düşünülmektedir.</p>
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36

Munkittrick, K. R., R. J. Martin, and D. G. Dixon. "Seasonal changes in whole brain amine levels of white sucker exposed to elevated levels of copper and zinc." Canadian Journal of Zoology 68, no. 5 (May 1, 1990): 869–73. http://dx.doi.org/10.1139/z90-126.

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Levels of dopamine, serotonin, and noradrenalin were measured in whole brains collected from white sucker (Catostomus commersoni) exposed to increased waterborne levels of copper and zinc associated with mining wastes. Few differences were detected between sites, and these findings are consistent with previous studies that failed to indicate chronic, direct effects of the metals on the white sucker populations. Levels of dopamine and serotonin were higher during postspawning periods than during prespawning or spawning. Noradrenalin levels showed parallel trends, although the differences were not significant owing to higher variability. Serotonin levels showed significant circadian variation at both sites, especially during the spawning season. Dopamine levels also showed circadian fluctuations, but only in females at one site. The results are discussed in relation to the potential use of whole brain amine levels as indicators of contaminant impact.
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37

Costa, Bárbara, Rita Matos, Irina Amorim, Fátima Gärtner, and Nuno Vale. "New Insight into Breast Cancer Cells Involving Drug Combinations for Dopamine and Serotonin Receptors." Applied Sciences 11, no. 13 (June 30, 2021): 6082. http://dx.doi.org/10.3390/app11136082.

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The breast cancer therapies available are insufficient, especially since first-line treatments, such as paclitaxel, result in drug resistance and their toxicity often limits their concentration. Strategies like drug repurposing are beneficial, and novel treatments can emerge by repurposing drugs that interfere with the dopamine and serotonin receptors, and thus influence tumor growth. In this study, the MTT assay was used to test the efficacy of such repurposed drugs commonly used for neurodegenerative disorders that act on the dopamine and serotonin receptors to reduce the MCF-7 cell’s viability, either by their single use or in combination with the reference drug paclitaxel. Furthermore, the expression of vimentin and E-cadherin was assayed by immunofluorescence. The dopamine receptor-altering drugs benztropine and thioridazine resulted in the strongest reduction of cell viability when combined with paclitaxel, which may be connected to the alteration of E-cadherin rather than vimentin expression. More studies are needed to understand the mechanism of action of the combinations tested and the efficacious role of dopamine and serotonin.
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38

Leonard, M. N., C. A. Macey, and P. G. Strange. "Heterogeneity of D2 dopamine receptors in different brain regions." Biochemical Journal 248, no. 2 (December 1, 1987): 595–602. http://dx.doi.org/10.1042/bj2480595.

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The binding of [3H]spiperone has been examined in membranes derived from different regions of bovine brain. In caudate nucleus, nucleus accumbens, olfactory tubercle and putamen binding is to D2 dopamine and 5HT2 serotonin receptors, whereas in cingulate cortex only serotonin 5HT2 receptor binding can be detected. D2 dopamine receptors were examined in detail in caudate nucleus, olfactory tubercle and putamen using [3H]spiperone binding in the presence of 0.3 microM-mianserin (to block 5HT2 serotonin receptors). No evidence for heterogeneity among D2 dopamine receptors either between brain regions or within a brain region was found from the displacements of [3H]spiperone binding by a range of antagonists, including dibenzazepines and substituted benzamides. Regulation of agonist binding by guanine nucleotides did, however, differ between regions. In caudate nucleus a population of agonist binding sites appeared resistant to guanine nucleotide regulation, whereas this was not the case in olfactory tubercle and putamen.
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39

GÜNGÖR, Sezen. "Genes Involved in both Dopaminergic and Serotonergic Pathways and Financial Decision Making." PRIZREN SOCIAL SCIENCE JOURNAL 3, no. 2 (August 24, 2019): 21. http://dx.doi.org/10.32936/pssj.v3i2.111.

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One of the most important assumption of rational choice theory is that individuals are purely self-interested utility maximizers. However research in economics and other social sciences has found that people can also be irrational and their choices can also be taken with some heuristics and biases. Laboratory experiments have documented substantial heterogeneity in irrational preferences, but little is known about the origins of such irrational financial behavior. Especially in recent studies, it is seen that the inheritance estimates of these differences are investigated by using quantitative and molecular genetic methods. The main purpose of this study is to investigate the effects of dopamine and serotonin-related genes on financial decisions. For this purpose, genes associated with dopamine and serotonin were identified. Some of the studies investigating the effects of these genes on financial decision making process have been examined. Key words: Genoeconomics, Financial Decision, Dopamine, Serotonin, MAOA gene.
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40

Islami, Hilmi, Sadi Bexheti, Ragip Shabani, Bajram Nuraj, Fehmi Zeqiri, Aziz Šukalo, Ilir Kurtishi, Skender Kutllovci, Hasime Qorraj, and Mentor Disha. "Role of Meconium in the Reaction of Airways Smooth Musculature in the Newborn with Meconium Aspiration Syndrome (Mas)." Bosnian Journal of Basic Medical Sciences 9, no. 4 (November 20, 2009): 342–248. http://dx.doi.org/10.17305/bjbms.2009.2791.

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The role of meconium in the respiratory system was studied in newborns, who died from various causes (250 up to 3000 g of weight). We monitored tracheal rings response to dopamine, serotonin and ethanol in different concentrations (dopamine: 0,05 mg/ml, 0,5 mg/ml, 5 mg/ml; serotonin (5-HT): 10-4, 10-3, 10-2, 10-1 mol/dm3; ethanol: 0,02 ml, 0,5 ml, 1,0 ml; 96%). Tracheal smooth musculature tonus (TSM) was examined in 48 tracheal preparations taken after the newborn exitus due to different reasons. Based on functional researche of isolated preparations of tracheas, it may be concluded that: aspiration of me-conium has not changed the response of TSM to dopamine, serotonin and ethanol (p>0,1) in comparison with the control group, which have died due to different lung inflammatory processes (e.g. pneumonia, bronchopneumonia, atelectasis, cerebral hemorrhage). The results suggest that meconium does not potentiate the constricting action of dopamine, serotonin and ethanol in tracheobronchial system. Meconium causes mild relaxation of the TSM through a mechanism that is not intermediated by the products of cyclooxygenases (prostaglandins, prostacyclins) from the tracheal epithelium or proteins. Also, as it seems, the direct activity of many tested acids in the smooth musculature has no significant impact on increase of the airways tonus in MAS syndrome.
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41

Griessenauer, Christoph J., Su-Youne Chang, Susannah J. Tye, Christopher J. Kimble, Kevin E. Bennet, Paul A. Garris, and Kendall H. Lee. "Wireless Instantaneous Neurotransmitter Concentration System: electrochemical monitoring of serotonin using fast-scan cyclic voltammetry—a proof-of-principle study." Journal of Neurosurgery 113, no. 3 (September 2010): 656–65. http://dx.doi.org/10.3171/2010.3.jns091627.

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Object The authors previously reported the development of the Wireless Instantaneous Neurotransmitter Concentration System (WINCS) for measuring dopamine and suggested that this technology may be useful for evaluating deep brain stimulation–related neuromodulatory effects on neurotransmitter systems. The WINCS supports fast-scan cyclic voltammetry (FSCV) at a carbon-fiber microelectrode (CFM) for real-time, spatially resolved neurotransmitter measurements. The FSCV parameters used to establish WINCS dopamine measurements are not suitable for serotonin, a neurotransmitter implicated in depression, because they lead to CFM fouling and a loss of sensitivity. Here, the authors incorporate into WINCS a previously described N-shaped waveform applied at a high scan rate to establish wireless serotonin monitoring. Methods Optimized for the detection of serotonin, FSCV consisted of an N-shaped waveform scanned linearly from a resting potential of +0.2 to +1.0 V, then to −0.1 V and back to +0.2 V, at a rate of 1000 V/second. Proof-of-principle tests included flow injection analysis and electrically evoked serotonin release in the dorsal raphe nucleus of rat brain slices. Results Flow cell injection analysis demonstrated that the N waveform, applied at a scan rate of 1000 V/second, significantly reduced serotonin fouling of the CFM, relative to that observed with FSCV parameters for dopamine. In brain slices, WINCS reliably detected subsecond serotonin release in the dorsal raphe nucleus evoked by local high-frequency stimulation. Conclusions The authors found that WINCS supported high-fidelity wireless serotonin monitoring by FSCV at a CFM. In the future such measurements of serotonin in large animal models and in humans may help to establish the mechanism of deep brain stimulation for psychiatric disease.
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42

Shin, Eunju, Elisabetta Tronci, and Manolo Carta. "Role of Serotonin Neurons in L-DOPA- and Graft-Induced Dyskinesia in a Rat Model of Parkinson's Disease." Parkinson's Disease 2012 (2012): 1–5. http://dx.doi.org/10.1155/2012/370190.

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L-DOPA, the most effective drug to treat motor symptoms of Parkinson's disease, causes abnormal involuntary movements, limiting its use in advanced stages of the disease. An increasing body of evidence points to the serotonin system as a key player in the appearance of L-DOPA-induced dyskinesia (LID). In fact, exogenously administered L-DOPA can be taken up by serotonin neurons, converted to dopamine and released as a false transmitter, contributing to pulsatile stimulation of striatal dopamine receptors. Accordingly, destruction of serotonin fibers or silencing serotonin neurons by serotonin agonists could counteract LID in animal models. Recent clinical work has also shown that serotonin neurons are present in the caudate/putamen of patients grafted with embryonic ventral mesencephalic cells, producing intense serotonin hyperinnervation. These patients experience graft-induced dyskinesia (GID), a type of dyskinesia phenotypically similar to the one induced by L-DOPA but independent from its administration. Interestingly, the 5-HT1Areceptor agonist buspirone has been shown to suppress GID in these patients, suggesting that serotonin neurons might be involved in the etiology of GID as for LID. In this paper we will discuss the experimental and clinical evidence supporting the involvement of the serotonin system in both LID and GID.
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43

Jørgensen, Louise M., Pia Weikop, Claus Svarer, Ling Feng, Sune H. Keller, and Gitte M. Knudsen. "Cerebral serotonin release correlates with [11C]AZ10419369 PET measures of 5-HT1B receptor binding in the pig brain." Journal of Cerebral Blood Flow & Metabolism 38, no. 7 (July 7, 2017): 1243–52. http://dx.doi.org/10.1177/0271678x17719390.

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Positron emission tomography (PET) can, when used with appropriate radioligands, non-invasively capture temporal and spatial information about acute changes in brain neurotransmitter systems. We here evaluate the 5-HT1B receptor partial agonist PET radioligand, [11C]AZ10419369, for its sensitivity to detect changes in endogenous cerebral serotonin levels, as induced by different pharmacological challenges. To enable a direct translation of PET imaging data to changes in brain serotonin levels, we compared the [11C]AZ10419369 PET signal in the pig brain to simultaneous measurements of extracellular serotonin levels with microdialysis after various acute interventions (saline, escitalopram, fenfluramine). The interventions increased the cerebral extracellular serotonin levels to two to six times baseline, with fenfluramine being the most potent pharmacological enhancer of serotonin release. The interventions induced a varying degree of decline in [11C]AZ10419369 binding in the brain, consistent with the occupancy competition model. The observed correlation between changes in the extracellular serotonin level in the pig brain and the 5-HT1B receptor occupancy indicates that [11C]AZ10419369 binding is sensitive to changes in endogenous serotonin levels to a degree equivalent to that reported of [11C]raclopride to dopamine, a much used approach to detect in vivo change in cerebral dopamine.
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44

Chanclrashekar-Reddy, K. M., M. I. Balabolkin, and L. D. Stoilov. "The sympathoadrenal system in diabetics with different patterns of the disease and its late complications." Problems of Endocrinology 40, no. 6 (December 15, 1994): 13–14. http://dx.doi.org/10.14341/probl12182.

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Blood plasma concentrations of noradrenaline, dopamine, serotonin and their metabolites (DOPAC, HVA) were measured in 28 patients with insulin-dependent and 32 with noninsulin-dependent diabetes mellitus (IDDM and NIDDM, respectively). The patients were divided into 4 groups. Group 1 were 15 patients without late diabetic complications, group 2 were 15 subjects with diabetic neuropathy, group 3 were patients with neuropathy and retinopathy (n=16), and group 4 were 14 patients with neuropathy, retinopathy, and nephropathy. The results showed an increase of serotonin levels in IDDM patients w. those with NIDDM, a positive correlation between serotonin and blood glucose levels in IDDM, increased concentration of dopamine and reduced plasma level of noradrenaline in patients with diabetic neuropathy vs. those without late diabetic complications. Plasma levels of dopamine were decreased in all the patients microvascular involvement. The findings indicate the development of changes in the sympathoadrenal system of patients with late diabetic vascular complications.
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45

Hagino, Y., Y. Takamatsu, H. Yamamoto, T. Iwamura, D. L. Murphy, G. R. Uhl, I. Sora, and K. Ikeda. "Effects of MDMA on Extracellular Dopamine and Serotonin Levels in Mice Lacking Dopamine and/or Serotonin Transporters." Current Neuropharmacology 9, no. 1 (March 1, 2011): 91–95. http://dx.doi.org/10.2174/157015911795017254.

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46

Masler, Edward. "Responses of Heterodera glycines and Meloidogyne incognita to exogenously applied biogenic amines." Nematology 10, no. 6 (2008): 911–17. http://dx.doi.org/10.1163/156854108786161436.

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AbstractHatching and head movement behaviours of second-stage juvenile (J2) of two agriculturally important plant-parasitic nematodes were affected by the in vitro application of biogenic amines. The behavioural responses of Heterodera glycines and Meloidogyne incognita to treatments of serotonin, octopamine and dopamine were qualitatively similar, but significant quantitative differences between the species were revealed. The frequency of J2 head movement was decreased by as little as 250 μM serotonin in H. glycines and 500 μM serotonin in M. incognita, with effective doses (ED50) of 0.73 mM for H. glycines and 1.72 mM for M. incognita. Octopamine had the opposite effect of serotonin, increasing J2 head movement frequency at thresholds of 2 mM in H. glycines and 1 mM in M. incognita. Octopamine ED50 values were 32.35 mM and 1.91 mM, respectively. Dopamine had no effect on head movement in either species up to concentrations of 20 mM. Serotonin inhibited hatch in both species but was more potent against H. glycines (90% inhibition at 1 mM) than M. incognita (40% inhibition at 5 mM). Octopamine reduced hatch equally in both species with over 95% inhibition at 80 mM. Dopamine had no effect on hatch in M. incognita but did inhibit H. glycines hatch over 60% at 40 mM. The value of detailed quantitative analyses of plant-parasitic nematode responses to biogenic amines for studies on nematode control is discussed.
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47

Masler, E. P. "Responses of Heterodera glycines and Meloidogyne incognita to exogenously applied neuromodulators." Journal of Helminthology 81, no. 4 (December 2007): 421–27. http://dx.doi.org/10.1017/s0022149x07850243.

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AbstractBiogenic amines regulate important behaviours in nematodes and are associated with pharyngeal activity in plant-parasitic nematodes. A robust behavioural assay based upon nematode body movements was developed to expand the study of these and other neuroregulators in plant-parasitic nematodes. Dopamine, octopamine and serotonin each had significant but differing effects on the behaviour of soybean cyst nematode Heterodera glycines and root-knot nematode Meloidogyne incognita juveniles. Body movement frequency was increased twofold in H.glycines by 5 mM dopamine (P = 0.0001), but decreased by 50 mM dopamine in H. glycines (88%) and M. incognita (53%) (P < 0.0001). Movement frequency in both species was increased by 50–70% (P < 0.0001) by 50 mM octopamine, and 5 mM octopamine increased M. incognita movement frequency more than twofold (P < 0.0001). Movement frequency in each species was reduced by more than 90% by 5 mM serotonin (P < 0.0001). While amplitude of body movement in H. glycines was unaffected by any amine, it was significantly reduced in M.incognita by all amines (P < 0.0006). Stylet pulsing frequencies in either species were unaffected by dopamine or octopamine, but 5 mM serotonin stimulated pulsing in H. glycines by nearly 13-fold (P < 0.0001) and in M. incognita by more than 14-fold (P < 0.0001). The invertebrate neuropeptide FLRFamide (N-Phe-Leu-Arg-Phe) increased M. incognita body movement frequency 45% (P = 0.02) at 1 mM but did not affect stylet activity. Finally, H. glycines egg hatch was completely suppressed by 50 mM serotonin, and partially suppressed by 50 mM dopamine (75%; P < 0.0001) and 50 mM octopamine (55%; P < 0.0001).
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48

Karpova, I. V., V. V. Mikheev, V. V. Marysheva, N. A. Kuritcyna, E. R. Bychkov, and P. D. Shabanov. "The time course of changes in the state of monoaminergic systems in the brain of mice under the acute hypoxia with hypercapnia." Biomeditsinskaya Khimiya 65, no. 6 (2019): 485–97. http://dx.doi.org/10.18097/pbmc20196506485.

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In socially isolated male outbred albino mice, the changes of monoaminergic systems under acute hypoxia with hypercapnia were studied. In cerebral cortex, hippocampus and striatum of the right and left sides of the brain, the concentrations of norepinephrine, dopamine, serotonin and their metabolites – dihydroxyphenylacetic, homovanillic and 5-hydroxyindoleacetic acids were investigated using the HPLC method. In isolated mice, which were not subjected to hypoxia with hypercapnia, higher levels of dopamine and serotonin in the left cortex were found. There was no asymmetry in monoamines and their metabolites in other studied brain structures. 10 min after the onset of exposure, acute hypoxia with hypercapnia resulted in a right-sided increase in norepinephrine levels and a decrease in dopamine levels in the striatum and serotonin levels in the hippocampus. In the cerebral cortex, 10 min after of hypoxic exposure beginning, there was a left-sided decrease in the dopamine content, while the original asymmetry found in the cortex of intact animals disappeared. In isolated mice perished of hypoxia with hypercapnia, almost all parameters returned to the control level. The exception was the ratio of serotonin metabolite level to the neurotransmitter, which in the right cortex became lower than in control animals. In white outbred mice, the brain monoaminergic systems are suggested to be relatively resistant to the negative consequences of hypoxia and hypercapnia, and corresponding shifts resulting in the reflex brain response to changes in the gas composition of the respiratory air.
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49

Park, Hyejin, Un-ho Jin, Keshav Karki, Arul Jayaraman, Clint Allred, Sharon K. Michelhaugh, Sandeep Mittal, Robert S. Chapkin, and Stephen Safe. "Dopamine is an aryl hydrocarbon receptor agonist." Biochemical Journal 477, no. 19 (October 16, 2020): 3899–910. http://dx.doi.org/10.1042/bcj20200440.

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Tryptophan metabolites exhibit aryl hydrocarbon receptor (AhR) agonist activity and recent studies show that the phenylalanine metabolites serotonin and carbidopa, a drug used in treating Parkinson's disease, activated the AhR. In this study, we identified the neuroactive hormone dopamine as an inducer of drug-metabolizing enzymes CYP1A1, CYP1B1, and UGT1A1 in colon and glioblastoma cells and similar results were observed for carbidopa. In contrast, carbidopa but not dopamine exhibited AhR activity in BxPC3 pancreatic cancer cells whereas minimal activity was observed for both compounds in Panc1 pancreatic cancer cells. In contrast with a previous report, the induction responses and cytotoxicity of carbidopa was observed only at high concentrations (100 µM) in BxPC3 cells. Our results show that similar to serotonin and several tryptophan metabolites, dopamine is also an AhR-active compound.
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50

De Deurwaerdère, Philippe, Norbert Bonhomme, Guillaume Lucas, Michel Le Moal, and Umberto Spampinato. "Serotonin Enhances Striatal Dopamine Outflow In Vivo Through Dopamine Uptake Sites." Journal of Neurochemistry 66, no. 1 (November 19, 2002): 210–15. http://dx.doi.org/10.1046/j.1471-4159.1996.66010210.x.

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