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Journal articles on the topic 'Serotonergic pathways'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 February 2022

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1

Burgard, Edward C., Mathew O. Fraser, and Karl B. Thor. "Serotonergic modulation of bladder afferent pathways." Urology 62, no. 4 (October 2003): 10–15. http://dx.doi.org/10.1016/s0090-4295(03)00590-9.

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2

Lin, Henry C., Corynn Neevel, Peng-Sheng Chen, Gina Suh, and Jin Hai Chen. "Slowing of intestinal transit by fat or peptide YY depends on β-adrenergic pathway." American Journal of Physiology-Gastrointestinal and Liver Physiology 285, no. 6 (December 2003): G1310—G1316. http://dx.doi.org/10.1152/ajpgi.00230.2003.

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Although the enteric reflex pathway triggered by volume distension is known to depend on an adrenergic nerve, it is not known whether the slowing of intestinal transit by fat or peptide YY (PYY) also depends on an adrenergic pathway. The aim of this study was to test the hypotheses that the slowing of transit by fat or PYY may depend on a β-adrenergic pathway, and this adrenergic pathway may act via the serotonergic and opioid pathways previously observed for the slowing of transit by fat. Eighteen dogs were equipped with duodenal and midgut fistulas. The small intestine was compartmentalized into the proximal and distal half of gut. The role of adrenergic, serotonergic, and opioid pathways was then tested in the slowing of intestinal transit by fat, PYY, and norepinephrine. Intestinal transit results were compared as the cumulative percent marker of recovery over 30 min. We found that the slowing of transit by fat, PYY, or norepinephrine was reversed by propranolol. In addition, the slowing effect of fat was reversed by metoprolol (β1-adrenoreceptor antagonist) but not phentolamine (α-adrenoreceptor antagonist). Furthermore, norepinephrine-induced slowing of transit was reversed by ondansetron (5-HT3 receptor antagonist) or naloxone (opioid receptor antagonist). Extending these physiological results, we also found by immunohistochemistry that β1-adrenoreceptors are expressed by neurons of the intrinsic plexuses of the small intestine. We conclude that the slowing of intestinal transit by fat or PYY depends on a β-adrenergic pathway and that this adrenergic pathway acts on serotonergic and opioid pathways.
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3

Lam, Daniel D., and Lora K. Heisler. "Serotonin and energy balance: molecular mechanisms and implications for type 2 diabetes." Expert Reviews in Molecular Medicine 9, no. 5 (February 2007): 1–24. http://dx.doi.org/10.1017/s1462399407000245.

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The neurotransmitter serotonin is an important regulator of energy balance. In the brain, serotonergic fibres from midbrain raphe nuclei project to key feeding centres, where serotonin acts on specific receptors to modulate the activity of various downstream neuropeptide systems and autonomic pathways and thus affects ingestive behaviour and energy expenditure. Serotonin, released by intestinal enterochromaffin cells, also appears to regulate energy homeostasis through peripheral mechanisms. Serotonergic effects on energy balance lead to secondary effects on glucose homeostasis, based on a well-established link between obesity and insulin resistance. However, serotonergic pathways may also directly affect glucose homeostasis through regulation of autonomic efferents and/or action on peripheral tissues. Several serotonergic compounds have been evaluated for clinical use in the treatment of obesity and type 2 diabetes; results of these trials are discussed here. Finally, future directions in the elucidation of serotonergic metabolic regulation are discussed.
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4

Torrico, Bàrbara, Judit Cabana-Domínguez, Anu Shivalikanjli, Noèlia Fernàndez-Castillo, and Bru Cormand. "S68EXPLORING DOPAMINERGIC AND SEROTONERGIC PATHWAYS IN PSYCHIATRIC DISORDERS." European Neuropsychopharmacology 29 (October 2019): S148—S149. http://dx.doi.org/10.1016/j.euroneuro.2019.08.069.

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5

Áfra, J., C. Ertsey, G. Bozsik, and I. Jelencsik. "Cluster Headache Patients Show Marked Intensity Dependence of Cortical Auditory Evoked Potentials during and outside the Bout." Cephalalgia 25, no. 1 (January 2005): 36–40. http://dx.doi.org/10.1111/j.1468-2982.2004.00801.x.

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Central serotonergic neurotransmission was assessed using intensity dependence of cortical auditory evoked potentials (IDAP) in cluster headache (CH) patients during both the active and interictal period. In 15 episodic CH patients and 13 controls previously described methods were used and amplitude-stimulus intensity function (ASF) slopes were computed. In the cluster group mean ASF slope was significantly steeper than in the control group both during the active period (1.53 + 0.90 vs. 0.77 + 0.85, P = 0031) and interictally (1.85 + 1.20 vs. 0.77 + 0.85, P = 0012). In the cluster group IDAPs of active and interictal period did not differ significantly ( P = 0378). Duration of the disease or the present bout, distance from the last attack did not correlate with ASF slopes. In conclusion, our results are compatible with decreased level of serotonergic neurotransmission in raphe-cortical pathways. Diminished serotonergic activity in raphe-hypothalamic serotonergic pathways might be hypothesized influencing the activity of hypothalamic neurons and thus play a role in the genesis of cluster headache.
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6

Sawynok, Jana. "The 1988 Merck Frosst Award.: The role of ascending and descending noradrenergic and serotonergic pathways in opioid and non-opioid antinociception as revealed by lesion studies." Canadian Journal of Physiology and Pharmacology 67, no. 9 (September 1, 1989): 975–88. http://dx.doi.org/10.1139/y89-154.

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Both ascending and descending noradrenergic and serotonergic pathways have been implicated in mechanisms of antinociception produced by systemic administration of morphine and the non-opioid drugs, baclofen and clonidine. These agents affect the turnover and release of noradrenaline and 5-hydroxytryptamine in various brain regions and the spinal cord, and alter neuronal activity in regions from which ascending and descending aminergic pathways originate. The role of specific pathways in morphine analgesia has been examined by applying electrolytic lesions to discrete brain regions. However, this technique is limited because lesions are nonselective for a particular neuronal population. More recent studies have used microinjection of the neurotoxins 6-hydroxydopamine and 5, 7-dihydroxytryptamine to lesion specific noradrenergic and serotonergic pathways, respectively. Although more selective, this approach may be limited by the development of receptor supersensitivity or other mechanisms of compensation, as certain changes seen soon after microinjection (days) are no longer apparent at later intervals (weeks). Systemic drug administration reveals drug actions at predominant but not clearly identified sites of action. The role of a particular aminergic pathway can be revealed most clearly by combining microinjection of drugs into discrete brain sites with neurotoxin-induced lesions, and examining the effects of such lesions at a range of time intervals. A differential role of a particular pathway may become apparent following systemic or intracerebral administration.Key words: neurotoxin lesions, antinociception, morphine, noradrenaline, baclofen.
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7

Keesom, Sarah M., and Laura M. Hurley. "Silence, Solitude, and Serotonin: Neural Mechanisms Linking Hearing Loss and Social Isolation." Brain Sciences 10, no. 6 (June 12, 2020): 367. http://dx.doi.org/10.3390/brainsci10060367.

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For social animals that communicate acoustically, hearing loss and social isolation are factors that independently influence social behavior. In human subjects, hearing loss may also contribute to objective and subjective measures of social isolation. Although the behavioral relationship between hearing loss and social isolation is evident, there is little understanding of their interdependence at the level of neural systems. Separate lines of research have shown that social isolation and hearing loss independently target the serotonergic system in the rodent brain. These two factors affect both presynaptic and postsynaptic measures of serotonergic anatomy and function, highlighting the sensitivity of serotonergic pathways to both types of insult. The effects of deficits in both acoustic and social inputs are seen not only within the auditory system, but also in other brain regions, suggesting relatively extensive effects of these deficits on serotonergic regulatory systems. Serotonin plays a much-studied role in depression and anxiety, and may also influence several aspects of auditory cognition, including auditory attention and understanding speech in challenging listening conditions. These commonalities suggest that serotonergic pathways are worthy of further exploration as potential intervening mechanisms between the related conditions of hearing loss and social isolation, and the affective and cognitive dysfunctions that follow.
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8

Lin, Henry C., Corynn Neevel, and Jin Hai Chen. "Slowing intestinal transit by PYY depends on serotonergic and opioid pathways." American Journal of Physiology-Gastrointestinal and Liver Physiology 286, no. 4 (April 2004): G558—G563. http://dx.doi.org/10.1152/ajpgi.00278.2003.

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Slowing of intestinal transit by fat is abolished by immunoneutralization of peptide YY (PYY), demonstrating a key role for this gut peptide. How PYY slows intestinal transit is not known. We tested the hypothesis that the slowing of intestinal transit by PYY may depend on an ondansetron-sensitive serotonergic pathway and a naloxone-sensitive opioid pathway. In a fistulated dog model, occluding Foley catheters were used to compartmentalize the small intestine into proximal (between fistulas) and distal (beyond midgut fistula) half of gut. Buffer (pH 7.0) was perfused into both proximal and distal gut, and PYY was delivered intravenously. Ondansetron or naloxone was mixed with buffer and delivered into either the proximal or distal half of gut. Intestinal transit was measured across the proximal half of the gut. The slowing of intestinal transit by PYY was abolished when either ondansetron or naloxone was delivered into the proximal, but not the distal gut, to localize the two pathways to the efferent limb of the slowing response. In addition, 5-HT slows intestinal transit with marker recovery decreased from 76.2 ± 3.6% (control) to 33.5 ± 2.4% (5-HT) ( P < 0.0001) but was reversed by naloxone delivered into the proximal gut with marker recovery increased to 79.9 ± 7.2% ( P < 0.0005). We conclude that the slowing of intestinal transit by PYY depends on serotonergic neurotransmission via an opioid pathway.
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9

Fajemiroye, James Oluwagbamigbe, Pablinny Moreira Galdino, Joelma Abadia Marciano De Paula, Fagundes Fabio Rocha, Moses A. Akanmu, Frederico Argollo Vanderlinde, Jordan K. Zjawiony, and Elson Alves Costa. "Anxiolytic and antidepressant like effects of natural food flavour (E)-methyl isoeugenol." Food Funct. 5, no. 8 (2014): 1819–28. http://dx.doi.org/10.1039/c4fo00109e.

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10

Stahl, S. "C.06.03 Targeting dopaminergic and serotonergic pathways in schizophrenia." European Neuropsychopharmacology 25 (September 2015): S667. http://dx.doi.org/10.1016/s0924-977x(15)30954-8.

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11

Coote, John H. "Bulbospinal Serotonergic Pathways in the Control of Blood Pressure." Journal of Cardiovascular Pharmacology 15 (1990): S35—S41. http://dx.doi.org/10.1097/00005344-199000157-00005.

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12

Coote, John H. "Bulbospinal Serotonergic Pathways in the Control of Blood Pressure." Journal of Cardiovascular Pharmacology 15 (January 1990): S35—S41. http://dx.doi.org/10.1097/00005344-199001001-00005.

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13

Schoofs, Andreas, Sebastian Hückesfeld, Sandya Surendran, and Michael J. Pankratz. "Serotonergic pathways in the Drosophila larval enteric nervous system." Journal of Insect Physiology 69 (October 2014): 118–25. http://dx.doi.org/10.1016/j.jinsphys.2014.05.022.

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14

Singh, Damanpreet, and Rajesh Kumar Goel. "Anticonvulsant effect of Ficus religiosa: Role of serotonergic pathways." Journal of Ethnopharmacology 123, no. 2 (June 2009): 330–34. http://dx.doi.org/10.1016/j.jep.2009.02.042.

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15

Carver, Charles S., Sheri L. Johnson, and Jutta Joormann. "Two-Mode Models of Self-Regulation as a Tool for Conceptualizing Effects of the Serotonin System in Normal Behavior and Diverse Disorders." Current Directions in Psychological Science 18, no. 4 (August 2009): 195–99. http://dx.doi.org/10.1111/j.1467-8721.2009.01635.x.

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The serotonin system is a collection of neural pathways whose overall level of functioning (from low to high) relates to diverse kinds of psychological and behavioral variability. Individual differences in serotonergic function are important both in personality and in vulnerability to psychological disorders. These disorders range widely—from impulsive aggression to depression. One way to understand such diverse reflections of differences in serotonergic function is by viewing serotonergic function through the lens of two-mode (or dual-process) models of self-regulation. Such theories posit a lower-order system that responds quickly to associative cues of the moment and a higher-order system that responds reflectively and planfully. Low serotonergic function appears to enhance influence of the lower-order system. This often yields impulsive reactivity. Why, then, does low serotonergic function also relate to depression, which is characterized by lethargy and unresponsiveness? The answer must be that ascendance of the lower system interacts with other factors. One hypothesis is that low serotonergic function plus high sensitivity to incentives yields vulnerability to impulsive approach, whereas low serotonergic function plus low incentive sensitivity yields vulnerability to depression. Conceptualizing serotonergic function this way helps integrate information pertaining to very different disorders into a coherent picture.
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16

Latorre, Eva, Jose Emilio Mesonero, and Lorna W. Harries. "Alternative splicing in serotonergic system: Implications in neuropsychiatric disorders." Journal of Psychopharmacology 33, no. 11 (June 18, 2019): 1352–63. http://dx.doi.org/10.1177/0269881119856546.

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Background:The serotonergic system is a key component of physiological brain function and is essential for proper neurological activity. Numerous neuropsychiatric disorders are associated with deregulation of the serotonergic system. Accordingly, many pharmacological treatments are focused on modulation of this system. While providing a promising line of therapeutic moderation, these approaches may be complicated due to the presence of alternative splicing events for key genes in this pathway. Alternative splicing is a co-transcriptional process by which different mRNA transcripts can be produced from the same gene. These different isoforms may have diverse activities and functions, and their relative balance is often critical for the maintenance of homeostasis. Alternative splicing greatly increases the production of proteins, augmenting cell plasticity, and provides an important control point for regulation of gene expression.Aim:The objective of this narrative review is to discuss the potential impact of alternative splicing of different components of the serotonergic system and speculate on their involvement in several neuropsychiatric disorders.Conclusions:The specific role of each isoform in disease and their relative activities in the signalling pathways involved are yet to be determined. We need to gain a better understanding of the basis of alternative isoforms of the serotonergic system in order to fully understand their impact and be able to develop new effective pharmacological isoform-specific targets.
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17

Lundwall, Rebecca A., Jordan Sgro, and Tyson Wade. "SLC6A3 Is Associated With Relational Aggression in Children." Journal of Individual Differences 38, no. 4 (November 2017): 220–29. http://dx.doi.org/10.1027/1614-0001/a000239.

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Abstract. Understanding the genetic influence on aggressive behavior in children is one way to understand pathways to the development of aggression in adults. While aggression is likely under some environmental influence, it is also likely under some genetic influence. Overt aggression associates with a variety of genes including dopaminergic and serotonergic genes. Dopaminergic and serotonergic genes are known to be associated with overt aggression. However, little is known regarding the genetic pathways associated with relational aggression. Detecting genetic associates of relational aggression is important to eventually understand pathways to socially aggressive behaviors in children. Therefore, we attempted to determine if relational aggression was also associated with dopaminergic and serotonergic genes. We invited the parents of 327 children to complete a modified version of the MacArthur Health and Behavior Questionnaire (HBQ-P), which has a subscale for relational aggression. We used logistic regression models that predicted relational aggression after controlling for covariates. One genetic predictor was added at a time until there was no model improvement. The covariates were overt aggression scores obtained from the HBQ-P and age. The final (best) model included as a significant predictor of relational aggression one single nucleotide polymorphisms (SNP) on SLC6A3 (rs2617605) and the covariates.
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18

Ruddick, Jon P., Andrew K. Evans, David J. Nutt, Stafford L. Lightman, Graham A. W. Rook, and Christopher A. Lowry. "Tryptophan metabolism in the central nervous system: medical implications." Expert Reviews in Molecular Medicine 8, no. 20 (August 2006): 1–27. http://dx.doi.org/10.1017/s1462399406000068.

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The metabolism of the amino acid l-tryptophan is a highly regulated physiological process leading to the generation of several neuroactive compounds within the central nervous system. These include the aminergic neurotransmitter serotonin (5-hydroxytryptamine, 5-HT), products of the kynurenine pathway of tryptophan metabolism (including 3-hydroxykynurenine, 3-hydroxyanthranilic acid, quinolinic acid and kynurenic acid), the neurohormone melatonin, several neuroactive kynuramine metabolites of melatonin, and the trace amine tryptamine. The integral role of central serotonergic systems in the modulation of physiology and behaviour has been well documented since the first description of serotonergic neurons in the brain some 40 years ago. However, while the significance of the peripheral kynurenine pathway of tryptophan metabolism has also been recognised for several decades, it has only recently been appreciated that the synthesis of kynurenines within the central nervous system has important consequences for physiology and behaviour. Altered kynurenine metabolism has been implicated in the pathophysiology of conditions such as acquired immunodeficiency syndrome (AIDS)-related dementia, Huntington's disease and Alzheimer's disease. In this review we discuss the molecular mechanisms involved in regulating the metabolism of tryptophan and consider the medical implications associated with dysregulation of both serotonergic and kynurenine pathways of tryptophan metabolism.
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19

Gotoh, E., K. Murakami, T. D. Bahnson, and W. F. Ganong. "Role of brain serotonergic pathways and hypothalamus in regulation of renin secretion." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 253, no. 1 (July 1, 1987): R179—R185. http://dx.doi.org/10.1152/ajpregu.1987.253.1.r179.

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To investigate the role of brain serotonergic neurons in the regulation of renin secretion, we measured changes in plasma renin activity (PRA), and, in some instances, plasma renin concentration (PRC), plasma angiotensinogen, and plasma adrenocorticotropic hormone (ACTH) in rats with lesions of the dorsal raphe nucleus and lesions of the paraventricular nuclei, dorsomedial nuclei, and ventromedial nuclei of the hypothalamus. We also investigated the effects of p-chloroamphetamine (PCA), immobilization, head-up tilt, and a low-sodium diet in the rats with dorsal raphe, paraventricular, and dorsomedial lesions. Lesions of the dorsal raphe nucleus abolished the increase in PRA produced by PCA but had no effect on the increase produced by immobilization, head-up tilt, and a low-sodium diet. Paraventricular lesions, which abolish the increase in plasma ACTH produced by PCA, immobilization, and head-up tilt, decreased plasma angiotensinogen. The paraventricular lesions abolished the PRA and the PRC responses to PCA and the PRA but not PRC response to immobilization, head-up tilt, and a low-sodium diet. The ventromedial lesions abolished the PRA and PRC responses to PCA and did not reduce plasma angiotensinogen. The data suggest that paraventricular lesions depress angiotensinogen production by the liver and that the paraventricular and ventromedial nuclei are part of the pathway by which serotonergic discharges increase renin secretion. They also suggest that the serotonergic pathway does mediate the increases in renin secretion produced by immobilization, head-up tilt, and a low-sodium diet.
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20

Pawlak, Dariusz, Yumiko Takada, Tetsumei Urano, and Akikazu Takada. "Serotonergic and kynurenic pathways in rats exposed to foot shock." Brain Research Bulletin 52, no. 3 (June 2000): 197–205. http://dx.doi.org/10.1016/s0361-9230(00)00252-5.

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21

Harris, Lorri T., and Robert B. McCall. "GABA-serotonergic interactions in the regulation of central sympathetic pathways." European Journal of Pharmacology 128, no. 1-2 (August 1986): 133–36. http://dx.doi.org/10.1016/0014-2999(86)90567-4.

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22

Doihara, Hitoshi, Katsura Nozawa, Eri Kawabata-Shoda, Ryosuke Kojima, Toshihide Yokoyama, and Hiroyuki Ito. "TRPA1 agonists delay gastric emptying in rats through serotonergic pathways." Naunyn-Schmiedeberg's Archives of Pharmacology 380, no. 4 (July 24, 2009): 353–57. http://dx.doi.org/10.1007/s00210-009-0435-7.

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23

Sizemore, Tyler R., Laura M. Hurley, and Andrew M. Dacks. "Serotonergic modulation across sensory modalities." Journal of Neurophysiology 123, no. 6 (June 1, 2020): 2406–25. http://dx.doi.org/10.1152/jn.00034.2020.

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The serotonergic system has been widely studied across animal taxa and different functional networks. This modulatory system is therefore well positioned to compare the consequences of neuromodulation for sensory processing across species and modalities at multiple levels of sensory organization. Serotonergic neurons that innervate sensory networks often bidirectionally exchange information with these networks but also receive input representative of motor events or motivational state. This convergence of information supports serotonin’s capacity for contextualizing sensory information according to the animal’s physiological state and external events. At the level of sensory circuitry, serotonin can have variable effects due to differential projections across specific sensory subregions, as well as differential serotonin receptor type expression within those subregions. Functionally, this infrastructure may gate or filter sensory inputs to emphasize specific stimulus features or select among different streams of information. The near-ubiquitous presence of serotonin and other neuromodulators within sensory regions, coupled with their strong effects on stimulus representation, suggests that these signaling pathways should be considered integral components of sensory systems.
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24

Mishima, Yoshiyuki, and Shunji Ishihara. "Enteric Microbiota-Mediated Serotonergic Signaling in Pathogenesis of Irritable Bowel Syndrome." International Journal of Molecular Sciences 22, no. 19 (September 23, 2021): 10235. http://dx.doi.org/10.3390/ijms221910235.

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Irritable bowel syndrome (IBS) is a chronic functional disorder that affects the gastrointestinal tract. Details regarding the pathogenesis of IBS remain largely unknown, though the dysfunction of the brain-gut-microbiome (BGM) axis is a major etiological factor, in which neurotransmitters serve as a key communication tool between enteric microbiota and the brain. One of the most important neurotransmitters in the pathology of IBS is serotonin (5-HT), as it influences gastrointestinal motility, pain sensation, mucosal inflammation, immune responses, and brain activity, all of which shape IBS features. Genome-wide association studies discovered susceptible genes for IBS in serotonergic signaling pathways. In clinical practice, treatment strategies targeting 5-HT were effective for a certain portion of IBS cases. The synthesis of 5-HT in intestinal enterochromaffin cells and host serotonergic signaling is regulated by enteric resident microbiota. Dysbiosis can trigger IBS development, potentially through aberrant 5-HT signaling in the BGM axis; thus, the manipulation of the gut microbiota may be an alternative treatment strategy. However, precise information regarding the mechanisms underlying the microbiota-mediated intestinal serotonergic pathway related to the pathogenesis of IBS remains unclear. The present review summarizes current knowledge and recent progress in understanding microbiome–serotonin interaction in IBS cases.
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25

Glass, J. David, Allison J. Brager, Adam C. Stowie, and Rebecca A. Prosser. "Cocaine modulates pathways for photic and nonphotic entrainment of the mammalian SCN circadian clock." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 302, no. 6 (March 15, 2012): R740—R750. http://dx.doi.org/10.1152/ajpregu.00602.2011.

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Cocaine abuse is highly disruptive to circadian physiological and behavioral rhythms. The present study was undertaken to determine whether such effects are manifest through actions on critical photic and nonphotic regulatory pathways in the master circadian clock of the mouse suprachiasmatic nucleus (SCN). Impairment of SCN photic signaling by systemic (intraperitoneal) cocaine injection was evidenced by strong (60%) attenuation of light-induced phase-delay shifts of circadian locomotor activity during the early night. A nonphotic action of cocaine was apparent from its induction of 1-h circadian phase-advance shifts at midday. The serotonin receptor antagonist, metergoline, blocked shifting by 80%, implicating a serotonergic mechanism. Reverse microdialysis perfusion of the SCN with cocaine at midday induced 3.7 h phase-advance shifts. Control perfusions with lidocaine and artificial cerebrospinal fluid had little shifting effect. In complementary in vitro experiments, photic-like phase-delay shifts of the SCN circadian neuronal activity rhythm induced by glutamate application to the SCN were completely blocked by cocaine. Cocaine treatment of SCN slices alone at subjective midday, but not the subjective night, induced 3-h phase-advance shifts. Lidocaine had no shifting effect. Cocaine-induced phase shifts were completely blocked by metergoline, but not by the dopamine receptor antagonist, fluphenazine. Finally, pretreatment of SCN slices for 2 h with a low concentration of serotonin agonist (to block subsequent serotonergic phase resetting) abolished cocaine-induced phase shifts at subjective midday. These results reveal multiple effects of cocaine on adult circadian clock regulation that are registered within the SCN and involve enhanced serotonergic transmission.
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Smith, Howard. "Potential Analgesic Mechanisms of Acetaminophen." Pain Physician 1;12, no. 1;1 (January 14, 2009): 269–80. http://dx.doi.org/10.36076/ppj.2009/12/269.

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Despite nearing the end of the decade of pain research, the analgesic mechanisms of one of the most widely used and popular analgesics remains uncertain. Acetaminophen (APAP) (paracetamol [PARA]) has been used clinically for over a half of a century and although clinicians seem to be comfortable with its benefits, risks, and limitations, they still remain in the dark as to precisely what is providing its pain relief. What does seem clearer is that the predominant mechanisms of APAP’s analgesic effects are in the central nervous system (CNS). Although, which central effects are largely responsible for APAP’s effects on pain continue to be uncertain. Perhaps, the most accepted theory is that of APAP’s positive effects on the serotonergic descending inhibitory pathways. However, interactions with opioidergic systems, eicosanoid systems, and/or nitric oxide containing pathways may be involved as well. Furthermore, endocannabinoid signaling may play a role in APAP’s activation of the serotonergic descending inhibitory pathways. A greater understanding of APAP’s analgesic mechanisms may promote optimal utilization of analgesic polypharmacy. Key words: Acetaminophen (APAP), paracetamol (PARA), pain, analgesia, mechanisms of action, serotonin, opioids, endocannabinoids
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Saedisomeolia, Ahmad, Mahsa Samadi, Fatemeh Gholami, Marzieh Seyedi, Mohammad Effatpanah, Rezvan Hashemi, Mina Abdolahi, and Niyaz Mohammadzadeh Honarvar. "Vitamin D’s Molecular Action Mechanism in Attention-Deficit/ Hyperactivity Disorder: A Review of Evidence." CNS & Neurological Disorders - Drug Targets 17, no. 4 (July 6, 2018): 280–90. http://dx.doi.org/10.2174/1871527317666180501111627.

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Background & Objective: Attention-deficit/hyperactivity disorder (ADHD) is a heterogeneous disorder characterized by hyperactivity, impulsivity and inattention. Children with ADHD have challenges with learning, behavior and psychosocial adjustments, sometimes retained into adulthood. The exact etiology of ADHD is unknown, and the pathophysiology of this disease is complex. Several hypotheses have been raised regarding ADHD pathogenesis, including serotonergic and catecholaminergic signalling pathway dysfunction, neurotropic-related factors, oxidative stress, or neuroinflammation. Vitamin D has an important protective effect against inflammation, oxidative stress and certain neurotrophic factors and neurotransmitter, as well as facilitating dopaminergic and serotonergic functions. Vitamin D levels in children with ADHD are lower than in healthy children, and thus may be involved in the pathogenesis of ADHD. These observations, therefore, confirm the neuroprotective role of vitamin D through multiple molecular mechanisms and can be considered as a promising target in understanding ADHD pathology. Conclusion: In this context, the present study reviews the molecular pathways of vitamin D in ADHD patients.
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Pottoo, Faheem Hyder, Md Noushad Javed, Md Abul Barkat, Md Sabir Alam, Javaid Ashraf Nowshehri, Dhafer Mahdi Alshayban, and Mohammad Azam Ansari. "Estrogen and Serotonin: Complexity of Interactions and Implications for Epileptic Seizures and Epileptogenesis." Current Neuropharmacology 17, no. 3 (February 14, 2019): 214–31. http://dx.doi.org/10.2174/1570159x16666180628164432.

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A burgeoning literature documents the confluence of ovarian steroids and central serotonergic systems in the injunction of epileptic seizures and epileptogenesis. Estrogen administration in animals reduces neuronal death from seizures by up-regulation of the prosurvival molecule i.e. Bcl-2, anti-oxidant potential and protection of NPY interneurons. Serotonin modulates epileptiform activity in either direction i.e administration of 5-HT agonists or reuptake inhibitors leads to the activation of 5-HT3 and 5-HT1A receptors tending to impede focal and generalized seizures, while depletion of brain 5-HT along with the destruction of serotonergic terminals leads to expanded neuronal excitability hence abatement of seizure threshold in experimental animal models. Serotonergic neurotransmission is influenced by the organizational activity of steroid hormones in the growing brain and the actuation effects of steroids which come in adulthood. It is further established that ovarian steroids bring induction of dendritic spine proliferation on serotonin neurons thus thawing a profound effect on serotonergic transmission. This review features 5-HT1A and 5-HT3 receptors as potential targets for ameliorating seizure-induced neurodegeneration and recurrent hypersynchronous neuronal activity. Indeed 5-HT3 receptors mediate cross-talk between estrogenic and serotonergic pathways, and could be well exploited for combinatorial drug therapy against epileptogenesis.
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Zhou, Ligang, Todd Williams, Jennifer L. Lachey, Toshiro Kishi, Michael A. Cowley, and Lora K. Heisler. "Serotonergic pathways converge upon central melanocortin systems to regulate energy balance." Peptides 26, no. 10 (October 2005): 1728–32. http://dx.doi.org/10.1016/j.peptides.2004.12.028.

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Bock, Matthias, Barbara Sinner, Martin Göttlicher, Eckhart Simon, Eike Martin, and Johann Motsch. "Involvement of serotonergic pathways in postanaesthetic cold defence: dolasetron prevents shivering." Journal of Thermal Biology 27, no. 2 (April 2002): 159–66. http://dx.doi.org/10.1016/s0306-4565(01)00080-8.

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Barnes, Nicholas M., and John Gordon. "Harnessing serotonergic and dopaminergic pathways for lymphoma therapy: Evidence and aspirations." Seminars in Cancer Biology 18, no. 3 (June 2008): 218–25. http://dx.doi.org/10.1016/j.semcancer.2007.12.007.

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Marshall, Sara E., Tom G. Bird, Keith Hart, and Kenneth I. Welsh. "Unified approach to the analysis of genetic variation in serotonergic pathways." American Journal of Medical Genetics 88, no. 6 (December 15, 1999): 621–27. http://dx.doi.org/10.1002/(sici)1096-8628(19991215)88:6<621::aid-ajmg9>3.0.co;2-h.

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Yanarates, Omer, Ahmet Dogrul, Vedat Yildirim, Altan Sahin, Ali Sizlan, Melik Seyrek, Özgür Akgül, Orhan Kozak, Ercan Kurt, and Ulku Aypar. "Spinal 5-HT7 Receptors Play an Important Role in the Antinociceptive and Antihyperalgesic Effects of Tramadol and Its Metabolite, O-Desmethyltramadol, via Activation of Descending Serotonergic Pathways." Anesthesiology 112, no. 3 (March 1, 2010): 696–710. http://dx.doi.org/10.1097/aln.0b013e3181cd7920.

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Background Tramadol is an analgesic drug, and its mechanism of action is believed to be mediated by the mu-opioid receptor. A further action of tramadol has been identified as blocking the reuptake of serotonin (5-HT). One of the most recently identified subtypes of 5-HT receptor is the 5-HT7 receptor. Thus, the authors aimed to examine the potential role of serotonergic descending bulbospinal pathways and spinal 5-HT7 receptors compared with that of the 5-HT2A and 5-HT3 receptors in the antinociceptive and antihyperalgesic effects of tramadol and its major active metabolite O-desmethyltramadol (M1) on phasic and postoperative pain models. Methods Nociception was assessed by the radiant heat tail-flick and plantar incision test in male Balb-C mice (25-30 g). The serotonergic pathways were lesioned with an intrathecal injection of 5,7-dihydroxytryptamine. The selective 5-HT7, 5-HT2, and 5-HT3 antagonists; SB-269970 and SB-258719; ketanserin and ondansetron were given intrathecally. Results Systemically administered tramadol and M1 produced antinociceptive and antihyperalgesic effects. The antinociceptive effects of both tramadol and M1 were significantly diminished in 5-HT-lesioned mice. Intrathecal injection of SB-269970 (10 microg) and SB-258719 (20 microg) blocked both tramadol- and M1-induced antinociceptive and antihyperalgesic effects. Ketanserin (20 mumicrog) and ondansetron (20 microg) were unable to reverse the antinociceptive and antihyperalgesic effects of tramadol and M1. Conclusions These findings suggest that the descending serotonergic pathways and spinal 5-HT7 receptors play a crucial role in the antinociceptive and antihyperalgesic effects of tramadol and M1.
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Loonen, Anton J. M., and Svetlana A. Ivanova. "New insights into the mechanism of drug-induced dyskinesia." CNS Spectrums 18, no. 1 (December 20, 2012): 15–20. http://dx.doi.org/10.1017/s1092852912000752.

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Dyskinesia is an extrapyramidal movement disorder characterized by involuntary, repetitive, irregular motions that affect the mouth and face and/or the limbs and trunk. Tardive dyskinesia (TD) is a well-known complication of long-term treatment with antipsychotic drugs. Dyskinesia is also induced with levodopa, a treatment for Parkinson's disease, and it occurs spontaneously as a symptom of Huntington's disease. Research on the pathogenesis of TD has focused on a dysfunction of either the dopaminergic or serotonergic system. However, recent evidence has suggested that we should focus on the possible damage of GABAergic medium spiny neurons (MSNs). MSNs are the first station in the cortico-striato-thalamo-cortical circuit that regulates the amplitude and velocity of movements. Two pathways can be distinguished in this circuit: a direct pathway, which increases movements (hyperkinesia), and an indirect pathway, which decreases movements (hypokinesia). Both pathways are activated by glutamatergic corticostriatal neurons. Here, we discuss some evidence that supports the hypothesis that indirect pathway MSNs are damaged in dyskinesia.
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Li, James J. "Assessing the interplay between multigenic and environmental influences on adolescent to adult pathways of antisocial behaviors." Development and Psychopathology 29, no. 5 (November 22, 2017): 1947–67. http://dx.doi.org/10.1017/s0954579417001511.

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AbstractThe current investigation utilized a developmental psychopathology approach to test the hypothesis that multigenic (i.e., dopaminergic and serotonergic genes) and multienvironmental factors interactively contribute to developmental pathways of antisocial behavior (ASB). A sample of 8,834 Caucasian individuals from the National Longitudinal Study of Adolescent to Adult Health (Add Health) were used to (a) examine the developmental pathways of ASB from age 13 to 32 using growth mixture modeling, (b) compute weighted multigenic risk scores (Add Health MRS) for ASB from six well-characterized polymorphisms in dopamine and serotonin genes, and (c) test the interaction between the Add Health MRS and a measures of support (incorporating indicators of both positive and negative support from parents and schools). Four pathways of adolescent to adult ASB emerged from the growth mixture models: low, adolescence-peaked, high decline, and persistent. Add Health MRS predicted the persistent ASB pathway, but not other ASB pathways. Males with high Add Health MRS, but not low MRS, had significantly greater odds of being in the adolescence-peaked pathway relative to the low pathway at low levels of school connectedness. Nonfamilial environmental influences during adolescence may have a cumulative impact on the development of ASB, particularly among males with greater underlying genetic risks.
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Marinesco, Stéphane, Nimalee Wickremasinghe, Kristine E. Kolkman, and Thomas J. Carew. "Serotonergic Modulation in Aplysia. II. Cellular and Behavioral Consequences of Increased Serotonergic Tone." Journal of Neurophysiology 92, no. 4 (October 2004): 2487–96. http://dx.doi.org/10.1152/jn.00210.2004.

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Serotonin (5-HT) plays an important role in sensitization of defensive reflexes in Aplysia and is also involved in several aspects of arousal, such as the control of locomotion and of cardiovascular tone. In the preceding paper, we showed that tail-nerve shock, a noxious stimulus that readily induces sensitization, increases the firing rate of a large number of serotonergic neurons throughout the CNS. However, the functional consequences of such an increase in serotonergic tone are still poorly understood. In this study, we examined this question by using the 5-HT precursor 5-hydroxytryptophan (5-HTP) to specifically increase 5-HT release in the CNS. Increased tonic 5-HT release after 5-HTP treatment was manifested by facilitation of sensorimotor (SN-MN) synapses, increased firing rate of serotonergic neurons in the pedal and abdominal ganglia, and enhanced 5-HT release evoked by tail-nerve shock. When 5-HTP was administered to freely moving animals, it produced a strong arousal response characterized by increased locomotion and heart rate, which was reminiscent of the defensive arousal reaction triggered by noxious stimulation such as tail-shock. In contrast, 5-HTP actually inhibited the tail-induced siphon-withdrawal reflex. It is possible that 5-HT-induced facilitation of SN-MN synapses was counteracted by inhibition of polysynaptic reflex pathways between SNs and MNs, resulting in transient behavioral inhibition of the reflex, which could favor escape locomotion and/or respiration shortly after an aversive stimulus. We conclude that a major function associated with the activation of the Aplysia serotonergic system evoked by noxious stimuli is the triggering of a defensive arousal response. It is known that tail-shock-induced serotonergic activation contributes to memory encoding at least in part by facilitating SN-MN synapses. However, this effect in isolation might not be sufficient for the behavioral expression of sensitization.
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Ślifirski, Grzegorz, Marek Król, and Jadwiga Turło. "5-HT Receptors and the Development of New Antidepressants." International Journal of Molecular Sciences 22, no. 16 (August 20, 2021): 9015. http://dx.doi.org/10.3390/ijms22169015.

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Serotonin modulates several physiological and cognitive pathways throughout the human body that affect emotions, memory, sleep, and thermal regulation. The complex nature of the serotonergic system and interactions with other neurochemical systems indicate that the development of depression may be mediated by various pathomechanisms, the common denominator of which is undoubtedly the disturbed transmission in central 5-HT synapses. Therefore, the deliberate pharmacological modulation of serotonergic transmission in the brain seems to be one of the most appropriate strategies for the search for new antidepressants. As discussed in this review, the serotonergic system offers great potential for the development of new antidepressant therapies based on the combination of SERT inhibition with different pharmacological activity towards the 5-HT system. The aim of this article is to summarize the search for new antidepressants in recent years, focusing primarily on the possibility of benefiting from interactions with various 5-HT receptors in the pharmacotherapy of depression.
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Cordeiro, Quirino, and Homero Vallada. "Lack of association between the G681C polimorphism in the 5-HT1Dbeta autoreceptor gene and schizophrenia." Arquivos de Neuro-Psiquiatria 63, no. 2b (June 2005): 380–82. http://dx.doi.org/10.1590/s0004-282x2005000300002.

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A major role of the serotonergic system has been hypothesized in the pathogenesis of schizophrenia, mostly based on the evidence of action of atypical antipsychotics. Disturbances of serotonergic pathways have been implicated in the etiology of schizophrenia. The aim of this study was to investigate the association between schizophrenia and the G861C polymorphism in the 5-HT1Dbeta autoreceptor gene. There was conducted a case-control analysis in a sample of 196 schizophrenic patients and 143 gender, age and ethnic matched controls. No statistically differences were found in allelic or genotypic distributions between cases and controls. Thus, the results do not support an association of the G861C polymorphism in the 5-HT1Dbeta autoreceptor gene with schizophrenia in the studied sample.
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Jagannathan, Ram, Azizi Seixas, David St-Jules, Lakshmanan Jagannathan, April Rogers, Lu Hu, Girardin Jean-Louis, and Mary Ann Sevick. "Systems Biology Genetic Approach Identifies Serotonin Pathway as a Possible Target for Obstructive Sleep Apnea: Results from a Literature Search Review." Sleep Disorders 2017 (2017): 1–8. http://dx.doi.org/10.1155/2017/6768323.

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Rationale. Overall validity of existing genetic biomarkers in the diagnosis of obstructive sleep apnea (OSA) remains unclear. The objective of this systematic genetic study is to identify “novel” biomarkers for OSA using systems biology approach. Methods. Candidate genes for OSA were extracted from PubMed, MEDLINE, and Embase search engines and DisGeNET database. The gene ontology (GO) analyses and candidate genes prioritization were performed using Enrichr tool. Genes pertaining to the top 10 pathways were extracted and used for Ingenuity Pathway Analysis. Results. In total, we have identified 153 genes. The top 10 pathways associated with OSA include (i) serotonin receptor interaction, (ii) pathways in cancer, (iii) AGE-RAGE signaling in diabetes, (iv) infectious diseases, (v) serotonergic synapse, (vi) inflammatory bowel disease, (vii) HIF-1 signaling pathway, (viii) PI3-AKT signaling pathway, (ix) regulation lipolysis in adipocytes, and (x) rheumatoid arthritis. After removing the overlapping genes, we have identified 23 candidate genes, out of which >30% of the genes were related to the genes involved in the serotonin pathway. Among these 4 serotonin receptors SLC6A4, HTR2C, HTR2A, and HTR1B were strongly associated with OSA. Conclusions. This preliminary report identifies several potential candidate genes associated with OSA and also describes the possible regulatory mechanisms.
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Menani, J. V., and A. K. Johnson. "Lateral parabrachial serotonergic mechanisms: angiotensin-induced pressor and drinking responses." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 269, no. 5 (November 1, 1995): R1044—R1049. http://dx.doi.org/10.1152/ajpregu.1995.269.5.r1044.

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This study investigated the effects of bilateral injections of serotonergic receptor ligands into the lateral parabrachial nucleus (LPBN) on the pressor and dipsogenic responses induced by intracerebroventricular (i.c.v.) injection of angiotensin II (ANG II). Rats with stainless steel cannulas implanted bilaterally into the LPBN and into the left lateral ventricle were used to study i.c.v. ANG II-induced water intake and pressor responses. Pretreatment with the serotonergic 5-HT1/5-HT2 receptor antagonist methysergide (1-8 micrograms/200 nl) bilaterally injected into the LPBN increased the water intake induced by i.c.v. ANG II (50 ng/microliters) administered via the lateral ventricle, but pretreatment with methysergide (4 micrograms/200 nl) did not change the pressor response produced by i.c.v. ANG II. After bilateral injection of either serotonin (5-HT, 5 micrograms/200 nl) or the serotonergic 5-HT2a/5-HT2c receptor agonist (+/-)-2,5-dimetoxy-4-iodoamphetamine hydrochloride (DOI; 0.5-10 micrograms/200 nl) into the LPBN, the water intake induced by ANG II was significantly reduced. These results are consistent with Other observations indicating that the LPBN is associated with inhibitory mechanisms controlling water intake induced by ANG II treatment and suggest that serotonergic pathways may be involved in this effect.
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Carmo, Helena, Fernando Remião, Félix Carvalho, Eduarda Fernandes, Douwe de Boer, Lesseps A. dos Reys, and Maria de Lourdes Bastos. "4-methylthioamphetamine-induced hyperthermia in mice: influence of serotonergic and catecholaminergic pathways." Toxicology and Applied Pharmacology 190, no. 3 (August 2003): 262–71. http://dx.doi.org/10.1016/s0041-008x(03)00190-x.

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42

Dogrul, Ahmet, Melik Seyrek, Bulent Yalcin, and Ahmet Ulugol. "Involvement of descending serotonergic and noradrenergic pathways in CB1 receptor-mediated antinociception." Progress in Neuro-Psychopharmacology and Biological Psychiatry 38, no. 1 (July 2012): 97–105. http://dx.doi.org/10.1016/j.pnpbp.2012.01.007.

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43

Berge, Odd-Geir, Ole Bernt Fasmer, Lars Tveiten, and Kjell Hole. "Selective Neurotoxic Lesions of Descending Serotonergic and Noradrenergic Pathways in the Rat." Journal of Neurochemistry 44, no. 4 (April 1985): 1156–61. http://dx.doi.org/10.1111/j.1471-4159.1985.tb08738.x.

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44

Alekseyenko, Olga V., Yick-Bun Chan, Benjamin W. Okaty, YoonJeung Chang, Susan M. Dymecki, and Edward A. Kravitz. "Serotonergic Modulation of Aggression in Drosophila Involves GABAergic and Cholinergic Opposing Pathways." Current Biology 29, no. 13 (July 2019): 2145–56. http://dx.doi.org/10.1016/j.cub.2019.05.070.

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45

�gren, Sven Ove, Odd-Geir Berge, and Christina Johansson. "Involvement of spinal serotonergic pathways in nociception but not in avoidance learning." Psychopharmacology 87, no. 3 (November 1985): 260–65. http://dx.doi.org/10.1007/bf00432704.

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Izquierdo, Patricia G., Fernando Calahorro, and Manuel Ruiz-Rubio. "Neuroligin modulates the locomotory dopaminergic and serotonergic neuronal pathways of C. elegans." neurogenetics 14, no. 3-4 (October 8, 2013): 233–42. http://dx.doi.org/10.1007/s10048-013-0377-6.

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Hunskaar, Steinar, Jan Henrik Rosland, and Kjell Hole. "Mechanisms of orhenadrine-induced antinociception in mice: a role for serotonergic pathways." European Journal of Pharmacology 160, no. 1 (January 1989): 83–91. http://dx.doi.org/10.1016/0014-2999(89)90656-0.

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48

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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Todurga, Zeynep Gizem, Ozgur Gunduz, Cetin Hakan Karadag, and Ahmet Ulugol. "Descending serotonergic and noradrenergic systems do not regulate the antipruritic effects of cannabinoids." Acta Neuropsychiatrica 28, no. 6 (April 8, 2016): 321–26. http://dx.doi.org/10.1017/neu.2016.16.

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BackgroundFor centuries, cannabinoids have been known to be effective in pain states. Itch and pain are two sensations sharing a lot in common.ObjectiveThe goal of this research was to observe whether the cannabinoid agonist WIN 55,212-2 reduces serotonin-induced scratching behaviour and whether neurotoxic destruction of descending serotonergic and noradrenergic pathways mediate the antipruritic effect of WIN 55,212-2.Material and methodsScratching behaviour was induced by intradermal injection of serotonin (50 µg/50 µl/mouse) to Balb/c mice. The neurotoxins 5,7-dihydroxytryptamine (5,7-DHT, 50 μg/mouse) and 6-hydroxydopamine (6-OHDA, 20 μg/mouse) are applied intrathecally to deplete serotonin and noradrenaline in the spinal cord. WIN 55,212-2 (1, 3, 10 mg/kg, i.p.) dose-dependently attenuated serotonin-induced scratches. Neurotoxic destruction of neither the serotonergic nor the noradrenergic systems by 5,7-DHT and 6-OHDA, respectively, had any effect on the antipruritic action of WIN 55,212-2.ConclusionOur findings indicate that cannabinoids dose-dependently reduce serotonin-induced scratching behaviour and neurotoxic destruction of descending inhibitory pathways does not mediate this antipruritic effect.
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Francescangeli, James, Kunal Karamchandani, Meghan Powell, and Anthony Bonavia. "The Serotonin Syndrome: From Molecular Mechanisms to Clinical Practice." International Journal of Molecular Sciences 20, no. 9 (May 9, 2019): 2288. http://dx.doi.org/10.3390/ijms20092288.

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The serotonin syndrome is a medication-induced condition resulting from serotonergic hyperactivity, usually involving antidepressant medications. As the number of patients experiencing medically-treated major depressive disorder increases, so does the population at risk for experiencing serotonin syndrome. Excessive synaptic stimulation of 5-HT2A receptors results in autonomic and neuromuscular aberrations with potentially life-threatening consequences. In this review, we will outline the molecular basis of the disease and describe how pharmacologic agents that are in common clinical use can interfere with normal serotonergic pathways to result in a potentially fatal outcome. Given that serotonin syndrome can imitate other clinical conditions, an understanding of the molecular context of this condition is essential for its detection and in order to prevent rapid clinical deterioration.
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