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1
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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Bush, V. L., D. N. Middlemiss, C. A. Marsden, and K. C. F. Fone. "Implantation of a Slow Release Corticosterone Pellet Induces Long-Term Alterations in Serotonergic Neurochemistry in the Rat Brain." Journal of Neuroendocrinology 15, no. 6 (April 28, 2003): 607–13. http://dx.doi.org/10.1046/j.1365-2826.2003.01034.x.
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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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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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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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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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D'Mello, Charlotte, and Mark G. Swain. "Liver-brain inflammation axis." American Journal of Physiology-Gastrointestinal and Liver Physiology 301, no. 5 (November 2011): G749—G761. http://dx.doi.org/10.1152/ajpgi.00184.2011.
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It is becoming increasingly evident that peripheral organ-centered inflammatory diseases, including chronic inflammatory liver diseases, are associated with changes in central neural transmission that result in alterations in behavior. These behavioral changes include sickness behaviors, such as fatigue, cognitive dysfunction, mood disorders, and sleep disturbances. While such behaviors have a significant impact on quality of life, the changes within the brain and the communication pathways between the liver and the brain that give rise to changes in central neural activity are not fully understood. Traditionally, neural and humoral communication pathways have been described, with the three cytokines TNFα, IL-1β, and IL-6 receiving the most attention in mediating communication between the periphery and the brain, in the setting of peripheral inflammation. However, more recently, we described an immune-mediated communication pathway in experimentally induced liver inflammation whereby, in response to activation of resident immune cells in the brain (i.e., the microglia), peripheral circulating monocytes transmigrate into the brain, leading to development of sickness behaviors. These signaling pathways drive changes in behavior by altering central neurotransmitter systems. Specifically, changes in serotonergic and corticotropin-releasing hormone neurotransmission have been demonstrated and implicated in liver inflammation-associated sickness behaviors. Understanding how the liver communicates with the brain in the setting of chronic inflammatory liver diseases will help delineate novel therapeutic targets that can reduce the burden of symptoms in patients with liver disease.
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Frawley, P. Joseph. "Neurobehavioral Model of Addiction." Journal of Drug Issues 17, no. 1 (January 1987): 29–46. http://dx.doi.org/10.1177/002204268701700103.
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A model is presented which shows addiction as a disease resulting from the involuntary adaptation of the nervous system to a drug. The ability of various addictive drugs to mimic neurotransmitters results not only in biochemical adaptation of these neurochemicals and other chemical elements of the brain but also programmed/trained/physically enhanced nervous pathways involved in drug-seeking behavior and weakened or inhibited pathways leading to non-chemical rewards. Recovery involves removal of the chemical and retraining the survival system. Counterconditioning retrains the system that the drug doesn't work. Counseling/support and positive training/experience teach the system that the individual does work. The model reviews the role of genetics, neurochemistry, conditioning, self-esteem, family, support and therapy in the progression of disease and its recovery.
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Holmes, Ben, Seung Ho Jung, Jing Lu, Jessica A. Wagner, Liudmilla Rubbi, Matteo Pellegrini, and Ryan Jankord. "Transcriptomic Modification in the Cerebral Cortex following Noninvasive Brain Stimulation: RNA-Sequencing Approach." Neural Plasticity 2016 (2016): 1–15. http://dx.doi.org/10.1155/2016/5942980.
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Transcranial direct current stimulation (tDCS) has been shown to modulate neuroplasticity. Beneficial effects are observed in patients with psychiatric disorders and enhancement of brain performance in healthy individuals has been observed following tDCS. However, few studies have attempted to elucidate the underlying molecular mechanisms of tDCS in the brain. This study was conducted to assess the impact of tDCS on gene expression within the rat cerebral cortex. Anodal tDCS was applied at 3 different intensities followed by RNA-sequencing and analysis. In each current intensity, approximately 1,000 genes demonstrated statistically significant differences compared to the sham group. A variety of functional pathways, biological processes, and molecular categories were found to be modified by tDCS. The impact of tDCS on gene expression was dependent on current intensity. Results show that inflammatory pathways, antidepressant-related pathways (GTP signaling, calcium ion binding, and transmembrane/signal peptide pathways), and receptor signaling pathways (serotonergic, adrenergic, GABAergic, dopaminergic, and glutamate) were most affected. Of the gene expression profiles induced by tDCS, some changes were observed across multiple current intensities while other changes were unique to a single stimulation intensity. This study demonstrates that tDCS can modify the expression profile of various genes in the cerebral cortex and that these tDCS-induced alterations are dependent on the current intensity applied.
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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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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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Meng, Ying, Susan W. Groth, Joyce A. Smith, and Harriet Kitzman. "2125 What genes are involved in the brain food reward circuitry: Findings from a large candidate gene analysis." Journal of Clinical and Translational Science 2, S1 (June 2018): 36. http://dx.doi.org/10.1017/cts.2018.149.
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OBJECTIVES/SPECIFIC AIMS: The food reward circuitry regulates hedonic eating especially in relation to palatable hypercaloric foods, which can lead to chronic overeating and consequent overweight and obesity. Evidence supports that there is considerable overlap within the brain reward circuitry between palatable hypercaloric food intake and substance addiction. The goal of this study was to identify associations between addiction-related genes and body mass index. We hypothesized that addiction-related genes potentially participate in the food reward circuitry if they are associated with obesity traits. METHODS/STUDY POPULATION: A secondary analysis was conducted with 1093 African American adolescents and young adults from the New Mother’s Study. Anthropometric, genetic, demographic and lifestyle measurements were available at the 18-year follow-up assessments. A total of 1350 single nucleotide polymorphisms mapped to 127 addiction-related genes were assessed. A total of 186 ancestry informative markers were used to adjust for population stratification. Generalized estimating equation models were used to identify genetic associations, including additive, dominant, and recessive models, and control for correlations within families. RESULTS/ANTICIPATED RESULTS: The participants ranged from 15 to 23 years of age. Of them, 42.7% were overweight or obese. Significant associations with body mass index were identified for 13 single nucleotide polymorphisms mapped to 11 addiction-related genes, including LEP (p 0.027–<0.001). Most of these genes are involved in dopaminergic, opioidergic, serotonergic pathways, and stress. DISCUSSION/SIGNIFICANCE OF IMPACT: Our results support the role of dopaminergic and opioidergic pathways in the food reward circuitry, and suggest a potential involvement of serotonergic pathways and genes related to stress in the food reward circuitry. Further investigation of the identified genes will facilitate delineation and understanding of the brain food reward system and its relationship with obesity.
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Monteiro, Bárbara C., Suzana Monteiro, Maristela Candida, Nathalia Adler, Flavia Paes, Nuno Rocha, Antonio Egidio Nardi, Eric Murillo-Rodriguez, and Sergio Machado. "Relationship Between Brain-Derived Neurotrofic Factor (Bdnf) and Sleep on Depression: A Critical Review." Clinical Practice & Epidemiology in Mental Health 13, no. 1 (November 21, 2017): 213–19. http://dx.doi.org/10.2174/1745017901713010213.
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The Brain-Derived Neurotrofic Factor (BDNF) is one of the most important neurotrophins in the brain and it is suggested influences the activity of the serotonergic, noradrenergic and dopaminergic pathways. In the last few years, it has been hypothesized that BDNF level is related with depression and sleep. Several studies show that depressive subjects present low levels of BDNF in the brain. Poor sleep quality is also related with alterations in the BDNF concentration. Some authors argue that most of the cases show that impaired sleep quality increases the stress and, consequently, the vulnerability to depressive disorders, suggesting that there is a relationship between sleep, depression and BDNF levels.
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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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Maron, Eduard, Jakov Shlik, and David J. Nutt. "Tryptophan Research in Panic Disorder." International Journal of Tryptophan Research 1 (January 2008): IJTR.S929. http://dx.doi.org/10.4137/ijtr.s929.
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A considerable body of evidence suggests the involvement of serotonin neurotransmission in the pathogenesis of panic disorder. Research on pathways and functions of tryptophan, an essential amino acid converted into serotonin, may advance our understanding of serotonergic actions in panic disorder and related phenomena. The investigative approaches in this field include manipulations of tryptophan availability as well as genetic association and functional brain imaging studies. In this review we examine the principle findings of these studies and propose further research directions.
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Bertola, Vivian, Quirino Cordeiro, Stevin Zung, Elisabete Cristina Miracca, and Homero Vallada. "Association analysis between the C516T polymorphism in the 5-HT2A receptor gene and schizophrenia." Arquivos de Neuro-Psiquiatria 65, no. 1 (March 2007): 11–14. http://dx.doi.org/10.1590/s0004-282x2007000100004.
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Data from epidemiological studies have demonstrated that genetics is an important risk factor for schizophrenia. Disturbances of serotonergic brain pathways have been implicated in the pathophysiology of schizophrenia. Some studies have suggested that the efficacy of atypical antipsychotics on schizophrenia treatment may be related to the serotonin 2A receptor (5-HT2A), and that serotonergic drugs may induce psychotic symptoms. Thus, the aim of this study was to investigate the association between the C516T polymorphism and schizophrenia in a Brazilian population composed by 246 patients and 315 healthy matched controls in a case-control approach. No statistically differences were observed in allelic (chi2=1.77, 1d.f., p=0.18) or genotypic (chi2=1.69, 2d.f., p=0.42) distributions between cases and controls. The results suggest that the C516T polymorphism of the 5-HT2A receptor gene is not related to the susceptibility for schizophrenia in our Brazilian sample.
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Westenberg, Herman G. M., Naomi A. Fineberg, and Damiaan Denys. "Neurobiology of Obsessive-Compulsive Disorder: Serotonin and Beyond." CNS Spectrums 12, S3 (February 2007): 14–27. http://dx.doi.org/10.1017/s1092852900002479.
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AbstractThe evidence for the involvement of the serotonergic system in the pathogenesis of obsessive-compulsive disorder (OCD) is circumstantial at best, despite being the focus for most pathophysiological research over the last 2 decades. This hypothesis was initially motivated by the observed differential efficacy of selective serotonin reuptake inhibitors in alleviating OCD symptoms. Direct evidence that serotonergic perturbations are implicated in the pathophysiology of OCD is still sparse. There is growing evidence, from both preclinical and clinical studies, that the dopamine system may also be involved in the pathogenesis of OCD, and that dopaminergic and serotonergic pathways play a role in the genesis and maintenance of obsessive-compulsive symptoms. The complex interactions between both systems, the phenotypic heterogeneity of the disorder, and the limitations of the available tests to probe both systems, make it as yet impossible to draw firm conclusions as to how these systems are implicated. Further studies with more selective pharmacologic agents and neurocognitive probes in humans, studies using deep brain stimulation in combination with neuroimaging, and the development of better animal models for OCD may further our understanding of this disabling condition.
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Fisher, Patrick M., and Ahmad R. Hariri. "Identifying serotonergic mechanisms underlying the corticolimbic response to threat in humans." Philosophical Transactions of the Royal Society B: Biological Sciences 368, no. 1615 (April 5, 2013): 20120192. http://dx.doi.org/10.1098/rstb.2012.0192.
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A corticolimbic circuit including the amygdala and medial prefrontal cortex (mPFC) plays an important role in regulating sensitivity to threat, which is heightened in mood and anxiety disorders. Serotonin is a potent neuromodulator of this circuit; however, specific serotonergic mechanisms mediating these effects are not fully understood. Recent studies have evaluated molecular mechanisms mediating the effects of serotonin signalling on corticolimbic circuit function using a multi-modal neuroimaging strategy incorporating positron emission tomography and blood oxygen level-dependent functional magnetic resonance imaging. This multi-modal neuroimaging strategy can be integrated with additional techniques including imaging genetics and pharmacological challenge paradigms to more clearly understand how serotonin signalling modulates neural pathways underlying sensitivity to threat. Integrating these methodological approaches offers novel opportunities to identify mechanisms through which serotonin signalling contributes to differences in brain function and behaviour, which in turn can illuminate factors that confer risk for illness and inform the development of more effective treatment strategies.
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Quirion, Rémi. "Atrial Natriuretic Factors and the Brain (Les facteurs natriurétiques auriculaires et le cerveau)." Canadian Journal of Physiology and Pharmacology 66, no. 3 (March 1, 1988): 253–54. http://dx.doi.org/10.1139/y88-043.
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Canadian scientists have played a major role in the discovery and characterization of various atrial natriuretic factors (ANF). It is now clear that this family of polypeptides induces multiple biological actions in a broad variety of peripheral tissues including the kidney, adrenal gland, and blood vessels. One generalized observation derived from multiple studies reveals that these peptides most likely act as important modulators of homeostasis by modulating the production of various body fluids. Recently, it became clear that the atrial natriuretic factors present in the central nervous system could influence various brain functions. Thus, the ANF-like peptides should be considered as a new family of brain–heart peptides.The present symposium, the first of its kind, was organized to examine and critically discuss the evidence for putative roles of atrial natriuretic peptides in the brain. It was clearly demonstrated that atrial natriuretic peptide-like immunoreactivity is widely distributed in mammalian and nonmammalian brains with a high number of cell bodies and (or) fiber terminals present in areas associated with water and salt intake and with the control of cardiovascular parameters. The gene transcripts responsible for the production of brain atrial natriuretic polypeptides have been isolated and their characteristics appear to be similar to those found in peripheral tissues. The presence and plasticity of specific brain ANF receptor sites have also been reported. It appears that at least one population of sites is associated with the activation of guanylate cyclase and it was also shown that specific ANF receptors are located on brain microvessels and can modulate the permeability of the blood-brain barrier. Finally, it has been shown that atrial natriuretic polypeptides exert various biological actions in the brain including electrophysiological effects in the hypothalamus, modulation of water and salt intake, alteration of various cardiovascular parameters, and release of certain pituitary hormones.Interactions with dopaminergic pathways, vasopressin, and (or) angiotensin II systems could be associated with some biological effects of atrial natriuretic peptides in the brain. Naturally, much remains to be known on the exact physiological role of brain atrial natriuretic factors, but this meeting represents the first attempt towards the integration of the most recent findings in this exciting research area.This symposium was an official satellite of the first joint meeting of the International Society for Neurochemistry and the American Society for Neurochemistry, held in Venezuela in May–June 1987. The success of the symposium has been ensured by generous donations from the International Society for Neurochemistry, the Medical Research Council of Canada, and various companies including Amersham International (England), ANAWA Trading SA (Switzerland), Ayerst Laboratories (U.S.A.), Bachem (Switzerland), Bayer AG (West Germany), Bio-Mega Inc. (Canada), Ciba-Geigy Corporation (U.S.A.), Dupont Canada – New England Nuclear Co. (Canada), Eli Lilly Research Laboratories (U.S.A.), Farmitalia Carlo Erba (Italy), Institut Henri Beaufour (France), Merck Sharp &Dohme Research Laboratories (U.S.A.), Miles Laboratories Inc. (U.S.A.), Monsanto Co. (U.S.A.), Novabiochem (Switzerland), Novopharm Ltd. (Canada), Peninsula Laboratories (U.S.A.), and the Peptide Institute and Protein Research Foundation (Japan).
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Reis, L. C., A. C. Almeida, P. L. Cedraz-Mercez, E. L. Olivares, A. Marinho Jr., and C. M. Thomaz. "Evidence indicating participation of the serotonergic system in controlling feeding behavior in Coturnix japonica (Galliformes: Aves)." Brazilian Journal of Biology 65, no. 2 (May 2005): 353–61. http://dx.doi.org/10.1590/s1519-69842005000200020.
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We investigated participation of the brain serotonergic system in food intake control by using oral and systemic administration of serotonin precursors in quails (Coturnix japonica). Dietary supplemental tryptophan (0.1-50.0 g/kg) provoked a dose-dependent inhibition of food intake during a 5-h observation period, which persisted up to 24 h for doses of 30.0 and 50.0 g/kg. Normally fed and fasted animals treated with hydroxytryptophan (12.5-50.0 mg/kg) by the intracoelomic route showed an acute inhibition of food intake. Hypophagia in fasted birds was only effective when the precursor was administered immediately before food presentation. A similar response was obtained by administering serotonin (0.125-2.5 mg/kg, sc), with animals showing a hypnogenic response within the first ten minutes after administration, suggesting that, in contrast to mammals, the amine crosses the blood-brain barrier in quails. Administration of hydroxytryptophan at all doses tested induced significant dipsogenic behavior despite the concomitant hypnogenic response. The results suggest the involvement of serotonergic pathways in food intake control in quails and also show, for the first time, hypnogenic action induced by serotonin and a hyperdipsic effect elicited by hydroxytryptophan.
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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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Anwar-Mohamed, Anwar, Osama H. Elshenawy, Ahmed A. El-Sherbeni, Mohamed Abdelrady, and Ayman O. S. El-Kadi. "Acute arsenic treatment alters arachidonic acid and its associated metabolite levels in the brain of C57Bl/6 mice." Canadian Journal of Physiology and Pharmacology 92, no. 8 (August 2014): 693–702. http://dx.doi.org/10.1139/cjpp-2014-0136.
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The toxic effects of arsenic on the whole brain, as well as the discrete regions, has been previously reported for mice. We investigated the effects of acute arsenite (As(III)) on brain levels of arachidonic acid (AA) and its associated metabolites generated through cytochrome P450 (CYP), cyclooxygenase (COX), and lipoxygenase (LOX) pathways. Our results demonstrated that acute As(III) treatment (12.5 mg·(kg body mass)−1) decreases cytosolic phospholipase A2 (cPLA2) with a subsequent decrease in its catalytic activity and brain AA levels. In addition, As(III) differentially altered CYP epoxygenases and CYP ω-hydroxylases, but it did not affect brain Ephx2 mRNA or sEH catalytic activity levels. As(III)-mediated effects on Cyps caused an increase in brain 5,6-epoxyeicosatrienoic acid (5,6-EET) and 16/17-hydroxyeicosatetreinoic acid (16/17-HETE) levels, and a decrease in 18- and 20-HETE levels. Furthermore, As(III) increased cyclooxygenase-2 (COX-2) mRNA while decreasing prostaglandins F2α (PGF2α) and PGJ2. As(III) also increased brain 5-lipoxygenase (5-LOX) and 15-LOX mRNA, but decreased 12-LOX mRNA. These changes in LOX mRNA were associated with a decrease in 8/12-HETE levels only. In conclusion, this is the first demonstration that As(III) decreases AA levels coinciding with alterations to EET, HETE, and PG levels, which affects brain development and neurochemistry.
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De Castro-e-Silva, E., MF Peres, P. Brito, C. Cobas, A. Saraiva, V. Silva, A. Chaves, L. Barros, and IR De Oliveira. "Reduced immobility time in the tail suspension test (TST) by chronic immobilization stress. Role of corticosterone and brain serotonergic and adrenergic receptors." European Psychiatry 7, no. 5 (1992): 235–38. http://dx.doi.org/10.1017/s0924933800003485.
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SummaryChronically stressed adult male Balb C mice were submitted to the tail suspension test. Chronic immobilization stress (6 h/d for 14 consecutive days) induced a significant reduction in immobility time when compared to non-stressed controls. Pretreatment with LY 53857, a serotonin 5HT2 antagonist, and IPS 339, a selective beta-2 adrenoceptor blocker, reversed immobility time to the levels of non-stressed controls. Chronic administration of corticosterone (100 mg/kg for 7 d) did not modify immobility time as compared to saline treated controls. It is suggested that both serotonergic and adrenergic pathways in the brain may participate in the stress-induced changes occurring in the tail suspension test response and that corticosterone does not appear to play a role in this process.
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Vogt, Katrin, David M. Zimmerman, Matthias Schlichting, Luis Hernandez-Nunez, Shanshan Qin, Karen Malacon, Michael Rosbash, Cengiz Pehlevan, Albert Cardona, and Aravinthan D. T. Samuel. "Internal state configures olfactory behavior and early sensory processing in Drosophila larvae." Science Advances 7, no. 1 (January 2021): eabd6900. http://dx.doi.org/10.1126/sciadv.abd6900.
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Animals exhibit different behavioral responses to the same sensory cue depending on their internal state at a given moment. How and where in the brain are sensory inputs combined with state information to select an appropriate behavior? Here, we investigate how food deprivation affects olfactory behavior in Drosophila larvae. We find that certain odors repel well-fed animals but attract food-deprived animals and that feeding state flexibly alters neural processing in the first olfactory center, the antennal lobe. Hunger differentially modulates two output pathways required for opposing behavioral responses. Upon food deprivation, attraction-mediating uniglomerular projection neurons show elevated odor-evoked activity, whereas an aversion-mediating multiglomerular projection neuron receives odor-evoked inhibition. The switch between these two pathways is regulated by the lone serotonergic neuron in the antennal lobe, CSD. Our findings demonstrate how flexible behaviors can arise from state-dependent circuit dynamics in an early sensory processing center.
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Battaglia, George, John Sharkey, Michael J. Kuhar, and Errol B. de Souza. "Neuroanatomic specificity and time course of alterations in rat brain serotonergic pathways induced by MDMA (3,4-methylenedioxymethamphetamine): Assessment using quantitative autoradiography." Synapse 8, no. 4 (August 1991): 249–60. http://dx.doi.org/10.1002/syn.890080403.
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Linck, Viviane M., Ana P. Herrmann, Ângelo L. Piato, Bernardo C. Detanico, Micheli Figueiró, Jorge Flório, Maurice M. Iwu, Christopher O. Okunji, Mirna B. Leal, and Elaine Elisabetsky. "Alstonine as an Antipsychotic: Effects on Brain Amines and Metabolic Changes." Evidence-Based Complementary and Alternative Medicine 2011 (2011): 1–7. http://dx.doi.org/10.1093/ecam/nep002.
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Managing schizophrenia has never been a trivial matter. Furthermore, while classical antipsychotics induce extrapyramidal side effects and hyperprolactinaemia, atypical antipsychotics lead to diabetes, hyperlipidaemia, and weight gain. Moreover, even with newer drugs, a sizable proportion of patients do not show significant improvement. Alstonine is an indole alkaloid identified as the major component of a plant-based remedy used in Nigeria to treat the mentally ill. Alstonine presents a clear antipsychotic profile in rodents, apparently with differential effects in distinct dopaminergic pathways. The aim of this study was to complement the antipsychotic profile of alstonine, verifying its effects on brain amines in mouse frontal cortex and striatum. Additionally, we examined if alstonine induces some hormonal and metabolic changes common to antipsychotics. HPLC data reveal that alstonine increases serotonergic transmission and increases intraneuronal dopamine catabolism. In relation to possible side effects, preliminary data suggest that alstonine does not affect prolactin levels, does not induce gains in body weight, but prevents the expected fasting-induced decrease in glucose levels. Overall, this study reinforces the proposal that alstonine is a potential innovative antipsychotic, and that a comprehensive understanding of its neurochemical basis may open new avenues to developing newer antipsychotic medications.
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Gorini, C., H. Jameson, A. L. Woerman, D. C. Perry, and D. Mendelowitz. "Prenatal nicotine exposure enhances the trigeminocardiac reflex via serotonin receptor facilitation in brainstem pathways." Journal of Applied Physiology 115, no. 4 (August 15, 2013): 415–21. http://dx.doi.org/10.1152/japplphysiol.00552.2013.
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In this study we used a rat model for prenatal nicotine exposure to test whether clinically relevant concentrations of brain nicotine and cotinine are passed from dams exposed to nicotine to her pups, whether this changes the trigeminocardiac reflex (TCR), and whether serotonergic function in the TCR brainstem circuitry is altered. Pregnant Sprague-Dawley dams were exposed to 6 mg·kg−1·day−1of nicotine via osmotic minipumps for the duration of pregnancy. Following birth dams and pups were killed, blood was collected, and brain nicotine and cotinine levels were measured. A separate group of prenatal nicotine-exposed pups was used for electrophysiological recordings. A horizontal brainstem slice was obtained by carefully preserving the trigeminal nerve with fluorescent identification of cardiac vagal neurons (CVNs) in the nucleus ambiguus. Stimulation of the trigeminal nerve evoked excitatory postsynaptic current in CVNs. Our data demonstrate that prenatal nicotine exposure significantly exaggerates both the TCR-evoked changes in heart rate in conscious unrestrained pups, and the excitatory neurotransmission to CVNs upon trigeminal afferent nerve stimulation within this brainstem reflex circuit. Application of the 5-HT1Areceptor antagonist WAY 100635 (100 μM) and 5-HT2A/Creceptor antagonist ketanserin (10 μM)significantly decreased neurotransmission, indicating an increased facilitation of 5-HT function in prenatal nicotine-exposed animals. Prenatal nicotine exposure enhances activation of 5-HT receptors and exaggerates the trigeminocardiac reflex.
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Nakamura, Kazuhiro, and Shaun F. Morrison. "Central efferent pathways mediating skin cooling-evoked sympathetic thermogenesis in brown adipose tissue." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 292, no. 1 (January 2007): R127—R136. http://dx.doi.org/10.1152/ajpregu.00427.2006.
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Control of thermoregulatory effectors by the autonomic nervous system is a critical component of rapid cold-defense responses, which are triggered by thermal information from the skin. However, the central autonomic mechanism driving thermoregulatory effector responses to skin thermal signals remains to be determined. Here, we examined the involvement of several autonomic brain regions in sympathetic thermogenic responses in brown adipose tissue (BAT) to skin cooling in urethane-chloralose-anesthetized rats by monitoring thermogenic [BAT sympathetic nerve activity (SNA) and BAT temperature], metabolic (expired CO2), and cardiovascular (arterial pressure and heart rate) parameters. Acute skin cooling, which did not reduce either rectal (core) or brain temperature, evoked increases in BAT SNA, BAT temperature, expired CO2, and heart rate. Skin cooling-evoked thermogenic, metabolic, and heart rate responses were inhibited by bilateral microinjections of bicuculline (GABAA receptor antagonist) into the preoptic area (POA), by bilateral microinjections of muscimol (GABAA receptor agonist) into the dorsomedial hypothalamic nucleus (DMH), or by microinjection of muscimol, glycine, 8-OH-DPAT (5-HT1A receptor agonist), or kynurenate (nonselective antagonist for ionotropic excitatory amino acid receptors) into the rostral raphe pallidus nucleus (rRPa) but not by bilateral muscimol injections into the lateral/dorsolateral part or ventrolateral part of the caudal periaqueductal gray. These results implicate the POA, DMH, and rRPa in the central efferent pathways for thermogenic, metabolic, and cardiac responses to skin cooling, and suggest that these pathways can be modulated by serotonergic inputs to the medullary raphe.
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Carvalho, F., D. Barros, J. Silva, E. Rezende, M. Soares, J. Fregoneze, and E. de Castro-e-Silva. "Hyperglycemia Induced by Pharmacological Activation of Central Serotonergic Pathways Depends on the Functional Integrity of Brain CRH System and 5-HT3 Receptors." Hormone and Metabolic Research 37, no. 8 (August 2005): 482–88. http://dx.doi.org/10.1055/s-2005-870323.
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Ruhlen, Rachel L., Grace Y. Sun, and Edward R. Sauter. "Black Cohosh: Insights into its Mechanism(s) of Action." Integrative Medicine Insights 3 (January 2008): 117863370800300. http://dx.doi.org/10.4137/117863370800300002.
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The Women's Health Initiative found that combination estrogen and progesterone hormone replacement therapy increases breast cancer and cardiovascular disease risk, which compelled many women to seek herbal alternatives such as black cohosh extract (BCE) to relieve their menopausal symptoms. While several clinical trials document the efficacy of BCE in alleviating menopausal symptoms, preclinical studies to determine how BCE works have yielded conflicting results. Part of this is because there is not a universally accepted method to standardize the dose of black cohosh triterpenes, the presumed active ingredients in the extract. Although the mechanism by which BCE relieves symptoms is unknown, several hypotheses have been proposed: it acts 1) as a selective estrogen receptor modulator, 2) through serotonergic pathways, 3) as an antioxidant, or 4) on inflammatory pathways. We found that while the most prominent triterpene in BCE, 23-epi-26-deoxyactein, suppresses cytokine-induced nitric oxide production in brain microglial cells, the whole BCE extract actually enhanced this pathway. A variety of activities have been reported for black cohosh and its compounds, but the absorption and tissue distribution of these compounds is unknown.
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Gorini, C., H. S. Jameson, and D. Mendelowitz. "Serotonergic Modulation of the Trigeminocardiac Reflex Neurotransmission to Cardiac Vagal Neurons in the Nucleus Ambiguus." Journal of Neurophysiology 102, no. 3 (September 2009): 1443–50. http://dx.doi.org/10.1152/jn.00287.2009.
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Stimulation of the trigeminal nerve evokes a dramatic decrease in heart rate and blood pressure, and this reflex has generally been termed the trigeminocardiac reflex. A subset of the trigeminocardiac reflex is the diving reflex in which the nasal mucosa is stimulated with water or air-borne chemical irritants. Activation of the diving reflex evokes a pronounced bradycardia, mediated by increased parasympathetic cardiac activity, and is the most powerful autonomic reflex. However, exaggeration of this protective response could be detrimental and has been implicated in Sudden Infant Death Syndrome (SIDS). Despite the importance and strength of the trigeminocardiac reflex, there is little information about the cellular mechanisms and brain stem pathways that constitute this reflex. To address these issues, stimulation of trigeminal afferent fibers and the evoked excitatory postsynaptic currents were recorded in cardiac vagal neurons (CVNs) in an in vitro brain stem slice preparation. This synaptic pathway is robust and activation of the trigeminal pathway often evoked action potentials in CVNs. Application of the serotonin (5-HT) reuptake inhibitor citalopram significantly enhanced these responses. Consistent with the hypothesis this pathway is endogenously modulated by 5-HT receptors the 5-HT1Areceptor antagonist, WAY 100635 inhibited, whereas the 5-HT2A/Creceptor antagonist, ketanserin facilitated the excitatory neurotransmission to CVNs. The 5-HT1Areceptor agonist 8-hydroxy-2-(dipropylamino)tetralin hydrobromide increased, whereas the 5-HT2receptor agonist, α-methylserotonin maleate salt inhibited this reflex pathway. These results indicate stimulation of trigeminal fibers evokes a powerful excitatory and polysynaptic pathway to CVNs, and this pathway is endogenously modulated and differentially enhanced and depressed, by 5-HT1Aand 5-HT2receptors, respectively.
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Kuner, Rohini, and Thomas Kuner. "Cellular Circuits in the Brain and Their Modulation in Acute and Chronic Pain." Physiological Reviews 101, no. 1 (January 1, 2021): 213–58. http://dx.doi.org/10.1152/physrev.00040.2019.
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Chronic, pathological pain remains a global health problem and a challenge to basic and clinical sciences. A major obstacle to preventing, treating, or reverting chronic pain has been that the nature of neural circuits underlying the diverse components of the complex, multidimensional experience of pain is not well understood. Moreover, chronic pain involves diverse maladaptive plasticity processes, which have not been decoded mechanistically in terms of involvement of specific circuits and cause-effect relationships. This review aims to discuss recent advances in our understanding of circuit connectivity in the mammalian brain at the level of regional contributions and specific cell types in acute and chronic pain. A major focus is placed on functional dissection of sub-neocortical brain circuits using optogenetics, chemogenetics, and imaging technological tools in rodent models with a view towards decoding sensory, affective, and motivational-cognitive dimensions of pain. The review summarizes recent breakthroughs and insights on structure-function properties in nociceptive circuits and higher order sub-neocortical modulatory circuits involved in aversion, learning, reward, and mood and their modulation by endogenous GABAergic inhibition, noradrenergic, cholinergic, dopaminergic, serotonergic, and peptidergic pathways. The knowledge of neural circuits and their dynamic regulation via functional and structural plasticity will be beneficial towards designing and improving targeted therapies.
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Cudennec, Annie, Danielle Duverger, André Serrano, Bernard Scatton, and Eric T. MacKenzie. "Influence of ascending serotonergic pathways on glucose use in the conscious rat brain. II. Effects of electrical stimulation of the rostral raphé nuclei." Brain Research 444, no. 2 (March 1988): 227–46. http://dx.doi.org/10.1016/0006-8993(88)90933-x.
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Villas-Boas, Gustavo R., Stefânia N. Lavorato, Marina M. Paes, Pablinny M. G. de Carvalho, Vanessa C. Rescia, Mila S. Cunha, Manoel F. de Magalhães-Filho, et al. "Modulation of the Serotonergic Receptosome in the Treatment of Anxiety and Depression: A Narrative Review of the Experimental Evidence." Pharmaceuticals 14, no. 2 (February 12, 2021): 148. http://dx.doi.org/10.3390/ph14020148.
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Serotonin (5-HT) receptors are found throughout central and peripheral nervous systems, mainly in brain regions involved in the neurobiology of anxiety and depression. 5-HT receptors are currently promising targets for discovering new drugs for treating disorders ranging from migraine to neuropsychiatric upsets, such as anxiety and depression. It is well described in the current literature that the brain expresses seven types of 5-HT receptors comprising eighteen distinct subtypes. In this article, we comprehensively reviewed 5-HT1-7 receptors. Of the eighteen 5-HT receptors known today, thirteen are G protein-coupled receptors (GPCRs) and represent targets for approximately 40% of drugs used in humans. Signaling pathways related to these receptors play a crucial role in neurodevelopment and can be modulated to develop effective therapies to treat anxiety and depression. This review presents the experimental evidence of the modulation of the “serotonergic receptosome” in the treatment of anxiety and depression, as well as demonstrating state-of-the-art research related to phytochemicals and these disorders. In addition, detailed aspects of the pharmacological mechanism of action of all currently known 5-HT receptor families were reviewed. From this review, it will be possible to direct the rational design of drugs towards new therapies that involve signaling via 5-HT receptors.
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Kasper, S. "Depression." European Psychiatry 26, S2 (March 2011): 2186. http://dx.doi.org/10.1016/s0924-9338(11)73889-5.
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Depression is one of the thoroughly evaluated diseases in psychiatry with regard to diagnosis as well as treatment variables. Like in other medical conditions, early treatment should be aimed and watchful waiting which is for instance also not done in the treatment of high blood pressure or diabetes, has not been proven to be a sophisticated approach based on neurobiological considerations. Like in other diseases, it is apparent that days of untreated depression may result in brain damage like reduced volume size of the hypocampus. The course of illness of depression shows that life events are less important in later stages of the illness than in earlier. The introduction of the group of selective serotonin reuptake inhibitors (SSRI) marked a revolution in the treatment of depression, since it was possible to treat patient for the first time effectively with a more minor side effect profile with this approach. Substantially more patients could be reached and the association with this phenomenon and the reduction of the suicide rates in different countries like Sweden, Austria and Hungary has been discussed. Dual reuptake inhibitors effecting both the serotonergic as well as the noradrenergic pathways and the dopaminergic noradrenergic medication bupropion have been introduced in the filed with specific angles of treatment goals like pain or somatic symptoms. With the introduction of agomelatine, a unique mechanism of action with the combination of melatonergic agonistic as well as serotonergic antagonistic activities has been achieved. With this approach a more potent influence on the circadian rhythm has been shown compared to other, previously used antidepressant properties. Deep brain stimulation and vagus nerve stimulation for treatment refractory depressed patients yield promising results. More thorough characterisation of the underlying pathophysiology of depression including brain imaging results as well as molecular biological variables will yield further inside of the understanding and treatment of depression.
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Hodgkinson, S., J. Steyer, M. Jandl, and W. P. Kaschka. "Action-inhibition hierarchies: Using a simple gastropod model to investigate serotonergic and dopaminergic control of action selection and reinforcement learning." European Psychiatry 26, S2 (March 2011): 905. http://dx.doi.org/10.1016/s0924-9338(11)72610-4.
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IntroductionBasal ganglia (BG) activity plays an important role in action selection and reinforcement learning. Inputs from and to other areas of the brain are modulated by a number of neurotransmitter pathways in the BG. Disturbances in the normal function of the BG may play a role in the aetiology of psychiatric disorders such as schizophrenia and bipolar disorder.AimsDevelop a simple animal model to evaluate interactions between glutamatergic, dopaminergic, serotonergic and GABAergic neurones in the modulation of action selection and reinforcement learning.ObjectivesTo characterise the effects of changing dopaminergic and serotonergic activity on action selection and reinforcement learning in an animal model.MethodsThe food seeking / consummation (FSC) activity of the gastropod Planorbis corneus was suppressed by operant conditioning using a repeated unconditioned stimulus-punishment regime. The effects of elevated serotonin or dopamine levels (administration into cerebral, pedal and buccal ganglia), on operantly-conditioned FSC activity was assessed.ResultsOperantly-conditioned behaviour was reversed by elevated ganglia serotonin levels but snails showed no food consummation motor activity in the absence of food. In contrast, elevated ganglia dopamine levels in conditioned snails elicited food consummation motor movements in the absence of food but not orientation towards a food source.ConclusionsThe modulation of FSC activity elicited by reinforcement learning is subject to hierarchical control in gastropods. Serotoninergic activity is responsible establishing the general activity level whilst dopaminergic activity appears to play a more localised and subordinate ‘command’ role.
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Turan Yücel, Nazlı, Ümmühan Kandemir, Ümide Demir Özkay, and Özgür Devrim Can. "5-HT1A Serotonergic, α-Adrenergic and Opioidergic Receptors Mediate the Analgesic Efficacy of Vortioxetine in Mice." Molecules 26, no. 11 (May 28, 2021): 3242. http://dx.doi.org/10.3390/molecules26113242.
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Vortioxetine is a multimodal antidepressant drug that affects several brain neurochemicals and has the potential to induce various pharmacological effects on the central nervous system. Therefore, we investigated the centrally mediated analgesic efficacy of this drug and the mechanisms underlying this effect. Analgesic activity of vortioxetine (5, 10 and 20 mg/kg, p.o.) was examined by tail-clip, tail-immersion and hot-plate tests. Motor performance of animals was evaluated using Rota-rod device. Time course measurements (30–180 min) showed that vortioxetine (10 and 20 mg/kg) administrations significantly increased the response latency, percent maximum possible effect and area under the curve values in all of the nociceptive tests. These data pointed out the analgesic effect of vortioxetine on central pathways carrying acute thermal and mechanical nociceptive stimuli. Vortioxetine did not alter the motor coordination of mice indicating that the analgesic activity of this drug was specific. In mechanistic studies, pre-treatments with p-chlorophenylalanine (serotonin-synthesis inhibitor), NAN-190 (serotonin 5-HT1A receptor antagonist), α-methyl-para-tyrosine (catecholamine-synthesis inhibitor), phentolamine (non-selective α-adrenoceptor blocker), and naloxone (non-selective opioid receptor blocker) antagonised the vortioxetine-induced analgesia. Obtained findings indicated that vortioxetine-induced analgesia is mediated by 5-HT1A serotonergic, α-adrenergic and opioidergic receptors, and contributions of central serotonergic and catecholaminergic neurotransmissions are critical for this effect.
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Lautenschlager, Nicola T., Ralf Ihl, and Walter E. Müller. "Ginkgo biloba extract EGb 761® in the context of current developments in the diagnosis and treatment of age-related cognitive decline and Alzheimer's disease: a research perspective." International Psychogeriatrics 24, S1 (July 12, 2012): S46—S50. http://dx.doi.org/10.1017/s1041610212001019.
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ABSTRACTIn June 2011 a two-day expert meeting “The Ageing Brain” took place in Amsterdam, The Netherlands. The main aim was to discuss the available preclinical and clinical data on Ginkgo biloba special extract EGb 761® in the context of current developments in the diagnosis and treatment of age-related cognitive decline and Alzheimer's disease. 19 dementia experts covering the disciplines bio- and neurochemistry, gerontology, neurology, pharmacology, and psychiatry from Australia, Asia, Europe and North America reviewed available preclinical and clinical data for EGb 761® and identified core topics for future research. Based on a wide range of preclinical effects demonstrated for Ginkgo biloba, EGb 761® can be conceptualized as a multi-target compound with activity on distinct pathophysiological pathways in Alzheimer's disease (AD) and age-related cognitive decline. While symptomatic efficacy in dementia and mild cognitive impairment (MCI) has been demonstrated, interpretation of data from dementia prevention trials is complicated by important methodological issues. Bridging pre-clinical research and clinical research as well as deciding on suitable study designs for future trials with EGb 761® remain important questions. The participants of the “Ageing Brain” meeting on Ginkgo biloba special extract EGb 761® concluded that there is plenty of promising data, both pre-clinical and clinical, to consider future research with the compound targeting cognitive impairment in old age as a worthwhile activity.
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Langhans, Wolfgang. "Signals generating anorexia during acute illness." Proceedings of the Nutrition Society 66, no. 3 (July 16, 2007): 321–30. http://dx.doi.org/10.1017/s0029665107005587.
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Anorexia is part of the body's acute-phase response to illness. Microbial products such as lipopolysaccharides (LPS), which are also commonly used to model acute illness, trigger the acute-phase response and cause anorexia mainly through pro-inflammatory cytokines. LPS stimulate cytokine production through the cell-surface structural molecule CD14 and toll-like receptor-4. Cytokines ultimately change neural activity in brain areas controlling food intake and energy balance. The blood–brain barrier endothelial cells (BBB EC) are an important site of cytokine action in this context. BBB EC and perivascular cells (microglia and macrophages) form a complex regulatory interface that modulates neuronal activity by the release of messengers (e.g. PG, NO) in response to peripheral challenges. Serotonergic neurons originating in the raphe nuclei and glucagon-like peptide-1-expressing neurons in the hindbrain may be among the targets of these messengers, because serotonin (5-HT), acting through the 5-HT2C receptor, and glucagon-like peptide-1 have recently emerged as neurochemical mediators of LPS anorexia. The central melanocortin system, which is a downstream target of serotonergic neurons, also appears to be involved in mediation of LPS anorexia. Interestingly, LPS also reduce orexin expression and the activity of orexin neurons in the lateral hypothalamic area of fasted mice. As the eating-stimulatory properties of orexin are apparently related to arousal, the inhibitory effect of LPS on orexin neurons might be involved in LPS-induced inactivity and anorexia. In summary, the immune signalling pathways of LPS-induced, and presumably acute illness-induced, anorexia converge on central neural signalling systems that control food intake and energy balance in healthy individuals.
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De Sousa, Thallysson Jose Dourado, Pedro Henrique Almeida De Faria, Kassyo Lenno Sousa Dantas, Monick Nielly Miranda Pinto, Gabriella de Assis Malerba, Milena Sousa Freitas, Sheyrlani Tatiany Da Silva, Paulo Cesar Morales Mayer, Domingos Magno Santos Pereira, and Cristiane Santos Silva e. Silva Figueiredo. "Plantas medicinales como alternativa terapéutica para el trastorno Depresivo Mayor (DMD)." Revista Eletrônica Acervo Saúde 13, no. 2 (February 6, 2021): e5646. http://dx.doi.org/10.25248/reas.e5646.2021.
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Objective: To review the antidepressant activity and mechanisms of action of plants that have antidepressant action. Literature Review: The use of plants for medicinal purposes has been used as an adjunct to the treatment of depression due to easy access by the population, few side effects and lower cost. Based on the studies, the plants St. John's wort, ground turmeric, anona and lavender have antidepressant potential for acting in different ways in depression, either by inhibiting the reuptake of serotonin or by modulation in the dopaminergic and serotonergic pathways. Final Considerations: From the studies of the mechanisms of action it was found that the plants studied can modulate the brain signaling pathways responsible for the patient's mood, with the reuptake of serotonin (inhibition of the serotonin transporter protein) the main mechanism of action shared between them. In addition, some of these plants can modulate not only the concentrations of serotonin in the synaptic cleft, but also dopamine. It is worth mentioning that, although these actions have been scientifically proven, much research is still needed to ensure the safe use of these agents as herbal medicines in the alternative or adjunctive treatment of depressive disorders.
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Chung, M. K., S. Wang, J. Yang, I. Alshanqiti, F. Wei, and J. Y. Ro. "Neural Pathways of Craniofacial Muscle Pain: Implications for Novel Treatments." Journal of Dental Research 99, no. 9 (May 6, 2020): 1004–12. http://dx.doi.org/10.1177/0022034520919384.
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Craniofacial muscle pain is highly prevalent in temporomandibular disorders but is difficult to treat. Enhanced understanding of neurobiology unique to craniofacial muscle pain should lead to the development of novel mechanism-based treatments. Herein, we review recent studies to summarize neural pathways of craniofacial muscle pain. Nociceptive afferents in craniofacial muscles are predominantly peptidergic afferents enriched with TRPV1. Signals from peripheral glutamate receptors converge onto TRPV1, leading to mechanical hyperalgesia. Further studies are needed to clarify whether hyperalgesic priming in nonpeptidergic afferents or repeated acid injections also affect craniofacial muscle pain. Within trigeminal ganglia, afferents innervating craniofacial muscles interact with surrounding satellite glia, which enhances the sensitivity of the inflamed neurons as well as nearby uninjured afferents, resulting in hyperalgesia and ectopic pain originating from adjacent orofacial tissues. Craniofacial muscle afferents project to a wide area within the trigeminal nucleus complex, and central sensitization of medullary dorsal horn neurons is a critical factor in muscle hyperalgesia related to ectopic pain and emotional stress. Second-order neurons project rostrally to pathways associated with affective pain, such as parabrachial nucleus and medial thalamic nucleus, as well as sensory-discriminative pain, such as ventral posteromedial thalamic nuclei. Abnormal endogenous pain modulation can also contribute to chronic muscle pain. Descending serotonergic circuits from the rostral ventromedial medulla facilitate activation of second-order neurons in the trigeminal nucleus complex, which leads to the maintenance of mechanical hyperalgesia of inflamed masseter muscle. Patients with temporomandibular disorders exhibit altered brain networks in widespread cortical and subcortical regions. Recent development of methods for neural circuit manipulation allows silencing of specific hyperactive neural circuits. Chemogenetic silencing of TRPV1-expressing afferents or rostral ventromedial medulla neurons attenuates hyperalgesia during masseter inflammation. It is likely, therefore, that further delineation of neural circuits mediating craniofacial muscle hyperalgesia potentially enhances treatment of chronic muscle pain conditions.
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Lizarraga-Mollinedo, Esther, Elisa Fernández-Millán, Juan de Toro Martín, Carlos Martínez-Honduvilla, Fernando Escrivá, and Carmen Álvarez. "Early undernutrition induces glucagon resistance and insulin hypersensitivity in the liver of suckling rats." American Journal of Physiology-Endocrinology and Metabolism 302, no. 9 (May 1, 2012): E1070—E1077. http://dx.doi.org/10.1152/ajpendo.00495.2011.
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Developing brains are vulnerable to nutritional insults. Early undernutrition alters their structure and neurochemistry, inducing long-term pathological effects whose causal pathways are not well defined. During suckling, the brain uses glucose and ketone bodies as substrates. Milk is a high-fat low-carbohydrate diet, and the liver must maintain high rates of gluconeogenesis and ketogenesis to address the needs of these substrates. Insulin and glucagon play major roles in this adaptation: throughout suckling, their blood concentrations are low and high, respectively, and the liver maintains low insulin sensitivity and increased glucagon responsiveness. We propose that disturbances in the endocrine profile and available plasma substrates along with undernutrition-related changes in brain cortex capacity for ketone utilization may cause further alterations in some brain functions. We explored this hypothesis in 10-day-old suckling rats whose mothers were severely food restricted from the 14th day of gestation. We measured the plasma/serum concentrations of glucose, ketone body, insulin and glucagon, and hepatic insulin and glucagon responses. Undernutrition led to hypoglycemia and hyperketonemia to 84% ( P < 0.001) and 144% ( P < 0.001) of control values, respectively. Liver responsiveness to insulin and glucagon became increased and reduced, respectively; intraperitoneal glucagon reduced liver glycogen by 90% ( P < 0.01) in control and by 35% ( P < 0.05) in restricted. Cortical enzymes of ketone utilization remained unchanged, but their carrier proteins were altered: monocarboxylate transporter (MCT) 1 increased: 73 ± 14, controls; 169 ± 20, undernourished ( P < 0.01; densitometric units); MCT2 decreased: 103 ± 3, controls; 37 ± 4, undernourished ( P < 0.001; densitometric units). All of these changes, coinciding with the brain growth spurt, may cause some harmful effects associated with early undernutrition.
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Keshavarz, Maryam, and Diethard Tautz. "The imprinted lncRNA Peg13 regulates sexual preference and the sex-specific brain transcriptome in mice." Proceedings of the National Academy of Sciences 118, no. 10 (March 3, 2021): e2022172118. http://dx.doi.org/10.1073/pnas.2022172118.
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Mammalian genomes include many maternally and paternally imprinted genes. Most of these are also expressed in the brain, and several have been implicated in regulating specific behavioral traits. Here, we have used a knockout approach to study the function of Peg13, a gene that codes for a fast-evolving lncRNA (long noncoding RNA) and is part of a complex of imprinted genes on chromosome 15 in mice and chromosome 8 in humans. Mice lacking the 3′ half of the transcript look morphologically wild-type but show distinct behavioral differences. They lose interest in the opposite sex, instead displaying a preference for wild-type animals of the same sex. Further, they show a higher level of anxiety, lowered activity and curiosity, and a deficiency in pup retrieval behavior. Brain RNA expression analysis reveals that genes involved in the serotonergic system, formation of glutamatergic synapses, olfactory processing, and estrogen signaling—as well as more than half of the other known imprinted genes—show significant expression changes in Peg13-deficient mice. Intriguingly, these pathways are differentially affected in the sexes, resulting in male and female brains of Peg13-deficient mice differing more from each other than those of wild-type mice. We conclude that Peg13 is part of a developmental pathway that regulates the neurobiology of social and sexual interactions.
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Bozzatello, Paola, Cecilia Blua, Paola Rocca, and Silvio Bellino. "Mental Health in Childhood and Adolescence: The Role of Polyunsaturated Fatty Acids." Biomedicines 9, no. 8 (July 21, 2021): 850. http://dx.doi.org/10.3390/biomedicines9080850.
Full textAbstract:
There is increasing awareness of the importance of polyunsaturated fatty acids (PUFAs) for optimal brain development and function. In recent decades, researchers have confirmed the central role of PUFAs in a variety of patho-physiological processes. These agents modulate the mechanisms of brain cell signalling including the dopaminergic and serotonergic pathways. Therefore, nutritional insufficiencies of PUFAs may have adverse effects on brain development and developmental outcomes. The role of n-3 PUFAs has been studied in several psychiatric disorders in adulthood: schizophrenia, major depression, bipolar disorder, anxiety disorders, obsessive-compulsive disorder, post-traumatic stress disorder, attention deficit hyperactivity disorder (ADHD), autism spectrum disorders, eating disorders, substance use disorder, and borderline personality disorder. In contrast to the great number of studies conducted in adults, there are only limited data on the effects of n-3 PUFA supplementation in children and adolescents who suffer from mental disorders or show a high risk of developing psychiatric disorders. The aim of this review is to provide a complete and updated account of the available evidence of the impact of polyunsaturated fatty acids on developmental psychopathology in children and adolescents and the effect of fatty acid supplementation during developmental milestones, particularly in high-risk populations of children with minimal but detectable signs or symptoms of mental disorders.
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Laflamme, N., E. Feuvrier, D. Richard, and S. Rivest. "Involvement of serotonergic pathways in mediating the neuronal activity and genetic transcription of neuroendocrine corticotropin-releasing factor in the brain of systemically endotoxin-challenged rats." Neuroscience 88, no. 1 (January 1999): 223–40. http://dx.doi.org/10.1016/s0306-4522(98)00369-8.
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Sharma, Vandana, and Sandeep Kaur. "The Effect of Probiotic Intervention in Ameliorating the Altered Central Nervous System Functions in Neurological Disorders: A Review." Open Microbiology Journal 14, no. 1 (February 10, 2020): 18–29. http://dx.doi.org/10.2174/1874285802014010018.
Full textAbstract:
There has been a significant rise in the occurrence of various neurological ailments worldwide. The need to investigate newer and safer intervention therapies with prophylactic and/or therapeutic effects is well understood. Probiotics have recently been shown to hold promise as an intervention option that warrants future work. Probiotic strains have shown beneficial treatment outcomes as evidenced in various animal and human studies. Although numerous articles have highlighted the role of gut microbiota and its cross-talk with human brain in modulating Central Nervous System (CNS) physiology and neurochemistry, the present review solely focuses on the ability of externally administered probiotic strains (that may or may not be part of the already existing gut microflora of an average human) in ameliorating the altered CNS functions in patients. The review aims at giving a comprehensive analysis of the studies performed on animals and humans and discusses the findings in different neurological and psychiatric disorders (Anxiety, Major Depressive disorder, bipolar disorder, schizophrenia, autism spectrum disorder, cognitive impairments etc). The article also highlights different mechanisms through which the probiotic bacteria operate in improving neurologic manifestations or decreasing the incidence of neurological disorders. These underlying mechanisms include both direct as well as indirect pathways involving neural, hormonal and immunological pathways. The potential of probiotics as an important dietary modification as well as a useful intervention therapy with preventive and therapeutic value for the target population holds strong. However, future evaluation into formulation designing, selecting the best probiotic strain(s) for each specific disease and safety and tolerability aspects in patients needs to be considered.
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Rock, Kylie D., Genevieve St Armour, Brian Horman, Allison Phillips, Matthew Ruis, Allison K. Stewart, Dereje Jima, David C. Muddiman, Heather M. Stapleton, and Heather B. Patisaul. "Effects of Prenatal Exposure to a Mixture of Organophosphate Flame Retardants on Placental Gene Expression and Serotonergic Innervation in the Fetal Rat Brain." Toxicological Sciences 176, no. 1 (April 3, 2020): 203–23. http://dx.doi.org/10.1093/toxsci/kfaa046.
Full textAbstract:
Abstract There is a growing need to understand the potential neurotoxicity of organophosphate flame retardants (OPFRs) and plasticizers because use and, consequently, human exposure, is rapidly expanding. We have previously shown in rats that developmental exposure to the commercial flame retardant mixture Firemaster 550 (FM 550), which contains OPFRs, results in sex-specific behavioral effects, and identified the placenta as a potential target of toxicity. The placenta is a critical coordinator of fetal growth and neurodevelopment, and a source of neurotransmitters for the developing brain. We have shown in rats and humans that flame retardants accumulate in placental tissue, and induce functional changes, including altered neurotransmitter production. Here, we sought to establish if OPFRs (triphenyl phosphate and a mixture of isopropylated triarylphosphate isomers) alter placental function and fetal forebrain development, with disruption of tryptophan metabolism as a primary pathway of interest. Wistar rat dams were orally exposed to OPFRs (0, 500, 1000, or 2000 μg/day) or a serotonin (5-HT) agonist 5-methoxytryptamine for 14 days during gestation and placenta and fetal forebrain tissues collected for analysis by transcriptomics and metabolomics. Relative abundance of genes responsible for the transport and synthesis of placental 5-HT were disrupted, and multiple neuroactive metabolites in the 5-HT and kynurenine metabolic pathways were upregulated. In addition, 5-HTergic projections were significantly longer in the fetal forebrains of exposed males. These findings suggest that OPFRs have the potential to impact the 5-HTergic system in the fetal forebrain by disrupting placental tryptophan metabolism.
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Problems of endocrinology, Editorial team of. "In memory to Ye. V. Naumenko." Problems of Endocrinology 41, no. 3 (June 15, 1995): 47. http://dx.doi.org/10.14341/probl11428.
Full textAbstract:
On November 13, 1994, science suffered a heavy loss - an outstanding Russian scientist, professor, doctor of medical sciences, the founder of a number of original directions in world neuroendocrinology Evgeny Vladimirovich Naumenko prematurely passed away. In the 60s, the scientific interests of E.V. Naumenko were focused on studying the role of biogenic brain amines in the neurochemical regulation of the hypothalamic-pituitary-adrenocortical system. In particular, he proved for the first time that one of the final hypothalamic neural pathways stimulating the synthesis and secretion of corticoliberin is serotonergic in nature. The results of these widely known studies at home and abroad brought well-deserved fame to a neuroendocrinologist from Siberia. In the last 20 years, the main work of E.V. Naumenko concerned the study of genetic evolutionary and ontogenetic aspects of stress, the role of neuroendocrine mechanisms in animal domestication processes, the role of neurochemical brain mechanisms in the dominant behavior of individuals in micropopulations, and the study of a new model of hereditary arterial hypertension. Professor E.V. Naumenko has published over 300 works, including more than a dozen major monographic publications published at home and abroad. These publications are widely known among specialists, they have made a significant contribution to the development of neuroendocrinology and brought well-deserved recognition to their author.
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Problems of endocrinology, Editorial team of. "In memory to Ye. V. Naumenko." Problems of Endocrinology 41, no. 3 (June 15, 1995): 48. http://dx.doi.org/10.14341/probl11431.
Full textAbstract:
On November 13, 1994, science suffered a heavy loss - an outstanding Russian scientist, professor, doctor of medical sciences, the founder of a number of original directions in world neuroendocrinology Evgeny Vladimirovich Naumenko prematurely passed away. In the 60s, the scientific interests of E.V. Naumenko were focused on studying the role of biogenic brain amines in the neurochemical regulation of the hypothalamic-pituitary-adrenocortical system. In particular, he proved for the first time that one of the final hypothalamic neural pathways stimulating the synthesis and secretion of corticoliberin is serotonergic in nature. The results of these widely known studies at home and abroad brought well-deserved fame to a neuroendocrinologist from Siberia. In the last 20 years, the main work of E.V. Naumenko concerned the study of genetic evolutionary and ontogenetic aspects of stress, the role of neuroendocrine mechanisms in animal domestication processes, the role of neurochemical brain mechanisms in the dominant behavior of individuals in micropopulations, and the study of a new model of hereditary arterial hypertension. Professor E.V. Naumenko has published over 300 works, including more than a dozen major monographic publications published at home and abroad. These publications are widely known among specialists, they have made a significant contribution to the development of neuroendocrinology and brought well-deserved recognition to their author.
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Song, Ji-Hye, Seul-Ki Won, Geun-Hyang Eom, Da-Som Lee, Byung-Jin Park, Jin-Seok Lee, Chang-Gue Son, and Ji-Yeun Park. "Improvement Effects of Myelophil on Symptoms of Chronic Fatigue Syndrome in a Reserpine-Induced Mouse Model." International Journal of Molecular Sciences 22, no. 19 (September 22, 2021): 10199. http://dx.doi.org/10.3390/ijms221910199.
Full textAbstract:
Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is associated with various symptoms, such as depression, pain, and fatigue. To date, the pathological mechanisms and therapeutics remain uncertain. The purpose of this study was to investigate the effect of myelophil (MYP), composed of Astragali Radix and Salviaemiltiorrhizae Radix, on depression, pain, and fatigue behaviors and its underlying mechanisms. Reserpine (2 mg/kg for 10 days, intraperitoneally) induced depression, pain, and fatigue behaviors in mice. MYP treatment (100 mg/kg for 10 days, intragastrically) significantly improved depression behaviors, mechanical and thermal hypersensitivity, and fatigue behavior. MYP treatment regulated the expression of c-Fos, 5-HT1A/B receptors, and transforming growth factor β (TGF-β) in the brain, especially in the motor cortex, hippocampus, and nucleus of the solitary tract. MYP treatment decreased ionized calcium binding adapter molecule 1 (Iba1) expression in the hippocampus and increased tyrosine hydroxylase (TH) expression and the levels of dopamine and serotonin in the striatum. MYP treatment altered inflammatory and anti-oxidative-related mRNA expression in the spleen and liver. In conclusion, MYP was effective in recovering major symptoms of ME/CFS and was associated with the regulation of dopaminergic and serotonergic pathways and TGF-β expression in the brain, as well as anti-inflammatory and anti-oxidant mechanisms in internal organs.