Relevant bibliographies by topics / Neurochemistry; Serotonergic pathways; Brain

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
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Academic literature on the topic 'Neurochemistry; Serotonergic pathways; Brain'

Author: Grafiati
Published: 4 June 2021
Last updated: 15 February 2022

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Journal articles on the topic "Neurochemistry; Serotonergic pathways; Brain"

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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Dissertations / Theses on the topic "Neurochemistry; Serotonergic pathways; Brain"

1

Series, Hugh George. "The characterisation of two distinct ascending serotonergic projections in rats by anatomical, pharmacological and functional methods." Thesis, University of Oxford, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.337566.

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Murphy, Niall P. "The role of noradrenergic pathways in the morphine withdrawal excitation of oxytocin neurones." Thesis, University of Cambridge, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.264283.

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Books on the topic "Neurochemistry; Serotonergic pathways; Brain"

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(Editor), T. Kumazawa, L. Kruger (Editor), and K. Mizumura (Editor), eds. The Polymodal Receptor - A Gateway to Pathological Pain (Progress in Brain Research). Elsevier Science, 1996.

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Takao, Kumazawa, Kruger Lawrence, and Mizumura Kazue, eds. The polymodal receptor: A gateway to pathological pain. Amsterdam: Elsevier, 1996.

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Book chapters on the topic "Neurochemistry; Serotonergic pathways; Brain"

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Edwards, Sandra, and Anna Valros. "Understanding and preventing tail biting in pigs." In Understanding the behaviour and improving the welfare of pigs, 361–400. Burleigh Dodds Science Publishing, 2021. http://dx.doi.org/10.19103/as.2020.0081.10.

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Tail biting is a behavioural problem of pigs which is associated with welfare detriment for both the perpetrator and victim. It is seen to some extent on most farms worldwide and causes considerable economic loss, leading to widespread adoption of tail docking for risk reduction. Its occurrence is often sporadic and unpredictable, as a result of the many different combinations of chronic and acute risk factors which can be present on individual farms. Understanding of the underlying (neuro)physiological mechanisms which lead an individual pig to initiate tail biting is still incomplete, but stress, pro-inflammatory cytokine production, changes in amino acid metabolism and serotonergic brain pathways have been implicated. Rearing pigs with undocked tails and without tail biting is still challenging in commercial practice and requires a high quality of management and stockmanship to minimise risk, detect early warning signs of biting and intervene appropriately.
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van den Brink, Wim, and Falk Kiefer. "Alcohol use disorder." In New Oxford Textbook of Psychiatry, edited by John R. Geddes, Nancy C. Andreasen, and Guy M. Goodwin, 498–506. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198713005.003.0050.

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Alcohol is one of the most frequently used substances, and alcohol-related disorders are common, especially in western societies. While there is no safe lower drinking level, a clear dose–response relationship has been shown between alcohol intake and organ damage. Conceptualization and diagnostic classification of alcohol use disorders have changed over time, focusing most recently on aspects of craving, loss of control, and continued use despite negative consequences. Alcohol acts via various binding sites in the brain and via downstream effects, including glutamatergic, GABAergic, serotonergic, dopaminergic, opioid, and neuroendocrine pathways. For its long-lasting, habit-forming effects, sensitization within the mesolimbic–mesocortical system is crucial. Psychological treatments traditionally focus on motivational enhancement, cognitive behaviour therapy, and the community reinforcement approach. Pharmacological treatment approaches range from aversive and reward-inhibiting to anti-craving compounds and cognitive enhancers, which target opioid, glutamatergic, and monoamine receptors. Improvement of treatment effects can be achieved by polypharmacy and use of personalized medicine, based on clinical characteristics, biomarkers, and genetic indicators.
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