Pub Date : 2021-05-19DOI: 10.5772/INTECHOPEN.96990
Janet Best, A. M. Buchanan, H. F. Nijhout, P. Hashemi, M. Reed
The coauthors have been working together for ten years on serotonin, dopamine, and histamine and their connection to neuropsychiatric illnesses. Hashemi has pioneered many new experimental techniques for measuring serotonin and histamine in real time in the extracellular space in the brain. Best, Reed, and Nijhout have been making mathematical models of brain metabolism to help them interpret Hashemi’s data. Hashemi demonstrated that brain histamine inhibits serotonin release, giving a direct mechanism by which inflammation can cause a decrease in brain serotonin and therefore depression. Many new biological phenomena have come out of their joint research including 1) there are two different reuptake mechanisms for serotonin; 2) the effect of the serotonin autoreceptors is not instantaneous and is long-lasting even when the extracellular concentrations have returned to normal; 3) that mathematical models of serotonin metabolism and histamine metabolism can explain Hashemi’s experimental data; 4) that variation in serotonin autoreceptors may be one of the causes of serotonin-linked mood disorders. Here we review our work in recent years for biological audiences, medical audiences, and researchers who work on mathematical modeling of biological problems. We discuss the experimental techniques, the creation and investigation of mathematical models, and the consequences for neuropsychiatric diseases.
{"title":"Mathematical Models of Serotonin, Histamine, and Depression","authors":"Janet Best, A. M. Buchanan, H. F. Nijhout, P. Hashemi, M. Reed","doi":"10.5772/INTECHOPEN.96990","DOIUrl":"https://doi.org/10.5772/INTECHOPEN.96990","url":null,"abstract":"The coauthors have been working together for ten years on serotonin, dopamine, and histamine and their connection to neuropsychiatric illnesses. Hashemi has pioneered many new experimental techniques for measuring serotonin and histamine in real time in the extracellular space in the brain. Best, Reed, and Nijhout have been making mathematical models of brain metabolism to help them interpret Hashemi’s data. Hashemi demonstrated that brain histamine inhibits serotonin release, giving a direct mechanism by which inflammation can cause a decrease in brain serotonin and therefore depression. Many new biological phenomena have come out of their joint research including 1) there are two different reuptake mechanisms for serotonin; 2) the effect of the serotonin autoreceptors is not instantaneous and is long-lasting even when the extracellular concentrations have returned to normal; 3) that mathematical models of serotonin metabolism and histamine metabolism can explain Hashemi’s experimental data; 4) that variation in serotonin autoreceptors may be one of the causes of serotonin-linked mood disorders. Here we review our work in recent years for biological audiences, medical audiences, and researchers who work on mathematical modeling of biological problems. We discuss the experimental techniques, the creation and investigation of mathematical models, and the consequences for neuropsychiatric diseases.","PeriodicalId":21701,"journal":{"name":"Serotonin and the CNS - New Developments in Pharmacology and Therapeutics [Working Title]","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-05-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"88881576","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2021-05-12DOI: 10.5772/INTECHOPEN.97221
T. Vitalis, C. Verney
Post-Traumatic Stress Disorder (PTSD) is characterized by substantial physiological and/or psychological distress following exposure to trauma. Intrusive fear memories often lead to persistent avoidance of stimuli associated with the trauma, detachment from others, irritability and sleep disturbances. Different key structures in the brain are involved with fear conditioning, fear extinction and coping. The limbic system, namely, the amygdala complex in close relationship with the hippocampal hub and the prefrontal cortex play central roles in the integration and in coping with fear memories. Serotonin acting both as a neurotransmitter and as a neurohormone participates in regulating the normal and pathological activity of these anatomic structures. We review the literature analyzing how the different actors of the serotoninergic system (5-HT receptors, transporters and anabolic and catabolic pathways) may be involved in regulating the sensitivity to highly stressful events and hopefully coping with them.
{"title":"Roles of the Serotoninergic System in Coping with Traumatic Stress","authors":"T. Vitalis, C. Verney","doi":"10.5772/INTECHOPEN.97221","DOIUrl":"https://doi.org/10.5772/INTECHOPEN.97221","url":null,"abstract":"Post-Traumatic Stress Disorder (PTSD) is characterized by substantial physiological and/or psychological distress following exposure to trauma. Intrusive fear memories often lead to persistent avoidance of stimuli associated with the trauma, detachment from others, irritability and sleep disturbances. Different key structures in the brain are involved with fear conditioning, fear extinction and coping. The limbic system, namely, the amygdala complex in close relationship with the hippocampal hub and the prefrontal cortex play central roles in the integration and in coping with fear memories. Serotonin acting both as a neurotransmitter and as a neurohormone participates in regulating the normal and pathological activity of these anatomic structures. We review the literature analyzing how the different actors of the serotoninergic system (5-HT receptors, transporters and anabolic and catabolic pathways) may be involved in regulating the sensitivity to highly stressful events and hopefully coping with them.","PeriodicalId":21701,"journal":{"name":"Serotonin and the CNS - New Developments in Pharmacology and Therapeutics [Working Title]","volume":"58 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-05-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"73580049","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2021-04-19DOI: 10.5772/INTECHOPEN.96525
V. Kovalzon
For most cases of endogenous depression (major depression), the hypothesis of monoamine deficiency, despite a number of limitations it faces, is still considered the most acceptable explanation. The main difficulty faced by this hypothesis is the reason for the decrease in the level of cerebral monoamines (primarily serotonin) during depression. It is assumed either increased activity of the MAO enzyme, which metabolizes serotonin, or a mutation with the loss of function of the gene of the Tph-2 enzyme, which synthesizes serotonin, as possible causes. In this review, a third cause is proposed, which can explain a number of cases of «spontaneous» onset of depressive symptoms in apparently healthy people, as well as links the hypotheses of “monoamine deficiency” and “disturbances in circadian rhythms.” It is assumed that the formation of endogenous depression is due to a combination of two factors: a reduced “basal” level of cerebral serotonin and excessively long pre-morning periods of REM sleep, during which the release of cerebral monoamines stops altogether. As a possible way to of non-drug treatment of depression, not deprivation, but fragmentation of this phase of sleep is suggested, that is much easier for patients to tolerate.
{"title":"Serotonin, Sleep and Depression: A Hypothesis","authors":"V. Kovalzon","doi":"10.5772/INTECHOPEN.96525","DOIUrl":"https://doi.org/10.5772/INTECHOPEN.96525","url":null,"abstract":"For most cases of endogenous depression (major depression), the hypothesis of monoamine deficiency, despite a number of limitations it faces, is still considered the most acceptable explanation. The main difficulty faced by this hypothesis is the reason for the decrease in the level of cerebral monoamines (primarily serotonin) during depression. It is assumed either increased activity of the MAO enzyme, which metabolizes serotonin, or a mutation with the loss of function of the gene of the Tph-2 enzyme, which synthesizes serotonin, as possible causes. In this review, a third cause is proposed, which can explain a number of cases of «spontaneous» onset of depressive symptoms in apparently healthy people, as well as links the hypotheses of “monoamine deficiency” and “disturbances in circadian rhythms.” It is assumed that the formation of endogenous depression is due to a combination of two factors: a reduced “basal” level of cerebral serotonin and excessively long pre-morning periods of REM sleep, during which the release of cerebral monoamines stops altogether. As a possible way to of non-drug treatment of depression, not deprivation, but fragmentation of this phase of sleep is suggested, that is much easier for patients to tolerate.","PeriodicalId":21701,"journal":{"name":"Serotonin and the CNS - New Developments in Pharmacology and Therapeutics [Working Title]","volume":"52 4 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-04-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89053108","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2021-03-16DOI: 10.5772/INTECHOPEN.96362
R. Nikolov, K. Koleva
Serotonin syndrome (SS) is a potentially life-threatening adverse drug effect that occurs after an overdose or combined administration of two or more drugs that increase the serotonin levels. In humans, SS is represented by a triad of symptoms including mental status changes, neuromuscular hyperactivity and autonomic dysfunction. The manifestations of the syndrome observed in rodents resemble the symptoms of SS in humans. Theoretically, SS can occur as a result of stimulation of any of the seven families of the serotonin receptors. However, most data support the involvement of 5-HT1A and 5-HT2A receptors. A number of studies indicate the effectiveness of 5-HT2 antagonists and GABA-ergic agents in the treatment of the hyperthermia and other symptoms of SS in rats. Therefore, animal models of SS may help to further elucidate the mechanism of its development and the possibilities for its treatment.
{"title":"Experimental Serotonin Syndrome: Effects of GABA-ergic Medications and 5-HT2-Antagonists","authors":"R. Nikolov, K. Koleva","doi":"10.5772/INTECHOPEN.96362","DOIUrl":"https://doi.org/10.5772/INTECHOPEN.96362","url":null,"abstract":"Serotonin syndrome (SS) is a potentially life-threatening adverse drug effect that occurs after an overdose or combined administration of two or more drugs that increase the serotonin levels. In humans, SS is represented by a triad of symptoms including mental status changes, neuromuscular hyperactivity and autonomic dysfunction. The manifestations of the syndrome observed in rodents resemble the symptoms of SS in humans. Theoretically, SS can occur as a result of stimulation of any of the seven families of the serotonin receptors. However, most data support the involvement of 5-HT1A and 5-HT2A receptors. A number of studies indicate the effectiveness of 5-HT2 antagonists and GABA-ergic agents in the treatment of the hyperthermia and other symptoms of SS in rats. Therefore, animal models of SS may help to further elucidate the mechanism of its development and the possibilities for its treatment.","PeriodicalId":21701,"journal":{"name":"Serotonin and the CNS - New Developments in Pharmacology and Therapeutics [Working Title]","volume":"55 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-03-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78189268","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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