Functional nausea and vomiting is a broad term used to be described a subset of individuals who have chronic nausea and vomiting without apparent cause, despite extensive evaluation. According to the Rome III criteria, functional nausea and vomiting can be subdivided into three separate entities: chronic idiopathic nausea, functional vomiting and cyclic vomiting syndrome. Although no specific test can diagnose these diseases, the diagnostic approach requires excellent history taking combined with judicious diagnostic testing to exclude some organic cause of chronic nausea and vomiting. These conditions are probably not psychogenic in origin. Treatment remains empirical for all patients with functional nausea and vomiting. Reassurance and supportive physician-patient relationship, along with use of low-dose tricyclic antidepressants, can be beneficial in caring for patients with chronic idiopathic nausea and functional vomiting. The cornerstones of management for patients with cyclic vomiting syndrome are identifying and avoidance of triggering factors, treatment with prophylactic antimigraine agents, 5-HT3 antagonists, benzodiazepines and 5-HT1 agonists (sumatriptan), with supportive therapy.
Antidepressive Agents, Tricyclic ; Benzodiazepines ; Diagnostic Tests, Routine ; Humans ; Nausea ; Rome ; Serotonin 5-HT1 Receptor Agonists ; Serotonin 5-HT3 Receptor Antagonists ; Vomiting

Irritable bowel syndrome is a group of symptoms that includes abdominal pain and changes in the form and frequency of stool. Since its symptoms are usually long-lasting, the disease significantly degrades quality of life. Several pharmacological therapies have been suggested according to the type of symptoms (e.g., abdominal pain, constipation, or diarrhea). In order to control abdominal pain, smooth muscle antispasmodics, antidepressants including tricyclic antidepressants and selective serotonin reuptake inhibitors, or 5-HT3 antagonists can be used. To improve constipation, dietary fiber or laxatives, 5-HT4 agonists, and chloride channel activators are available. Opioid agonists, mixed opioid agonists/antagonists such as eluxadoline, and bile salt sequestrants can be considered for diarrhea. In addition, probiotics and non-absorbable oral antibiotics can be used for the normalization of the gut microbiome and the treatment of small intestinal bacterial overgrowth, respectively. It is necessary to understand the characteristics of each drug and their combinations, because any single regimen cannot improve all symptoms in patients with irritable bowel syndrome. In this review, the mechanisms of action, efficacy, and adverse events associated with drugs used for irritable bowel syndrome are summarized.
Abdominal Pain ; Anti-Bacterial Agents ; Antidepressive Agents ; Antidepressive Agents, Tricyclic ; Bile ; Chloride Channel Agonists ; Constipation ; Diarrhea ; Dietary Fiber ; Drug Therapy* ; Gastrointestinal Microbiome ; Humans ; Irritable Bowel Syndrome* ; Laxatives ; Muscle, Smooth ; Parasympatholytics ; Probiotics ; Quality of Life ; Serotonin 5-HT3 Receptor Antagonists ; Serotonin 5-HT4 Receptor Agonists ; Serotonin Uptake Inhibitors

Irritable bowel syndrome is a group of symptoms that includes abdominal pain and changes in the form and frequency of stool. Since its symptoms are usually long-lasting, the disease significantly degrades quality of life. Several pharmacological therapies have been suggested according to the type of symptoms (e.g., abdominal pain, constipation, or diarrhea). In order to control abdominal pain, smooth muscle antispasmodics, antidepressants including tricyclic antidepressants and selective serotonin reuptake inhibitors, or 5-HT3 antagonists can be used. To improve constipation, dietary fiber or laxatives, 5-HT4 agonists, and chloride channel activators are available. Opioid agonists, mixed opioid agonists/antagonists such as eluxadoline, and bile salt sequestrants can be considered for diarrhea. In addition, probiotics and non-absorbable oral antibiotics can be used for the normalization of the gut microbiome and the treatment of small intestinal bacterial overgrowth, respectively. It is necessary to understand the characteristics of each drug and their combinations, because any single regimen cannot improve all symptoms in patients with irritable bowel syndrome. In this review, the mechanisms of action, efficacy, and adverse events associated with drugs used for irritable bowel syndrome are summarized.
Abdominal Pain ; Anti-Bacterial Agents ; Antidepressive Agents ; Antidepressive Agents, Tricyclic ; Bile ; Chloride Channel Agonists ; Constipation ; Diarrhea ; Dietary Fiber ; Drug Therapy* ; Gastrointestinal Microbiome ; Humans ; Irritable Bowel Syndrome* ; Laxatives ; Muscle, Smooth ; Parasympatholytics ; Probiotics ; Quality of Life ; Serotonin 5-HT3 Receptor Antagonists ; Serotonin 5-HT4 Receptor Agonists ; Serotonin Uptake Inhibitors

It has been known that central tryptaminergic system is closely related with the regulation of renal function, and that central 5-HT1 receptors mediate diuresis and natriuresis, whereas central 5-HT2 and 5-HT3 receptors mediate antidiuresis and antinatriuresis. Among many subtypes of 5-HT1 receptors, central 5-HT1A subtype has been suggested to exert diuretic and natriuretic effets. Further, it was recently observed that TFMPP, 5-HT1B agonist, elicited profound diuresis and natriuresis when administered intracerebroventricularly(icv). Present study is therefore undertaken to delineate the mechanism involved in the natriuresis and diuresis induced by icv TFMPP, employing the denervated and vagotomized rabbits. The influence of icv TFMPP on the plasma level of ANP was also observed. TFMPP 250 microgram/kg icv produced marked diuresis and natriuresis. Renal hemodynamics showed significant increase only in the first 10-min period after administration and thereafter tended to recover. However, natriuretic action lasted even after the increased renal hemodynamics returned to the control level, suggesting the decreased Na reabsorption in the tubules by humoral natriuretic factors. Systemic blood pressure transiently increased. In rabbits in which one kidney is denervated, with the contralateral intact as the control kidney, the denervated kidney also responded with natriuresis and diuresis like that of the normal rabbit. The contralateral kidney responded with typical diuretic and natriuretic effects, along with the marked increased of renal hemodynamics. The plasma ANP, one of humoral natriuretic factors, increased after administration of icv TFMPP, peaking at about 15min. In bilaterally vagotomized rabbits, the natriuretic and diuretic effects produced by icv TFMPP were greater than that of the normal rabbits. These observations suggest that the natriuresis and diuresis elicited by icv TFMPP result from the inhibition of tubular Na reabsorption mainly through mediation of ANP. It has been also suggested that vagus nerve might exert inhibitory influence on the diuretic action of icv TFMPP, because the renal effects was augmented in the vagotomized rabbits.
Atrial Natriuretic Factor ; Blood Pressure ; Diuresis ; Diuretics ; Hemodynamics ; Kidney ; Natriuresis ; Natriuretic Agents ; Negotiating ; Plasma ; Rabbits* ; Receptors, Serotonin, 5-HT1 ; Receptors, Serotonin, 5-HT3 ; Serotonin 5-HT1 Receptor Agonists ; Vagus Nerve

Rabbit Syndrome is an uncommon side effect of antipsychotic treatment. Although it is usually associated with typical antipsychotics, it can also be related to atypical antipsychotics. Anticholinergics are the most accepted treatment approach in treating Rabbit Syndrome. Fluvoxamine is a member of selective serotonin reuptake inhibitors and it is a potent agonist of sigma 1 receptors. In this article, we report a Rabbit Syndrome case who has benefited from fluvoxamine, in terms of both depressive disorder and Rabbit Syndrome; and present the data on the effects of sigma 1 agonist fluvoxamine on numerous movement disorders.
Antipsychotic Agents ; Cholinergic Antagonists ; Depressive Disorder ; Fluvoxamine ; Movement Disorders ; Receptors, sigma ; Serotonin Uptake Inhibitors

Serotonin is one of the most important neurotransmitters involved in the pathophysiology of depressive illness. The assessment of alteration of cerebral serotonin has been still controversial but interesting topic to study. Recently, increasing evidence has accumulated that the N100 amplitude slope reflects cerebral serotonin activity and treatment response of selective serotonin reuptake inhibitors (SSRIs). We report on two patients who showed abrupt mood changes and side effects after taking SSRI antidepressants. In both patients, aberrantly high N100 amplitude slopes were observed. Our cases suggest that the N100 amplitude slope may be a reliable indicator for predicting manic conversion and side effects in the SSRI treatment of depressive patients. Controlled studies are necessary to confirm whether a high N100 amplitude slope is a useful indicator of SSRI supersensitivity.
Antidepressive Agents ; Depression ; Humans ; Neurotransmitter Agents ; Serotonin ; Serotonin Uptake Inhibitors

AIMTo determine whether serotonin, a major neurotransmitter in brain, can modulate the production of secretory beta-amyloid protein precursor (sAPP) by activation of serotonin 5-HT2C receptor.

METHODSThe hippocampal slices of rats were incubated with various concentrations of serotonin, M-110, or L-107. sAPP released into the incubation medium were assayed by Western blot analysis assay with monoclonal antibody 22C11 for 2 h.

RESULTSVarious concentrations of serotonin (1.0 x 10(-2) - 1.0 x 10(3) micromol x L(-1)), M-110, a serotonin 5-HT2C agonist (1.5 x 10(-6) - 1.5 x 10(3) micromol x L(-1)), showed positive effect on the production of sAPP while L-107, a serotonin 5-HT2C antagonist (1.0 x 10(-9) - 1.0 x 10(3) micromol x L(-1)), showed negative effect on the production of sAPP over controls.

CONCLUSIONSerotonin modulates production of secretory amyloid beta-protein precursor through serotonin 5-HT2C receptor in incubated rat hippocampal slices.

Amyloid beta-Protein Precursor ; secretion ; Animals ; Hippocampus ; metabolism ; In Vitro Techniques ; Male ; Peptide Fragments ; secretion ; Rats ; Rats, Sprague-Dawley ; Receptor, Serotonin, 5-HT2C ; Serotonin ; pharmacology ; Serotonin 5-HT2 Receptor Agonists ; Serotonin 5-HT2 Receptor Antagonists

Serotonin syndrome (SS) is a potentially life-threatening drug reaction characterized by mental status change, increased neuromuscular tone, and autonomic instability. Linezolid, an oxazolidinone antibacterial agent, is widely used in general hospitals; however, it interacts with some serotonin agonists and may cause SS. We report a case of SS caused by linezolid, without the concomitant use of serotonin agonist. A 72-year-old patient was admitted due to recurrent wound infection of his left ankle. He developed fever, skin rash, and renal function deterioration, and blood eosinophils and liver enzymes increased after administration of vancomycin. The antibiotic was changed to linezolid against methicillin-resistant Staphylococcus aureus. Four days later, he developed agitation, fever, increased blood pressure, and tachycardia. There were no abnormal findings in laboratory and image tests, including brain and chest computed tomography suggesting the cause of his symptoms. He had not taken any serotonin agonists, including serotonin uptake inhibitors and monoamineoxidase-inhibiting antidepressants. When administration of linezolid was stopped, his symptoms improved within 24 hours and fully recovered within 2 days without additional treatments.
Aged ; Ankle ; Antidepressive Agents ; Blood Pressure ; Brain ; Dihydroergotamine ; Eosinophils ; Exanthema ; Fever ; Hospitals, General ; Humans ; Liver ; Methicillin-Resistant Staphylococcus aureus ; Serotonin Receptor Agonists ; Serotonin Syndrome* ; Serotonin Uptake Inhibitors ; Tachycardia ; Thorax ; Vancomycin ; Wound Infection ; Linezolid

Development of various antidepressants such as monoamine oxidase inhibitors, tricyclic antidepressants, selective serotonin reuptake inhibitors, serotonin norepinephrine reuptake inhibitors, and noradrenergic and specific serotonergic antidepressant has led to a tremendous progression of pharmaceutical treatment for depression, but still there are some limitations of current antidepressants, such as treatment-resistant depression and delayed onset of antidepressants. The pathogenesis of depression is unclear because depression is a heterogeneous disease state, and the mechanisms of antidepressants remain uncertain as well. Nevertheless, in an attempt to develop novel antidepressants, some trials have been conducted based on the potential biological mechanism discovered in the numerous research results. This review will provide information about the potential novel antidepressants and the current states of clinical studies using them. In particular, some potential novel antidepressants anti-inflammatory agents, antioxidants, anticholinergics, modulators of Hypothalamic Pituitary Adrenal Axis, glutamate, and opioid systems, as well as some neuropeptides such as susbstance P, neuropeptide Y, and galanin will be discussed.
Anti-Inflammatory Agents ; Antidepressive Agents ; Antidepressive Agents, Tricyclic ; Antioxidants ; Axis, Cervical Vertebra ; Cholinergic Antagonists ; Depression* ; Depressive Disorder ; Drug Therapy ; Galanin ; Glutamic Acid ; Monoamine Oxidase Inhibitors ; Neuropeptide Y ; Neuropeptides ; Norepinephrine ; Serotonin ; Serotonin Uptake Inhibitors

Selective serotonin reuptake inhibitors (SSRIs) are currently the treatment of choice in depression and constitute major portion of prescription in depressive patients. The role of serotonin receptors in bone is emerging, raising certain questions regarding the effect of blockade of serotonin reuptake in the bone metabolism. Clinical studies have reported an association of SSRI antidepressants which with increase in fracture and decrease in bone mineral density. This review focus on recent evidence that evaluate the association of SSRIs with the risk of fracture and bone mineral density and also the probable mechanisms that might be involved in such effects.
Antidepressive Agents ; Bone Density ; Depression ; Humans ; Metabolism ; Prescriptions ; Receptors, Serotonin ; Serotonin Uptake Inhibitors* ; Serotonin*