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Hyperkinetic Movement Disorders
Published in Philip B. Gorelick, Fernando D. Testai, Graeme J. Hankey, Joanna M. Wardlaw, Hankey's Clinical Neurology, 2020
Morales-Briceno Hugo, Victor S.C. Fung, Annu Aggarwal, Philip Thompson
A potentially life-threatening disorder resulting from excessive stimulation of central and peripheral serotonin receptors by therapeutic or recreational drugs, often when taken in combination.49
Environmental Emergencies
Published in Anthony FT Brown, Michael D Cadogan, Emergency Medicine, 2020
Anthony FT Brown, Michael D Cadogan
Serotonin syndrome This is a clinical manifestation of excessive stimulation of serotonin receptors in the central nervous system (CNS).It follows drug combinations with selective serotonin reuptake inhibitors (SSRIs), monoamine-uptake inhibitors, lithium, analgesics such as fentanyl or tramadol, antiemetics such as ondansetron, and illicit drugs such as amphetamine or cocaine.It has a spectrum of severity ranging from agitation and hyperreflexia through to generalized rigidity worse in the legs, myoclonus, autonomic instability, mental status changes and hyperthermia.
Rational Medical Therapy of Functional GI Disorders
Published in Kevin W. Olden, Handbook of Functional Gastrointestinal Disorders, 2020
Richard M. Sperling, Kenneth R. McQuaid
Substituted benzamides and the gut serotonin system—the two substituted benzamides inclinical use in the United States are metoclopramide and cisapride. These agents have prokinetic effects throughout the GI tract. Although its mechanism of action has not been wholly worked out, cisapride has been shown to cause the release of acetylcholine from postganglionic nerves in the gut intramural plexus, resulting in smooth-muscle contraction (209,212). This effect may be mediated by a complex interaction involving serotonin receptors.
Efficacy of dextromethorphan for the treatment of depression: a systematic review of preclinical and clinical trials
Published in Expert Opinion on Emerging Drugs, 2021
Amna Majeed, Jiaqi Xiong, Kayla M. Teopiz, Jason Ng, Roger Ho, Joshua D. Rosenblat, Lee Phan, Bing Cao, Roger S. McIntyre
In recognition of the importance of examining other avenues of depression management (i.e. aside from traditional antidepressant drugs [e.g. SNRIs] that act through norepinephrine and serotonin receptors), various antidepressants with novel mechanisms of action have emerged in recent decades [13]. For example, agomelatine, a melatonergic receptor agonist and a 5-HT2C antagonist has been shown to be effective and well-tolerated in MDD patients [14]. Another novel molecule, neuropeptide Y (NPY), has also been reported to exert positive antidepressant effects in both preclinical and clinical studies [15,16]. The discovery that the N-methyl-D-aspartate (NMDA) receptor antagonist, ketamine, is capable of rapid-onset efficacy in adults with treatment resistant depression (TRD) provides proof of principle that pharmacologic agents that primarily target glutamate signaling may also be capable of symptom relief in MDD [17]. Indeed, intranasal esketamine has been approved and received Breakthrough Designation by the US Food and Drug Administration for adults with TRD as well as adults with MDD and suicidality [18–21].
Carcinoid Heart Disease
Published in Structural Heart, 2020
Amin Sabet, Mina Haghighiabyaneh, Chirag Rajyaguru, Ajit Raisinghani, Daniel Kupsky, Anthony N. DeMaria
The pathogenesis of carcinoid heart disease and the development of carcinoid plaques remain obscure. Carcinoid tumors produce a variety of vasoactive substances including 5-HT (serotonin), histamine, bradykinin, prostaglandins, and other substances with fibroblast proliferative properties such as transforming growth factor-β (TGF-β) or tachykinins (neurokinin A, substance P, neuropeptide K). These peptides ultimately cause the deposition of plaques on the endocardial surfaces of valve leaflets, subvalvular apparatus (tendinous chords, papillary muscles), and cardiac chambers and occasionally within the intima of the pulmonary arteries and the aorta. These plaque-like-fibrotic lesions result from the proliferation of myofibroblasts, smooth muscle cells and the deposition of extracellular matrix (ECM); they typically have a white appearance. These lesions result in thickening of the valve leaflets and chordal structures 12–16 (Figure 1). There is a growing body of evidence that serotonin (5-HT) plays a key role in forming these plaques and producing CHD. Serotonin activity is mediated by interaction with seven serotonin receptor classes located on the cell membrane of neurons and of many other cells in the body. The 5-HT 2B receptor subtype has been found to be present in the cardiovascular system.17 The signal transduction induced by 5-HT 2B receptor activation has been shown to initiate the mitosis of fibroblasts and smooth muscle cells. It can also up-regulate the cytokine transforming growth factor-β, which is known to stimulate fibroblasts to produce ECM proteins.18–20
Association of HTR1A gene polymorphisms with obsessive–compulsive disorder and its treatment response: the influence of sex and clinical characteristics
Published in International Journal of Neuroscience, 2019
Niyousha Alizadeh, Nasim Nosrat, Zohreh Jahani, Abolhassan Ahmadiani, Sareh Asadi, Jamal Shams
Obsessive–Compulsive Disorder (OCD) is a relatively common psychological disorder with a prevalence rate of 1% to 3% of the world population [1]. The classification and diagnosis of OCD are characterized by unwanted and disturbing thoughts, images, or urges (obsessions) along with repetitive behaviours [2]. These repetitive activities can negatively affect a person’s daily life. Selective serotonin reuptake inhibitors (SSRIs) are first-line pharmacotherapy for OCD treatment that inhibits the serotonin reuptake, increasing the level of serotonin in the synaptic cleft [3]. Currently, at least 14 mammalian serotonin receptor subtypes have been identified which differ in structure and distribution [4]. In the human brain, the serotonin 1A receptor (5-HTR1A) is highly abundant [5]; it is expressed presynaptically on serotonin (5-HT) cell bodies in the raphe (somatodendritic autoreceptors), and post-synaptically in limbic and cortex regions [6]. The therapeutic effects of SSRI seem to be associated with the desensitization of somatodendritic HTR1A in the raphe nuclei (according to both animal and human studies results), which is induced by an increase of serotonin in the extracellular space [7].