5-HT receptors (nomenclature as agreed by the NC-IUPHAR Subcommittee on 5-HT receptors [202] and subsequently revised [184, 26]) are, with the exception of the ionotropic 5-HT3 class, GPCRs where the endogenous agonist is 5-hydroxytryptamine. The diversity of metabotropic 5-HT receptors is increased by alternative splicing that produces isoforms of the 5-HT2A (non-functional), 5-HT2C (non-functional), 5-HT4, 5-HT6 (non-functional) and 5-HT7 receptors. Unique amongst the GPCRs, RNA editing produces 5-HT2C receptor isoforms that differ in function, such as efficiency and specificity of coupling to Gq/11 and also pharmacology [42, 501]. Most 5-HT receptors (except 5-ht1e and 5-ht5b) play specific roles mediating functional responses in different tissues (reviewed by [480, 396]).

5-HT receptors (nomenclature as agreed by the NC-IUPHAR Subcommittee on 5-HT receptors [200] and subsequently revised [182]) are, with the exception of the ionotropic 5-HT3 class, GPCRs where the endogenous agonist is 5-hydroxytryptamine. The diversity of metabotropic 5-HT receptors is increased by alternative splicing that produces isoforms of the 5-HT2A (non-functional), 5-HT2C (non-functional), 5-HT4, 5-HT6 (non-functional) and 5-HT7 receptors. Unique amongst the GPCRs, RNA editing produces 5-HT2C receptor isoforms that differ in function, such as efficiency and specificity of coupling to Gq/11 and also pharmacology [40, 499]. Most 5-HT receptors (except 5-ht1e and 5-ht5b) play specific roles mediating functional responses in different tissues (reviewed by [478, 394]).

5-HT receptors (nomenclature as agreed by the NC-IUPHAR Subcommittee on 5-HT receptors [201] and subsequently revised [183]) are, with the exception of the ionotropic 5-HT3 class, GPCRs where the endogenous agonist is 5-hydroxytryptamine. The diversity of metabotropic 5-HT receptors is increased by alternative splicing that produces isoforms of the 5-HT2A (non-functional), 5-HT2C (non-functional), 5-HT4, 5-HT6 (non-functional) and 5-HT7 receptors. Unique amongst the GPCRs, RNA editing produces 5-HT2C receptor isoforms that differ in function, such as efficiency and specificity of coupling to Gq/11 and also pharmacology [41, 500]. Most 5-HT receptors (except 5-ht1e and 5-ht5b) play specific roles mediating functional responses in different tissues (reviewed by [479, 395]).

This chapter summarizes data concerning the pharmacological characteristics and possible functional correlates of central 5-hydroxytryptamine (HT) receptors, and discusses the potential clinical significance of each 5-HT receptor subtype. Recent clinical investigations have focused on the ability of selective agents to act as human anxiolytics. Buspirone is the first pharmacological agent in this class of drugs to be approved for human use. The recent work of Sanders-Bush and colleagues has convincingly demonstrated that 5-HT stimulation of phosphatidylinositol hydrolysis is mediated by the 5-HT1C site in choroid plexus membranes. The existence of a variety of other 5-HT receptor subtypes has been hypothesized, as well. In general, the feature that distinguishes the following sites from the foregoing receptors is that they have only been identified in a single laboratory.

5-HT receptors (nomenclature as agreed by the NC-IUPHAR Subcommittee on 5-HT receptors [198] and subsequently revised [180]) are, with the exception of the ionotropic 5-HT3 class, GPCRs where the endogenous agonist is 5-hydroxytryptamine. The diversity of metabotropic 5-HT receptors is increased by alternative splicing that produces isoforms of the 5-HT2A (non-functional), 5-HT2C (non-functional), 5-HT4, 5-HT6 (non-functional) and 5-HT7 receptors. Unique amongst the GPCRs, RNA editing produces 5-HT2C receptor isoforms that differ in function, such as efficiency and specificity of coupling to Gq/11 and also pharmacology [40, 491]. Most 5-HT receptors (except 5-ht1e and 5-ht5b) play specific roles mediating functional responses in different tissues (reviewed by [471, 387]).

This section of Headache annually reviews the status of recently completed and ongoing major clinical trials involving common headache disorders. The review will focus on multicenter trials of new therapies, as well as novel formulations of previously approved therapeutics. The Table summarizes the major therapeutic headache trials that were ongoing at the end of 2015, according to data obtained from both the "ClinicalTrials.Gov" website and from corporate press releases and presentations.

A role for calcitonin gene-related peptide (CGRP) in the pathophysiology of migraine has been established over the past 25 years. There have now been at least five different small-molecule CGRP antagonists that have demonstrated statistical proof of efficacy in the acute treatment of migraine. At present, multiple clinical trials are underway that are assessing the ability of long-acting antibodies against CGRP to prevent frequent migraine attacks. This review summarizes the existing data concerning the role of CGRP in migraine and attempts to highlight some possible outcomes from the ongoing anti-CGRP antibody trials.

Migraine attacks rarely occur spontaneously in the absence of any possible precipitating factors. A systematic literature review of 25 publications revealed a consistent set of stimuli that have been identified as factors associated with the onset of a migraine attack. The weighted average of the “Top 10” trigger factors was determined. Stress was cited as the overall most common migraine precipitating factor, which was identified as a trigger factor by 58 % of 7187 migraineurs. The incidence of migraine precipitating factors, across various populations globally, demonstrates the clinical consistency of migraine in the human population. Future efforts aimed at mitigating these precipitating factors have the potential to significantly improve migraine management. However, the current healthcare system is unlikely to be able to develop detailed personalized management plans. There is a need to develop a novel approach to the identification and management of multiple trigger factors in individual migraineurs.

Letter to the Editor Not All CGRP Antagonists Are Created Equal Stephen J. Peroutka MD, PhD, Stephen J. Peroutka MD, PhD NeurogesX, Inc., San Mateo, CA, USASearch for more papers by this author Stephen J. Peroutka MD, PhD, Stephen J. Peroutka MD, PhD NeurogesX, Inc., San Mateo, CA, USASearch for more papers by this author First published: 30 May 2013 https://doi.org/10.1111/head.12107Citations: 1Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Citing Literature Volume53, Issue6June 2013Pages 1004-1006 RelatedInformation

This section of Headache annually reviews the status of recently completed and ongoing major clinical trials involving common headache disorders. The review will focus on multicenter trials of new therapies, as well as novel formulations of previously approved therapeutics. Table 1 summarizes the major therapeutic headache trials that are ongoing at the present time, according to data obtained from both the "ClinicalTrials.Gov" website and from corporate press releases and presentations.

An annual review of the status of recently completed and ongoing major clinical trials involving common headache disorders is presented. The review will focus on multicenter trials of new therapies as well as novel formulations of previously approved therapeutics. The article also presents a tabulated summary of the major therapeutic headache trials that are ongoing at the present time, according to data obtained from both the ClinicalTrials.gov Web site and corporate press releases.

1. The American College of Neuropsychopharmacology (ACNP) presents the Efron Award to an individual on the basis of outstanding basic research contributions to neuropsychopharmacology. The contributions may be preclinical or work that emphasizes the interface between basic and clinical research. The selection of the awardee is based on the quality of the contribution and its impact in advancing neuropsychopharmacology. Award recipients will receive a monetary award and a plaque to be given at the ACNP Annual Meeting in Hollywood, Florida, December 812, 2013. Award recipients who are not members of the ACNP may also be reimbursed for their expenses to attend the Annual Meeting. The Award winner must attend the Annual Meeting. 2. Any scientist, worldwide, may nominate an individual for this award by submitting to the Awards Committee: a. The nominating letter (no more than three pages) should include a description of the contribution(s) of the candidate and also the significance of his/her contribution(s); (additional supporting letters are not needed and will not be considered); b. The curriculum vitae of the candidate; c. No more than three papers representing the contribution(s) (career contributions or specific works) upon which the Award would be based.

1. The American College of Neuropsychopharmacology (ACNP) presents the Efron Award to an individual on the basis of outstanding basic research contributions to neuropsychopharmacology. The contributions may be preclinical or work that emphasizes the interface between basic and clinical research. The selection of the awardee is based on the quality of the contribution and its impact in advancing neuropsychopharmacology. Award recipients will receive a monetary award and a plaque to be given at the ACNP Annual Meeting in Hollywood, Florida, December 26, 2012. Award recipients who are not members of the ACNP may also be reimbursed for their expenses to attend the Annual Meeting. The Award winner must attend the Annual Meeting. 2. Any scientist, worldwide, may nominate an individual for this award by submitting to the Awards Committee: a. The nominating letter (no more than three pages) should include a description of the contribution(s) of the candidate and also the significance of his/her contribution(s); (additional supporting letters are not needed and will not be considered); b. The curriculum vitae of the candidate; c. No more than three papers representing the contribution(s) (career contributions or specific works) upon which the Award would be based.

This section of Headache annually reviews the status of recently completed and ongoing clinical trials involving headache disorders. The review will focus on multicenter trials of new therapies as well as novel formulations of previously approved therapeutics. Table 1 summarizes major migraine therapeutic trials that have been completed recently, according to data obtained from the "ClinicalTrials.Gov" website as well as from corporate press releases. Table 2 summarizes the major therapeutic trials that are ongoing at the present time.

2008: The Year in Review Stephen J. Peroutka MD, PhD, Stephen J. Peroutka MD, PhD From the Clinical Neurosciences, PRA International, Carmel, CA, USA.Search for more papers by this author Stephen J. Peroutka MD, PhD, Stephen J. Peroutka MD, PhD From the Clinical Neurosciences, PRA International, Carmel, CA, USA.Search for more papers by this author First published: 27 April 2009 https://doi.org/10.1111/j.1526-4610.2009.01422.xCitations: 4Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat Citing Literature Volume49, Issue5May 2009Pages 796-802 RelatedInformation

Antidepressants compete at several neurotransmitter receptor binding sites, but drug affinities do not correlate with clinical efficacy. Long-term, but not short-term, antidepressant treatment decreases the numbers of both serotonin and β-adrenergic receptors. The decrease in the number of receptor sites is most marked for [ 3 H]spiroperidol-labeled serotonin receptors and is characteristic for antidepressants of several classes.