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5‐HT 1B receptor: a target for antidepressant drugs?
Author(s) -
Chenu Franck,
Dailly Eric,
Bourin Michel
Publication year - 2005
Publication title -
drug development research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.582
H-Index - 60
eISSN - 1098-2299
pISSN - 0272-4391
DOI - 10.1002/ddr.20017
Subject(s) - antidepressant , serotonergic , monoamine neurotransmitter , mechanism of action , serotonin , pharmacology , receptor , depression (economics) , neurotransmission , medicine , psychology , neuroscience , chemistry , hippocampus , biochemistry , economics , in vitro , macroeconomics
It is generally accepted that about two thirds of patients treated for depression respond only after several weeks (2 to 8 weeks) whilst a third do not respond at all. A depressed patient's response to a treatment is defined by at least 50% reduction of the symptoms evaluated on a standard instrument (i.e., Hamilton Depression Rating Scale). Thus, a response to an antidepressant treatment cannot be considered as a remission. Remission can take many months to occur. It is then crucial to find new targets for antidepressants development or co‐administration strategies in order to reduce the long delay in onset of action and improve the efficiency of current treatments. According to their mechanism of action, current antidepressants induce an increase in serotonin and/or noradrenaline neurotransmission by increasing the monoamine extracellular level available in the synaptic cleft. It is then highly possible that the antidepressant effect depends on the synaptic receptor(s) activated. In the case of serotonergic compounds, 14 subtypes of receptors could be stimulated. In this short review, we focus on the impact of 5‐HT 1B receptor activation in the mediation of antidepressant‐like effect. Drug Dev. Res. 65:141–146, 2005. © 2005 Wiley‐Liss, Inc.