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      Antidepressant-like Effects of δ Opioid Receptor Agonists in Animal Models

      research-article
      Author(s): * ,
      Publication date (Electronic):
      Journal: Current Neuropharmacology
      Publisher: Bentham Science Publishers
      Keywords: Anxiety, depression, KNT-127, naltrindole, SNC80, TAN-67.

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          Abstract

          Recently, δ opioid receptor agonists have been proposed to be attractive targets for the development of novel antidepressants. Several studies revealed that single treatment of δ opioid receptor agonists produce antidepressant-like effects in the forced swimming test, which is one of the most popular animal models for screening antidepressants. In addition, subchronic treatment with δ opioid receptor agonists has been shown to completely attenuate the hyperemotional responses found in olfactory bulbectomized rats. This animal model exhibits hyperemotional behavior that may mimic the anxiety, aggression, and irritability found in depressed patients, suggesting that δ opioid receptor agonists could be effective in the treatment of these symptoms in depression. On the other hand, prototype δ opioid receptor agonists produce convulsive effects, which limit their therapeutic potential and clinical development. In this review, we presented the current knowledge regarding the antidepressant-like effects of δ opioid receptor agonists, which include some recently developed drugs lacking convulsive effects.

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          Most cited references72

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          Depression: a new animal model sensitive to antidepressant treatments.

          R. PORSOLT, M. LE PICHON, M Jalfre (1977)
          Article 0 comments Cited 736 times – based on 0 reviews     Review now
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            Acute and longer-term outcomes in depressed outpatients requiring one or several treatment steps: a STAR*D report.

            D Kupfer, George Niederehe, Andrew Nierenberg … (2006)
            This report describes the participants and compares the acute and longer-term treatment outcomes associated with each of four successive steps in the Sequenced Treatment Alternatives to Relieve Depression (STAR*D) trial. A broadly representative adult outpatient sample with nonpsychotic major depressive disorder received one (N=3,671) to four (N=123) successive acute treatment steps. Those not achieving remission with or unable to tolerate a treatment step were encouraged to move to the next step. Those with an acceptable benefit, preferably symptom remission, from any particular step could enter a 12-month naturalistic follow-up phase. A score of or=11 (HRSD(17)>or=14) defined relapse. The QIDS-SR(16) remission rates were 36.8%, 30.6%, 13.7%, and 13.0% for the first, second, third, and fourth acute treatment steps, respectively. The overall cumulative remission rate was 67%. Overall, those who required more treatment steps had higher relapse rates during the naturalistic follow-up phase. In addition, lower relapse rates were found among participants who were in remission at follow-up entry than for those who were not after the first three treatment steps. When more treatment steps are required, lower acute remission rates (especially in the third and fourth treatment steps) and higher relapse rates during the follow-up phase are to be expected. Studies to identify the best multistep treatment sequences for individual patients and the development of more broadly effective treatments are needed.
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              Assessing substrates underlying the behavioral effects of antidepressants using the modified rat forced swimming test.

              John F. Cryan, Rita J. Valentino, Irwin Lucki (2005)
              Selective serotonin reuptake inhibitors (SSRIs) are the most widely prescribed antidepressant class today and exert their antidepressant-like effects by increasing synaptic concentrations of serotonin (5-HT). The rat forced swim test (FST) is the most widely used animal test predictive of antidepressant action. Procedural modifications recently introduced by our laboratory have enabled SSRI-induced behavioral responses to be measured in the modified FST. The use of this model to understand the pharmacological and physiological mechanisms underlying the role of 5-HT in the behavioral effects of antidepressant drugs is reviewed. Although all antidepressants reduced behavioral immobility, those antidepressants that increase serotonergic neurotransmission predominantly increase swimming behavior whereas those that increase catacholaminergic neurotransmission increase climbing behavior. The 5-HT(1A), 5-HT(1B/1D) and 5-HT(2C) receptors are the 5-HT receptors most important to the therapeutic effects of SSRIs, based on extensive evaluation of agonists and antagonists of individual 5-HT receptor subtypes. Studies involving chronic administration have shown that the effects of antidepressants are augmented following chronic treatment. Other studies have demonstrated strain differences in the response to serotonergic compounds. Finally, a physiological model of performance in the rat FST has been proposed involving the regulation of 5-HT transmission by corticotropin releasing factor (CRF).
              Article 0 comments Cited 193 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-ta): Curr Neuropharmacol
                Journal ID (iso-abbrev): Curr Neuropharmacol
                Journal ID (publisher-id): CN
                Title: Current Neuropharmacology
                Publisher: Bentham Science Publishers
                ISSN (Print): 1570-159X
                ISSN (Electronic): 1875-6190
                Publication date (Print): September 2012
                Publication date (Electronic): September 2012
                Volume: 10
                Issue: 3
                Pages: 231-238
                Affiliations
                Department of Neuropsychopharmacology, National Institute of Mental Health, National Center of Neurology and Psychiatry, Tokyo 187-8553, Japan
                Author notes
                [* ]Address correspondence to this author at the Department of Neuropsychopharmacology, National Institute of Mental Health, National Center of Neurology and Psychiatry, 4-1-1 Ogawahigashimachi, Kodaira, Tokyo 187-8553, Japan; Tel: +81-42-346-1987; Fax: +81-42-346-1987; E-mail: asaitoh@ 123456ncnp.go.jp
                Article
                Publisher ID: CN-10-231
                DOI: 10.2174/157015912803217314
                PMC ID: 3468877
                PubMed ID: 23449756
                SO-VID: 554e6934-cde9-41c1-a4db-8e5f5cb9e3aa
                Copyright © ©2012 Bentham Science Publishers
                License:

                This is an open access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/2.5/), which permits unrestrictive use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 5 January 2012
                Date revision received : 9 March 2012
                Date accepted : 5 April 2012
                Categories
                Subject: Article

                ScienceOpen disciplines: Pharmacology & Pharmaceutical medicine
                Keywords: anxiety,depression,knt-127,naltrindole,snc80,tan-67.
                Data availability:
                ScienceOpen disciplines: Pharmacology & Pharmaceutical medicine
                Keywords: anxiety, depression, knt-127, naltrindole, snc80, tan-67.

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