Pub Date : 2010-11-01DOI: 10.1017/S1461145710001124
F. Sulser
| | || With the death of Norbert Matussek on 10 November 2009, the international communities of Biological Psychiatry and Psychopharmacology lost one of their foremost members. The CINP lost one of its Honorary Fellows and all of us a dear friend and trusted colleague. Norbert Matussek was born in 1922 in Berlin. He studied medicine and chemistry in Heidelberg, Tuebingen and Munich and received his M.D. degree in 1952 from the University of Munich and his Dipl.Chem. in 1955 from the University of Heidelberg. From 1954 to 1956, he worked with Adolf Butenandt, a Nobel Laureate in Medicine, at the Max-Planck Institute in Tuebingen where he pursued studies on Ecdyson which he characterized as a steroid hormone, and on the isolation and structural characterization …
{"title":"Norbert Matussek (1922–2009)","authors":"F. Sulser","doi":"10.1017/S1461145710001124","DOIUrl":"https://doi.org/10.1017/S1461145710001124","url":null,"abstract":"| |\u0000||\u0000\u0000With the death of Norbert Matussek on 10 November 2009, the international communities of Biological Psychiatry and Psychopharmacology lost one of their foremost members. The CINP lost one of its Honorary Fellows and all of us a dear friend and trusted colleague.\u0000\u0000Norbert Matussek was born in 1922 in Berlin. He studied medicine and chemistry in Heidelberg, Tuebingen and Munich and received his M.D. degree in 1952 from the University of Munich and his Dipl.Chem. in 1955 from the University of Heidelberg.\u0000\u0000From 1954 to 1956, he worked with Adolf Butenandt, a Nobel Laureate in Medicine, at the Max-Planck Institute in Tuebingen where he pursued studies on Ecdyson which he characterized as a steroid hormone, and on the isolation and structural characterization …","PeriodicalId":394244,"journal":{"name":"The International Journal of Neuropsychopharmacology","volume":"46 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2010-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"124037193","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2010-08-01DOI: 10.1017/S1461145710000477
E. Vieta, C. Franco, N. Cruz
Krishnadas & Livingston (2010) make the case for caution when interpreting the results of our meta-analysis showing the efficacy of some second-generation antipsychotics in bipolar depression, as well as their apparent rapid onset of action (Cruz et al. 2010). While we generally agree that in the case of olanzapine the only items that significantly separated from placebo were those assessing sleep, inner tension and appetite (Tohen et al. 2003) and this, plus the fact that the combination of olanzapine with fluoxetine was significantly superior to …
{"title":"Antipsychotics in bipolar depression: in reply","authors":"E. Vieta, C. Franco, N. Cruz","doi":"10.1017/S1461145710000477","DOIUrl":"https://doi.org/10.1017/S1461145710000477","url":null,"abstract":"Krishnadas & Livingston (2010) make the case for caution when interpreting the results of our meta-analysis showing the efficacy of some second-generation antipsychotics in bipolar depression, as well as their apparent rapid onset of action (Cruz et al. 2010). While we generally agree that in the case of olanzapine the only items that significantly separated from placebo were those assessing sleep, inner tension and appetite (Tohen et al. 2003) and this, plus the fact that the combination of olanzapine with fluoxetine was significantly superior to …","PeriodicalId":394244,"journal":{"name":"The International Journal of Neuropsychopharmacology","volume":"15 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2010-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"121284495","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2010-07-01DOI: 10.1017/S1461145709990964
M. Sandler
| | || Professor Philip Bradley, who died on 27 August 2009, at the age of 90, rose from humble beginnings to become one of the doyens of the new scientific discipline of Neuropsychopharmacology. He was the youngest of the six children of a struggling Bristol printer. With Europe hovering on the brink of war, he managed to obtain a rare educational grant to study Zoology and Chemistry at Bristol University, which would preserve him from the attentions of the Armed Forces Recruiting Board for 4 years, until he qualified as a schoolteacher. And then there was a hiccup! Because he failed one of his Chemistry exams, he was no longer exempt from military service. Although his knowledge of electronics at that time was vanishingly small, the British Army, for its own arcane reasons, ordered him to teach it to recruits! He managed to stay two steps ahead of his students and, after 6 years of service, had amassed considerable …
| ||| Philip Bradley教授于2009年8月27日去世，享年90岁，他从卑微的起点成长为神经精神药理学这一新科学学科的几十位专家之一。他是布里斯托尔一个苦苦挣扎的印刷工的六个孩子中最小的一个。当时欧洲正处于战争的边缘，他设法获得了一笔罕见的教育补助金，在布里斯托尔大学学习动物学和化学，这使他在四年里不受武装部队招募委员会的关注，直到他获得了教师资格。然后出现了一个小嗝嗝!因为有一次化学考试不及格，他不再被免除兵役。尽管当时他对电子学的了解非常少，但英国军队出于自己神秘的原因，命令他向新兵教授电子学!他设法领先他的学生两步，经过六年的服务，积累了相当可观的……
{"title":"Professor Philip Bradley (1919–2009)","authors":"M. Sandler","doi":"10.1017/S1461145709990964","DOIUrl":"https://doi.org/10.1017/S1461145709990964","url":null,"abstract":"| |\u0000||\u0000\u0000Professor Philip Bradley, who died on 27 August 2009, at the age of 90, rose from humble beginnings to become one of the doyens of the new scientific discipline of Neuropsychopharmacology. He was the youngest of the six children of a struggling Bristol printer. With Europe hovering on the brink of war, he managed to obtain a rare educational grant to study Zoology and Chemistry at Bristol University, which would preserve him from the attentions of the Armed Forces Recruiting Board for 4 years, until he qualified as a schoolteacher. And then there was a hiccup! Because he failed one of his Chemistry exams, he was no longer exempt from military service. Although his knowledge of electronics at that time was vanishingly small, the British Army, for its own arcane reasons, ordered him to teach it to recruits! He managed to stay two steps ahead of his students and, after 6 years of service, had amassed considerable …","PeriodicalId":394244,"journal":{"name":"The International Journal of Neuropsychopharmacology","volume":"34 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2010-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"129672534","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2010-06-01DOI: 10.1017/S1461145710000131
D. Grayson, A. Guidotti
| | || Erminio (Mimo) Costa, one of the co-founding members of the CINP, died on Saturday, 28 November 2009 from complications of multiple myeloma. Dr Costa is survived by his wife Ingeborg Hanbauer and sons Michael and Max. His son Robert passed away on 1 September 2006. In 1970, when Dr Alessandro Guidotti (Sandro) joined Dr Costa's laboratory at NIMH as a visiting scientist, his intent was to spend 2 years as a research trainee but he found Mimo's take on the various fields of neuroscience so exciting and rewarding, he became his close colleague for the next 40 years. Sandro was one of many who could not fail to be positively affected by Dr Costa's passion for science, by his rigorous approach to the analyses of experimental results, and by the long working hours he spent with each of his pupils in formulating hypotheses, in designing appropriate experiments and in discussing the development of state-of-the-art technologies to implement these studies. Mimo always encouraged and fostered discussion, exchange of ideas, a multidisciplinary approach and top-level scientific interactions … (Email: dgrayson{at}psych.uic.edu) (Email: AGuidotti{at}psych.uic.edu)
{"title":"Erminio Costa, M.D. (1924–2009)","authors":"D. Grayson, A. Guidotti","doi":"10.1017/S1461145710000131","DOIUrl":"https://doi.org/10.1017/S1461145710000131","url":null,"abstract":"| |\u0000||\u0000\u0000Erminio (Mimo) Costa, one of the co-founding members of the CINP, died on Saturday, 28 November 2009 from complications of multiple myeloma. Dr Costa is survived by his wife Ingeborg Hanbauer and sons Michael and Max. His son Robert passed away on 1 September 2006.\u0000\u0000In 1970, when Dr Alessandro Guidotti (Sandro) joined Dr Costa's laboratory at NIMH as a visiting scientist, his intent was to spend 2 years as a research trainee but he found Mimo's take on the various fields of neuroscience so exciting and rewarding, he became his close colleague for the next 40 years. Sandro was one of many who could not fail to be positively affected by Dr Costa's passion for science, by his rigorous approach to the analyses of experimental results, and by the long working hours he spent with each of his pupils in formulating hypotheses, in designing appropriate experiments and in discussing the development of state-of-the-art technologies to implement these studies. Mimo always encouraged and fostered discussion, exchange of ideas, a multidisciplinary approach and top-level scientific interactions … \u0000\u0000(Email: dgrayson{at}psych.uic.edu)\u0000\u0000(Email: AGuidotti{at}psych.uic.edu)","PeriodicalId":394244,"journal":{"name":"The International Journal of Neuropsychopharmacology","volume":"222 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2010-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"114597151","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2009-07-01DOI: 10.1017/S1461145708009760
E. Calcagno, S. Guzzetti, Alessandro Canetta, C. Fracasso, S. Caccia, L. Cervo, R. Invernizzi
We recently found that the response of DBA/2 mice to SSRIs in the forced swim test (FST) was impaired and they also had a smaller basal and citalopram-stimulated increase in brain extracellular serotonin (5-HT) than 'responder' strains. We employed intracerebral microdialysis, FST and selective antagonists of 5-HT1A and 5-HT2C receptors to investigate whether enhancing the increase in extracellular 5-HT reinstated the anti-immobility effect of citalopram in the FST. WAY 100635 (0.3 mg/kg s.c.) or SB 242084 (1 mg/kg s.c.), respectively a selective 5-HT1A and 5-HT2C receptor antagonist, raised the effect of citalopram (5 mg/kg) on extracellular 5-HT in the medial prefrontal cortex of DBA/2N mice (citalopram alone 5.2+/-0.3 fmol/20 microl, WAY 100635+citalopram 9.9+/-2.1 fmol/20 microl, SB 242084+ citalopram 7.6+/-1.0 fmol/20 microl) to the level reached in 'responder' mice given citalopram alone. The 5-HT receptor antagonists had no effect on the citalopram-induced increase in extracellular 5-HT in the dorsal hippocampus. The combination of citalopram with WAY 100635 or SB 242084 significantly reduced immobility time in DBA/2N mice that otherwise did not respond to either drug singly. Brain levels of citalopram in mice given citalopram alone or with 5-HT antagonists did not significantly differ. The results confirm that impaired 5-HT transmission accounts for the lack of effect of citalopram in the FST and suggest that enhancing the effect of SSRIs on extracellular 5-HT, through selective blockade of 5-HT1A and 5-HT2C receptors, could be a useful strategy to restore the response in treatment-resistant depression.
{"title":"Enhancement of cortical extracellular 5-HT by 5-HT1A and 5-HT2C receptor blockade restores the antidepressant-like effect of citalopram in non-responder mice.","authors":"E. Calcagno, S. Guzzetti, Alessandro Canetta, C. Fracasso, S. Caccia, L. Cervo, R. Invernizzi","doi":"10.1017/S1461145708009760","DOIUrl":"https://doi.org/10.1017/S1461145708009760","url":null,"abstract":"We recently found that the response of DBA/2 mice to SSRIs in the forced swim test (FST) was impaired and they also had a smaller basal and citalopram-stimulated increase in brain extracellular serotonin (5-HT) than 'responder' strains. We employed intracerebral microdialysis, FST and selective antagonists of 5-HT1A and 5-HT2C receptors to investigate whether enhancing the increase in extracellular 5-HT reinstated the anti-immobility effect of citalopram in the FST. WAY 100635 (0.3 mg/kg s.c.) or SB 242084 (1 mg/kg s.c.), respectively a selective 5-HT1A and 5-HT2C receptor antagonist, raised the effect of citalopram (5 mg/kg) on extracellular 5-HT in the medial prefrontal cortex of DBA/2N mice (citalopram alone 5.2+/-0.3 fmol/20 microl, WAY 100635+citalopram 9.9+/-2.1 fmol/20 microl, SB 242084+ citalopram 7.6+/-1.0 fmol/20 microl) to the level reached in 'responder' mice given citalopram alone. The 5-HT receptor antagonists had no effect on the citalopram-induced increase in extracellular 5-HT in the dorsal hippocampus. The combination of citalopram with WAY 100635 or SB 242084 significantly reduced immobility time in DBA/2N mice that otherwise did not respond to either drug singly. Brain levels of citalopram in mice given citalopram alone or with 5-HT antagonists did not significantly differ. The results confirm that impaired 5-HT transmission accounts for the lack of effect of citalopram in the FST and suggest that enhancing the effect of SSRIs on extracellular 5-HT, through selective blockade of 5-HT1A and 5-HT2C receptors, could be a useful strategy to restore the response in treatment-resistant depression.","PeriodicalId":394244,"journal":{"name":"The International Journal of Neuropsychopharmacology","volume":"159 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2009-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"116544619","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2009-07-01DOI: 10.1017/S1461145708009759
J. Borg, S. Henningsson, Tomoyuki Saijo, M. Inoue, J. Bah, L. Westberg, J. Lundberg, H. Jovanovic, B. Andrée, A. Nordstrom, C. Halldin, E. Eriksson, L. Farde
The human serotonin transporter (5-HTT) gene is one of the most extensively studied in psychiatry. A functional polymorphism in the promoter region of the 5-HTT gene (5-HTTLPR) has been associated with several psychiatric disorders as well as anxiety-related personality traits. In search of a mechanistic understanding of the functional implications of 5-HTTLPR, the influence of this polymorphism on regional 5-HT1A receptor density has previously been examined in two positron emission tomography (PET) studies in humans, yielding, however, contradictory results. In the present study, 54 control subjects were examined with [11C]WAY 100635 PET and a battery of cognitive tests. Regional binding potential (BP) of [11C]WAY 100635 to 5-HT1A receptor was calculated for the dorsal raphe nuclei, the hippocampus, the anterior cingulate, the insula, the temporal cortex and the frontal cortex. The influence of 5-HTTLPR genotype on regional 5-HT1A BP and cognitive performance was investigated. No differences in 5-HT1A receptor density between carriers and non-carriers of the S allele were found. Thus, we could not replicate any of the previously reported associations between 5-HTTLPR and 5-HT1A density. There was, however, a highly significant association between 5-HTTLPR genotype and performance in Wisconsin Card Sorting Test; carriers of the S allele had a superior performance compared to the LL carriers. These observations suggest that functional implications of the 5-HTTLPR polymorphism are not likely to be mediated by differences in 5-HT1A expression levels and that other biomarkers must be considered for future investigations at phenotype level.
{"title":"Serotonin transporter genotype is associated with cognitive performance but not regional 5-HT1A receptor binding in humans.","authors":"J. Borg, S. Henningsson, Tomoyuki Saijo, M. Inoue, J. Bah, L. Westberg, J. Lundberg, H. Jovanovic, B. Andrée, A. Nordstrom, C. Halldin, E. Eriksson, L. Farde","doi":"10.1017/S1461145708009759","DOIUrl":"https://doi.org/10.1017/S1461145708009759","url":null,"abstract":"The human serotonin transporter (5-HTT) gene is one of the most extensively studied in psychiatry. A functional polymorphism in the promoter region of the 5-HTT gene (5-HTTLPR) has been associated with several psychiatric disorders as well as anxiety-related personality traits. In search of a mechanistic understanding of the functional implications of 5-HTTLPR, the influence of this polymorphism on regional 5-HT1A receptor density has previously been examined in two positron emission tomography (PET) studies in humans, yielding, however, contradictory results. In the present study, 54 control subjects were examined with [11C]WAY 100635 PET and a battery of cognitive tests. Regional binding potential (BP) of [11C]WAY 100635 to 5-HT1A receptor was calculated for the dorsal raphe nuclei, the hippocampus, the anterior cingulate, the insula, the temporal cortex and the frontal cortex. The influence of 5-HTTLPR genotype on regional 5-HT1A BP and cognitive performance was investigated. No differences in 5-HT1A receptor density between carriers and non-carriers of the S allele were found. Thus, we could not replicate any of the previously reported associations between 5-HTTLPR and 5-HT1A density. There was, however, a highly significant association between 5-HTTLPR genotype and performance in Wisconsin Card Sorting Test; carriers of the S allele had a superior performance compared to the LL carriers. These observations suggest that functional implications of the 5-HTTLPR polymorphism are not likely to be mediated by differences in 5-HT1A expression levels and that other biomarkers must be considered for future investigations at phenotype level.","PeriodicalId":394244,"journal":{"name":"The International Journal of Neuropsychopharmacology","volume":"1 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2009-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"132744027","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2009-06-01DOI: 10.1017/S1461145708009590
R. Singh, Y. Dai, Jeff L. Staudinger, N. Muma
We have previously demonstrated that olanzapine-induced desensitization of 5-HT2A receptor-stimulated phospholipase C (PLC) activity is associated with increases in RGS7 protein levels both in vivo and in cells in culture, and the increase in RGS7 is dependent on activation of the JAK-STAT pathway in cells in culture. In the present study, we found that desensitization of 5-HT2A receptor-stimulated PLC activity induced by olanzapine is dependent on activation of the JAK-STAT pathway. Similar to olanzapine, clozapine-induced desensitization of 5-HT2A receptor signalling is accompanied by increases in RGS7 and activation of JAK2. Treatment with the selective 5-HT2A receptor antagonist MDL 100907 also increased RGS7 protein levels and JAK2 activation. Using a JAK2 inhibitor AG490, we found that clozapine and MDL 100907-induced increases in RGS7 are dependent on activation of the JAK-STAT pathway. Olanzapine, clozapine, and MDL 100907 treatment increased mRNA levels of RGS7. Using a chromatin immunoprecipitation assay we found STAT3 binding to the putative RGS7 promoter region. Taken together, olanzapine-induced activation of the JAK-STAT pathway, and STAT3 binding to the RGS7 gene could underlie the increase in RGS7 mRNA which could subsequently increase protein expression. Furthermore, the increase in RGS7 protein could play a role in the desensitization of 5-HT2A receptor signalling by terminating the activated Galphaq/11 proteins more rapidly. Overall, our data suggest that the complete desensitization of 5-HT2A receptor-stimulated PLC activity by olanzapine, clozapine and MDL 100907 requires activation of the JAK-STAT pathway, which in turn increases RGS7 expression probably by direct transcriptional activity of STAT3.
{"title":"Activation of the JAK-STAT pathway is necessary for desensitization of 5-HT2A receptor-stimulated phospholipase C signalling by olanzapine, clozapine and MDL 100907.","authors":"R. Singh, Y. Dai, Jeff L. Staudinger, N. Muma","doi":"10.1017/S1461145708009590","DOIUrl":"https://doi.org/10.1017/S1461145708009590","url":null,"abstract":"We have previously demonstrated that olanzapine-induced desensitization of 5-HT2A receptor-stimulated phospholipase C (PLC) activity is associated with increases in RGS7 protein levels both in vivo and in cells in culture, and the increase in RGS7 is dependent on activation of the JAK-STAT pathway in cells in culture. In the present study, we found that desensitization of 5-HT2A receptor-stimulated PLC activity induced by olanzapine is dependent on activation of the JAK-STAT pathway. Similar to olanzapine, clozapine-induced desensitization of 5-HT2A receptor signalling is accompanied by increases in RGS7 and activation of JAK2. Treatment with the selective 5-HT2A receptor antagonist MDL 100907 also increased RGS7 protein levels and JAK2 activation. Using a JAK2 inhibitor AG490, we found that clozapine and MDL 100907-induced increases in RGS7 are dependent on activation of the JAK-STAT pathway. Olanzapine, clozapine, and MDL 100907 treatment increased mRNA levels of RGS7. Using a chromatin immunoprecipitation assay we found STAT3 binding to the putative RGS7 promoter region. Taken together, olanzapine-induced activation of the JAK-STAT pathway, and STAT3 binding to the RGS7 gene could underlie the increase in RGS7 mRNA which could subsequently increase protein expression. Furthermore, the increase in RGS7 protein could play a role in the desensitization of 5-HT2A receptor signalling by terminating the activated Galphaq/11 proteins more rapidly. Overall, our data suggest that the complete desensitization of 5-HT2A receptor-stimulated PLC activity by olanzapine, clozapine and MDL 100907 requires activation of the JAK-STAT pathway, which in turn increases RGS7 expression probably by direct transcriptional activity of STAT3.","PeriodicalId":394244,"journal":{"name":"The International Journal of Neuropsychopharmacology","volume":"77 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2009-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"134608353","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2009-05-01DOI: 10.1017/S1461145708009619
K. Nonogaki, Yukie Ohba, M. Wakameda, T. Tamari
Serotonin (5-hydroxytryptamine; 5-HT) 2C receptors and the downstream melanocortin pathway are suggested to mediate the anorexic effects of m-chlorophenylpiperazine (mCPP) and fenfluramine. We previously reported that fluvoxamine, a selective serotonin reuptake inhibitor, together with pharmacological inactivation of 5-HT2C receptors exert feeding suppression through activation of 5-HT1B receptors in mice. Here, we report that fluvoxamine exerted anorexic effects in 5-HT2C receptor mutant mice with heterozygous mutation of beta-endorphin gene (2CREnd mice), whereas fluvoxamine had no effect on food intake in age-matched wild-type mice and 5-HT2C receptor mutant mice, which are associated with decreases in hypothalamic proopiomelanocortin (POMC) expression. mCPP suppressed food intake in 5-HT2C receptor mutant mice, 2CREnd mice and age-matched wild-type mice. These results suggest that fluvoxamine-induced feeding suppression requires a perturbation of 5-HT2C receptor and beta-endorphin signalling plus functional hypothalamic POMC activity, whereas mCPP-induced feeding suppression does not always require functional 5-HT2C receptor, beta-endorphin, and POMC activity in mice.
{"title":"Fluvoxamine exerts anorexic effect in 5-HT2C receptor mutant mice with heterozygous mutation of beta-endorphin gene.","authors":"K. Nonogaki, Yukie Ohba, M. Wakameda, T. Tamari","doi":"10.1017/S1461145708009619","DOIUrl":"https://doi.org/10.1017/S1461145708009619","url":null,"abstract":"Serotonin (5-hydroxytryptamine; 5-HT) 2C receptors and the downstream melanocortin pathway are suggested to mediate the anorexic effects of m-chlorophenylpiperazine (mCPP) and fenfluramine. We previously reported that fluvoxamine, a selective serotonin reuptake inhibitor, together with pharmacological inactivation of 5-HT2C receptors exert feeding suppression through activation of 5-HT1B receptors in mice. Here, we report that fluvoxamine exerted anorexic effects in 5-HT2C receptor mutant mice with heterozygous mutation of beta-endorphin gene (2CREnd mice), whereas fluvoxamine had no effect on food intake in age-matched wild-type mice and 5-HT2C receptor mutant mice, which are associated with decreases in hypothalamic proopiomelanocortin (POMC) expression. mCPP suppressed food intake in 5-HT2C receptor mutant mice, 2CREnd mice and age-matched wild-type mice. These results suggest that fluvoxamine-induced feeding suppression requires a perturbation of 5-HT2C receptor and beta-endorphin signalling plus functional hypothalamic POMC activity, whereas mCPP-induced feeding suppression does not always require functional 5-HT2C receptor, beta-endorphin, and POMC activity in mice.","PeriodicalId":394244,"journal":{"name":"The International Journal of Neuropsychopharmacology","volume":"1 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2009-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"128843252","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2009-05-01DOI: 10.1017/S1461145708009607
B. Ryan, L. Musazzi, A. Mallei, D. Tardito, S. Gruber, A. El Khoury, R. Anwyl, G. Racagni, A. Mathé, M. Rowan, M. Popoli
An animal model of depression combining genetic vulnerability and early-life stress (ELS) was prepared by submitting the Flinders Sensitive Line (FSL) rats to a standard paradigm of maternal separation. We analysed hippocampal synaptic transmission and plasticity in vivo and ionotropic receptors for glutamate in FSL rats, in their controls Flinders Resistant Line (FRL) rats, and in both lines subjected to ELS. A strong inhibition of long-term potentiation (LTP) and lower synaptic expression of NR1 subunit of the NMDA receptor were found in FSL rats. Remarkably, ELS induced a remodelling of synaptic plasticity only in FSL rats, reducing inhibition of LTP; this was accompanied by marked increase of synaptic NR1 subunit and GluR2/3 subunits of AMPA receptors. Chronic treatment with escitalopram inhibited LTP in FRL rats, but this effect was attenuated by prior ELS. The present results suggest that early gene-environment interactions cause lifelong synaptic changes affecting functional and molecular aspects of plasticity, partly reversed by antidepressant treatments.
{"title":"Remodelling by early-life stress of NMDA receptor-dependent synaptic plasticity in a gene-environment rat model of depression.","authors":"B. Ryan, L. Musazzi, A. Mallei, D. Tardito, S. Gruber, A. El Khoury, R. Anwyl, G. Racagni, A. Mathé, M. Rowan, M. Popoli","doi":"10.1017/S1461145708009607","DOIUrl":"https://doi.org/10.1017/S1461145708009607","url":null,"abstract":"An animal model of depression combining genetic vulnerability and early-life stress (ELS) was prepared by submitting the Flinders Sensitive Line (FSL) rats to a standard paradigm of maternal separation. We analysed hippocampal synaptic transmission and plasticity in vivo and ionotropic receptors for glutamate in FSL rats, in their controls Flinders Resistant Line (FRL) rats, and in both lines subjected to ELS. A strong inhibition of long-term potentiation (LTP) and lower synaptic expression of NR1 subunit of the NMDA receptor were found in FSL rats. Remarkably, ELS induced a remodelling of synaptic plasticity only in FSL rats, reducing inhibition of LTP; this was accompanied by marked increase of synaptic NR1 subunit and GluR2/3 subunits of AMPA receptors. Chronic treatment with escitalopram inhibited LTP in FRL rats, but this effect was attenuated by prior ELS. The present results suggest that early gene-environment interactions cause lifelong synaptic changes affecting functional and molecular aspects of plasticity, partly reversed by antidepressant treatments.","PeriodicalId":394244,"journal":{"name":"The International Journal of Neuropsychopharmacology","volume":"45 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2009-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"127953001","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2009-04-01DOI: 10.1017/S1461145708009413
Tetsuya Marui, Ikuko Funatogawa, Shinko Koishi, Kenji Yamamoto, H. Matsumoto, O. Hashimoto, E. Nanba, Hisami Nishida, Toshiro Sugiyama, K. Kasai, Kei-ichiro Watanabe, Y. Kano, N. Kato
doi:10.1017/S1461145708009127. Published online by Cambridge University Press, 30 July 2008. Owing to an oversight by the authors the paper by Marui et al. (2008), was published with the name of a co-author, Tsukasa Sasaki, being omitted. The correct version of the author group and affiliations is reproduced …
doi: 10.1017 / S1461145708009127。剑桥大学出版社于2008年7月30日在线出版。由于作者的疏忽，Marui et al.(2008)发表的论文省略了合著者Tsukasa Sasaki的名字。正确版本的作者组和从属关系被复制…
{"title":"Association of the neuronal cell adhesion molecule (NRCAM) gene variants with autism – Corrigendum","authors":"Tetsuya Marui, Ikuko Funatogawa, Shinko Koishi, Kenji Yamamoto, H. Matsumoto, O. Hashimoto, E. Nanba, Hisami Nishida, Toshiro Sugiyama, K. Kasai, Kei-ichiro Watanabe, Y. Kano, N. Kato","doi":"10.1017/S1461145708009413","DOIUrl":"https://doi.org/10.1017/S1461145708009413","url":null,"abstract":"doi:10.1017/S1461145708009127. Published online by Cambridge University Press, 30 July 2008.\u0000\u0000Owing to an oversight by the authors the paper by Marui et al. (2008), was published with the name of a co-author, Tsukasa Sasaki, being omitted. The correct version of the author group and affiliations is reproduced …","PeriodicalId":394244,"journal":{"name":"The International Journal of Neuropsychopharmacology","volume":"4 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2009-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"124986997","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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