Pub Date : 2002-06-01DOI: 10.1017/S1461145702002882
M. Doat, R. Rabin, J. C. Winter
The present study investigated the effects of chronic treatment with the atypical antipsychotic, clozapine, or the typical antipsychotic, haloperidol, on the stimulus properties of 2,5-dimethoxy-4-methylamphetamine ([-]-DOM) in rats trained to discriminate [-]-DOM (0.3 mg/kg; 75 min pre-treatment time) from vehicle. As compared with control values, treatment with clozapine (25 mg/kg.d) for 7 d caused a statistically significant 57% reduction in [-]-DOM-appropriate responding. Unlike clozapine, treatment with haloperidol (1 mg/kg.d) for 7 d did not affect the stimulus properties of [-]-DOM. These findings demonstrate that a functionally significant decrease in 5-HT2A receptor-mediated activity is a unique component of the in-vivo response to chronic treatment with clozapine but not haloperidol and, therefore, might account for some of the clinical differences associated with atypical antipsychotics.
{"title":"The effect of chronic treatment with clozapine and haloperidol on stimulus control by DOM.","authors":"M. Doat, R. Rabin, J. C. Winter","doi":"10.1017/S1461145702002882","DOIUrl":"https://doi.org/10.1017/S1461145702002882","url":null,"abstract":"The present study investigated the effects of chronic treatment with the atypical antipsychotic, clozapine, or the typical antipsychotic, haloperidol, on the stimulus properties of 2,5-dimethoxy-4-methylamphetamine ([-]-DOM) in rats trained to discriminate [-]-DOM (0.3 mg/kg; 75 min pre-treatment time) from vehicle. As compared with control values, treatment with clozapine (25 mg/kg.d) for 7 d caused a statistically significant 57% reduction in [-]-DOM-appropriate responding. Unlike clozapine, treatment with haloperidol (1 mg/kg.d) for 7 d did not affect the stimulus properties of [-]-DOM. These findings demonstrate that a functionally significant decrease in 5-HT2A receptor-mediated activity is a unique component of the in-vivo response to chronic treatment with clozapine but not haloperidol and, therefore, might account for some of the clinical differences associated with atypical antipsychotics.","PeriodicalId":394244,"journal":{"name":"The International Journal of Neuropsychopharmacology","volume":"7 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2002-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"128542314","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 : 2002-06-01DOI: 10.1017/S1461145702002845
S. Faraone, E. Short, J. Biederman, R. Findling, Christine Roe, M. Manos
Stimulant medication has, for many years, been the pharmacological treatment of choice for children and adults with attention deficit hyperactivity disorder (ADHD). Recently, several studies have documented the efficacy of a new stimulant, Adderall. Although these initial studies provide useful information for clinicians treating ADHD children, their method of data presentation has provided limited information about the clinical significance of drug effects. Thus, to address the issue of clinical significance, we completed drug-placebo response curve analyses of a blinded, placebo-controlled study of Adderall and methylphenidate (MPH). Our results show that the efficacy of Adderall and MPH to improve functioning is seen throughout the full range of improvement scores. Both drugs prevent worsening and, for a majority of patients, lead to improvements that are well into the normal range. The analyses also highlight an important subgroup of placebo responders, which suggests that future research should focus on how to predict robust placebo response in ADHD patients.
{"title":"Efficacy of Adderall and methylphenidate in attention deficit hyperactivity disorder: a drug-placebo and drug-drug response curve analysis of a naturalistic study.","authors":"S. Faraone, E. Short, J. Biederman, R. Findling, Christine Roe, M. Manos","doi":"10.1017/S1461145702002845","DOIUrl":"https://doi.org/10.1017/S1461145702002845","url":null,"abstract":"Stimulant medication has, for many years, been the pharmacological treatment of choice for children and adults with attention deficit hyperactivity disorder (ADHD). Recently, several studies have documented the efficacy of a new stimulant, Adderall. Although these initial studies provide useful information for clinicians treating ADHD children, their method of data presentation has provided limited information about the clinical significance of drug effects. Thus, to address the issue of clinical significance, we completed drug-placebo response curve analyses of a blinded, placebo-controlled study of Adderall and methylphenidate (MPH). Our results show that the efficacy of Adderall and MPH to improve functioning is seen throughout the full range of improvement scores. Both drugs prevent worsening and, for a majority of patients, lead to improvements that are well into the normal range. The analyses also highlight an important subgroup of placebo responders, which suggests that future research should focus on how to predict robust placebo response in ADHD patients.","PeriodicalId":394244,"journal":{"name":"The International Journal of Neuropsychopharmacology","volume":"3 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2002-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"125132307","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 : 2002-06-01DOI: 10.1017/S1461145702002869
D. Marazziti, L. Palego, A. Giromella, M. Mazzoni, F. Borsini, N. Mayer, A. Naccarato, A. Lucacchini, G. Cassano
The mode of action of antidepressant drugs may be related to mechanisms of receptor adaptation, involving overall the serotonin 1A (5-HT1A) receptor subtype. However, so far, the clinical effectiveness of selective compounds acting at this level has proved disappointing. This could be explained by the heterogeneity of 5-HT1A receptors within the central nervous system. In animals, two 5-HT1A agonists, flibanserin and buspirone, have shown different pharmacological properties, depending on the brain region. Since no evidence supports this observation in humans, this study sought to investigate whether these two drugs exert different effects on 5-HT1A receptor activation in three different human brain areas: the prefrontal cortex, hippocampus and raphe nuclei. 5-HT1A-mediated inhibition of forskolin-stimulated adenylyl cyclase (AC) was taken as an index of 5-HT1A receptor activation. Flibanserin significantly reduced the activity of AC post-synaptically, i.e. in the prefrontal cortex [EC50 (mean +/- S.E.M.), 28 +/- 10.2 nM; Emax, 18 +/- 2.3%] and in the hippocampus (EC50, 3.5 +/- 3.1 nM; Emax, 20 +/- 4.0%), but had no effect in the raphe nuclei, i.e. at pre-synaptic level. Vice versa, buspirone was only slightly but significantly effective in the raphe (EC50, 3.0 +/- 2.8 nM; Emax, 12 +/- 1.9%). Agonist effects were sensitive to the 5-HT1A antagonists WAY-100135 and pindobind 5-HT1A in the cortex and raphe nuclei, whereas buspirone antagonized flibanserin in the hippocampus. These findings suggest a region-related action of flibanserin and buspirone on forskolin-stimulated AC activity in human brain.
{"title":"Region-dependent effects of flibanserin and buspirone on adenylyl cyclase activity in the human brain.","authors":"D. Marazziti, L. Palego, A. Giromella, M. Mazzoni, F. Borsini, N. Mayer, A. Naccarato, A. Lucacchini, G. Cassano","doi":"10.1017/S1461145702002869","DOIUrl":"https://doi.org/10.1017/S1461145702002869","url":null,"abstract":"The mode of action of antidepressant drugs may be related to mechanisms of receptor adaptation, involving overall the serotonin 1A (5-HT1A) receptor subtype. However, so far, the clinical effectiveness of selective compounds acting at this level has proved disappointing. This could be explained by the heterogeneity of 5-HT1A receptors within the central nervous system. In animals, two 5-HT1A agonists, flibanserin and buspirone, have shown different pharmacological properties, depending on the brain region. Since no evidence supports this observation in humans, this study sought to investigate whether these two drugs exert different effects on 5-HT1A receptor activation in three different human brain areas: the prefrontal cortex, hippocampus and raphe nuclei. 5-HT1A-mediated inhibition of forskolin-stimulated adenylyl cyclase (AC) was taken as an index of 5-HT1A receptor activation. Flibanserin significantly reduced the activity of AC post-synaptically, i.e. in the prefrontal cortex [EC50 (mean +/- S.E.M.), 28 +/- 10.2 nM; Emax, 18 +/- 2.3%] and in the hippocampus (EC50, 3.5 +/- 3.1 nM; Emax, 20 +/- 4.0%), but had no effect in the raphe nuclei, i.e. at pre-synaptic level. Vice versa, buspirone was only slightly but significantly effective in the raphe (EC50, 3.0 +/- 2.8 nM; Emax, 12 +/- 1.9%). Agonist effects were sensitive to the 5-HT1A antagonists WAY-100135 and pindobind 5-HT1A in the cortex and raphe nuclei, whereas buspirone antagonized flibanserin in the hippocampus. These findings suggest a region-related action of flibanserin and buspirone on forskolin-stimulated AC activity in human brain.","PeriodicalId":394244,"journal":{"name":"The International Journal of Neuropsychopharmacology","volume":"215 ","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2002-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"120942089","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 : 2002-03-01DOI: 10.1017/S1461145701002747
Hakuei Yamashita, T. Kazawa, Y. Minatogawa, T. Ebisawa, T. Yamauchi
Recent studies indicate that carbamazepine (CBZ) induces hepatic cytochrome p450 (CYP) protein subfamilies. The present study examines the time-course of the appearance of hepatic CYP subfamilies (2B, 3A) and serum levels of CBZ and its metabolite, CBZ epoxide (CBZE), induced by CBZ treatment in rats. Male Wistar rats were given 5 g of CBZ (CBZ-treated) per 1 kg of feed for 3, 7, 14, 28 and 42 d or feed without CBZ (control). Serum levels of CBZ and CBZE were evaluated by HPLC. Induction ratios of CYP2B and CYP3A were evaluated by Western blotting. Serum levels of CBZ and CBZE became maximal after 14 and 7 d, respectively, after CBZ treatment. Both levels gradually, then significantly decreased after 42 d CBZ compared with maximal levels. The induction ratio of CYP2B did not differ between 3, 7, 14, 28 and 42 d CBZ treatment. The induction ratio of CYP3A reached a maximum after 14 d CBZ, then significantly decreased after 28 and 42 d CBZ compared to the maximal rate. The difference between CYP2B and CYP3A induction by CBZ chronic treatment is a novel finding.
最近的研究表明卡马西平(CBZ)诱导肝细胞色素p450 (CYP)蛋白亚家族。本研究检测了大鼠肝CYP亚家族(2B, 3A)出现的时间过程，以及CBZ治疗诱导的CBZ及其代谢物CBZ环氧化物(CBZE)的血清水平。雄性Wistar大鼠每1 kg饲料给予5 g CBZ (CBZ处理)，连续饲喂3、7、14、28和42 d或不饲喂CBZ(对照组)。采用高效液相色谱法测定血清CBZ、CBZE水平。Western blotting检测CYP2B和CYP3A的诱导率。CBZ和CBZE分别在给药14 d和7 d后达到最大。与最大剂量相比，42 d CBZ后两者均逐渐降低。在CBZ处理3、7、14、28和42 d时，CYP2B的诱导率无显著差异。CYP3A的诱导率在CBZ 14 d时达到最大值，在CBZ 28和42 d时显著降低。CBZ慢性治疗诱导CYP2B和CYP3A的差异是一个新的发现。
{"title":"Time-course of hepatic cytochrome p450 subfamily induction by chronic carbamazepine treatment in rats.","authors":"Hakuei Yamashita, T. Kazawa, Y. Minatogawa, T. Ebisawa, T. Yamauchi","doi":"10.1017/S1461145701002747","DOIUrl":"https://doi.org/10.1017/S1461145701002747","url":null,"abstract":"Recent studies indicate that carbamazepine (CBZ) induces hepatic cytochrome p450 (CYP) protein subfamilies. The present study examines the time-course of the appearance of hepatic CYP subfamilies (2B, 3A) and serum levels of CBZ and its metabolite, CBZ epoxide (CBZE), induced by CBZ treatment in rats. Male Wistar rats were given 5 g of CBZ (CBZ-treated) per 1 kg of feed for 3, 7, 14, 28 and 42 d or feed without CBZ (control). Serum levels of CBZ and CBZE were evaluated by HPLC. Induction ratios of CYP2B and CYP3A were evaluated by Western blotting. Serum levels of CBZ and CBZE became maximal after 14 and 7 d, respectively, after CBZ treatment. Both levels gradually, then significantly decreased after 42 d CBZ compared with maximal levels. The induction ratio of CYP2B did not differ between 3, 7, 14, 28 and 42 d CBZ treatment. The induction ratio of CYP3A reached a maximum after 14 d CBZ, then significantly decreased after 28 and 42 d CBZ compared to the maximal rate. The difference between CYP2B and CYP3A induction by CBZ chronic treatment is a novel finding.","PeriodicalId":394244,"journal":{"name":"The International Journal of Neuropsychopharmacology","volume":"19 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2002-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"114284570","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 : 2002-03-01DOI: 10.1017/S1461145701002693
S. Nyberg, Y. Chou, C. Halldin
Positron emission tomography (PET) studies have demonstrated low striatal D2 dopamine receptor occupancy in clozapine-treated schizophrenic patients. The aim of this pilot study was to explore if this low receptor occupancy indeed represents partial saturability of striatal D2 dopamine receptors by clozapine. Three anaesthetized Cynomolgus monkeys were examined during one day with PET and [11C]raclopride at baseline and after intravenous injections of clozapine 1.5 mg/kg followed by 18.5 mg/kg. The estimated corresponding human oral doses were approx. 210 mg/d and 2800 mg/d. D2 dopamine receptor occupancy was calculated using an equilibrium-ratio analysis and ranged from 54 to 58% after 1.5 mg/kg and 87 to 89% after the total dose 20 mg/kg. The calculated maximal occupancy was 93%. We conclude that PET-measured D2 dopamine receptor occupancy by clozapine can be described using a model based on the law of mass action, previously validated for conventional antipsychotics. Therefore, sufficiently high doses of clozapine are expected to produce complete striatal D2 dopamine receptor occupancy. The findings further support our previous findings of low D2 dopamine receptor occupancy in patients treated with standard doses of clozapine.
{"title":"Saturation of striatal D(2) dopamine receptors by clozapine.","authors":"S. Nyberg, Y. Chou, C. Halldin","doi":"10.1017/S1461145701002693","DOIUrl":"https://doi.org/10.1017/S1461145701002693","url":null,"abstract":"Positron emission tomography (PET) studies have demonstrated low striatal D2 dopamine receptor occupancy in clozapine-treated schizophrenic patients. The aim of this pilot study was to explore if this low receptor occupancy indeed represents partial saturability of striatal D2 dopamine receptors by clozapine. Three anaesthetized Cynomolgus monkeys were examined during one day with PET and [11C]raclopride at baseline and after intravenous injections of clozapine 1.5 mg/kg followed by 18.5 mg/kg. The estimated corresponding human oral doses were approx. 210 mg/d and 2800 mg/d. D2 dopamine receptor occupancy was calculated using an equilibrium-ratio analysis and ranged from 54 to 58% after 1.5 mg/kg and 87 to 89% after the total dose 20 mg/kg. The calculated maximal occupancy was 93%. We conclude that PET-measured D2 dopamine receptor occupancy by clozapine can be described using a model based on the law of mass action, previously validated for conventional antipsychotics. Therefore, sufficiently high doses of clozapine are expected to produce complete striatal D2 dopamine receptor occupancy. The findings further support our previous findings of low D2 dopamine receptor occupancy in patients treated with standard doses of clozapine.","PeriodicalId":394244,"journal":{"name":"The International Journal of Neuropsychopharmacology","volume":"5 1 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2002-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"129418275","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 : 2002-03-01DOI: 10.1017/S1461145701002735
F. Lichtigfeld, M. Gillman
We read, with interest, the paper by Khan et al. (2001), which confirms earlier conclusions that approximately 75% of any treatment effect caused by antidepressants is held to be in common with that attributed to a placebo response alone (Kirsch and Sapirstein, 1998). Kirsch and Sapirstein (1998) concluded from their work that only 25% of the response to antidepressants was uniquely related to their specific therapeutic action.
我们饶有兴趣地阅读了Khan et al.(2001)的论文，该论文证实了早期的结论，即抗抑郁药引起的任何治疗效果中约有75%被认为与单独归因于安慰剂反应的效果相同(Kirsch和Sapirstein, 1998)。Kirsch和Sapirstein(1998)从他们的工作中得出结论，对抗抑郁药的反应中只有25%是与它们的特定治疗作用唯一相关的。
{"title":"Possible role of the endogenous opioid system in the placebo response in depression.","authors":"F. Lichtigfeld, M. Gillman","doi":"10.1017/S1461145701002735","DOIUrl":"https://doi.org/10.1017/S1461145701002735","url":null,"abstract":"We read, with interest, the paper by Khan et al. (2001), which confirms earlier conclusions that approximately 75% of any treatment effect caused by antidepressants is held to be in common with that attributed to a placebo response alone (Kirsch and Sapirstein, 1998). Kirsch and Sapirstein (1998) concluded from their work that only 25% of the response to antidepressants was uniquely related to their specific therapeutic action.","PeriodicalId":394244,"journal":{"name":"The International Journal of Neuropsychopharmacology","volume":"32 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2002-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"128903253","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 : 2002-03-01DOI: 10.1017/S1461145701002711
C. Cusin, A. Serretti, R. Zanardi, E. Lattuada, D. Rossini, R. Lilli, C. Lorenzi, E. Smeraldi
The aim of the present study was to test a possible effect of the monoamine oxidase A (MAOA) and serotonin receptor 2A (5-HT-2A) gene variants on the antidepressant activity of fluvoxamine and paroxetine in a sample of major (n = 248) and bipolar (n = 195) depressives, with or without psychotic features. A total of 443 in-patients were treated with 300 mg fluvoxamine (n = 307) or 20-40 mg paroxetine (n = 136) for 6 wk. The severity of depressive symptoms was assessed weekly with the Hamilton Rating Scale for Depression (HAMD). Allele variants were determined in each subject using a PCR-based technique. We observed a marginal association between 5-HT-2A variants and antidepressant response while MAOA genotypes were not associated. Possible stratification factors, such as sex, diagnosis, presence of psychotic features, HAMD scores at baseline, pindolol augmentation and SSRIs plasma levels did not significantly influence the observed results. The investigated MAOA and 5-HT-2A gene variants, therefore, do not seem to play a major role in SSRI antidepressant activity.
{"title":"Influence of monoamine oxidase A and serotonin receptor 2A polymorphisms in SSRI antidepressant activity.","authors":"C. Cusin, A. Serretti, R. Zanardi, E. Lattuada, D. Rossini, R. Lilli, C. Lorenzi, E. Smeraldi","doi":"10.1017/S1461145701002711","DOIUrl":"https://doi.org/10.1017/S1461145701002711","url":null,"abstract":"The aim of the present study was to test a possible effect of the monoamine oxidase A (MAOA) and serotonin receptor 2A (5-HT-2A) gene variants on the antidepressant activity of fluvoxamine and paroxetine in a sample of major (n = 248) and bipolar (n = 195) depressives, with or without psychotic features. A total of 443 in-patients were treated with 300 mg fluvoxamine (n = 307) or 20-40 mg paroxetine (n = 136) for 6 wk. The severity of depressive symptoms was assessed weekly with the Hamilton Rating Scale for Depression (HAMD). Allele variants were determined in each subject using a PCR-based technique. We observed a marginal association between 5-HT-2A variants and antidepressant response while MAOA genotypes were not associated. Possible stratification factors, such as sex, diagnosis, presence of psychotic features, HAMD scores at baseline, pindolol augmentation and SSRIs plasma levels did not significantly influence the observed results. The investigated MAOA and 5-HT-2A gene variants, therefore, do not seem to play a major role in SSRI antidepressant activity.","PeriodicalId":394244,"journal":{"name":"The International Journal of Neuropsychopharmacology","volume":"1 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2002-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"125563677","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 : 2002-03-01DOI: 10.1017/S1461145702002778
P. Delgado, F. Moreno, Larry Onate, A. Gelenberg
This study was aimed at determining whether patient- or antidepressant-related variables are most important to the mood response to serotonin (5-HT) or catecholamine depletion. Depressed patients treated with open-label mirtazapine (>or=6 wk) received two depletion tests (5-HT and catecholamine depletion) 1 wk apart. Both 5-HT and catecholamine depletion led to a partial return of depression in most patients. Antidepressant response to mirtazapine is dependent on its dual actions on norepinephrine and 5-HT neurotransmission. Mood response to tryptophan or catecholamine depletion is dependent on the pharmacological properties of the antidepressant being taken during depletion.
{"title":"Sequential catecholamine and serotonin depletion in mirtazapine-treated depressed patients.","authors":"P. Delgado, F. Moreno, Larry Onate, A. Gelenberg","doi":"10.1017/S1461145702002778","DOIUrl":"https://doi.org/10.1017/S1461145702002778","url":null,"abstract":"This study was aimed at determining whether patient- or antidepressant-related variables are most important to the mood response to serotonin (5-HT) or catecholamine depletion. Depressed patients treated with open-label mirtazapine (>or=6 wk) received two depletion tests (5-HT and catecholamine depletion) 1 wk apart. Both 5-HT and catecholamine depletion led to a partial return of depression in most patients. Antidepressant response to mirtazapine is dependent on its dual actions on norepinephrine and 5-HT neurotransmission. Mood response to tryptophan or catecholamine depletion is dependent on the pharmacological properties of the antidepressant being taken during depletion.","PeriodicalId":394244,"journal":{"name":"The International Journal of Neuropsychopharmacology","volume":"14 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2002-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"126800375","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 : 2002-03-01DOI: 10.1017/S1461145702002791
T. Burt, S. Lisanby, H. Sackeim
Transcranial magnetic stimulation (TMS) is a technology that allows for non-invasive modulation of the excitability and function of discrete brain cortical areas. TMS uses alternating magnetic fields to induce electric currents in cortical tissue. In psychiatry, TMS has been studied primarily as a potential treatment for major depression. Most studies indicate that slow-frequency repetitive TMS (rTMS) and higher frequency rTMS have antidepressant properties. A meta-analysis of controlled studies indicates that this effect is fairly robust from a statistical viewpoint. However, effect sizes are heterogeneous, and few studies have shown that rTMS results in substantial rates of clinical response or remission, and the durability of antidepressant effects is largely unknown. We review in detail rTMS studies in the treatment of depression, as well as summarize treatment studies of mania, obsessive-compulsive disorder, post-traumatic stress disorder, and schizophrenia. We also review the application of TMS in the study of the pathophysiology of psychiatric disorders and summarize studies of the safety of TMS in human subjects.
{"title":"Neuropsychiatric applications of transcranial magnetic stimulation: a meta analysis.","authors":"T. Burt, S. Lisanby, H. Sackeim","doi":"10.1017/S1461145702002791","DOIUrl":"https://doi.org/10.1017/S1461145702002791","url":null,"abstract":"Transcranial magnetic stimulation (TMS) is a technology that allows for non-invasive modulation of the excitability and function of discrete brain cortical areas. TMS uses alternating magnetic fields to induce electric currents in cortical tissue. In psychiatry, TMS has been studied primarily as a potential treatment for major depression. Most studies indicate that slow-frequency repetitive TMS (rTMS) and higher frequency rTMS have antidepressant properties. A meta-analysis of controlled studies indicates that this effect is fairly robust from a statistical viewpoint. However, effect sizes are heterogeneous, and few studies have shown that rTMS results in substantial rates of clinical response or remission, and the durability of antidepressant effects is largely unknown. We review in detail rTMS studies in the treatment of depression, as well as summarize treatment studies of mania, obsessive-compulsive disorder, post-traumatic stress disorder, and schizophrenia. We also review the application of TMS in the study of the pathophysiology of psychiatric disorders and summarize studies of the safety of TMS in human subjects.","PeriodicalId":394244,"journal":{"name":"The International Journal of Neuropsychopharmacology","volume":"40 6 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2002-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"131450704","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 : 2002-03-01DOI: 10.1017/S1461145701002723
Y. Kaneda, I. Kawamura, A. Fujii, T. Ohmori
The serotonin syndrome is thought to be caused by excess serotonin availability in the CNS, especially at the 5-HT-1A receptor (Sternbach, 1991). Although the syndrome is produced most often by the concurrent use of monoamine oxidase inhibitors and other serotonergic agents (Sternbach, 1991), more recent reports suggest that selective serotonin reuptake inhibitor (SSRI) monotherapy induces the syndrome (Bastani et al., 1996; Fischer, 1995; Gill et al., 1999; Lenzi et al., 1993). For the SSRI paroxetine, there is only one case report of serotonin syndrome connected with its sole use (Cavallazzi and Grezesiuk, 1999). We report here on the rare case of a patient who developed the syndrome after receiving a single dose of paroxetine.
5-羟色胺综合征被认为是由于中枢神经系统，特别是5-HT-1A受体中5-羟色胺过量而引起的(Sternbach, 1991)。虽然该综合征最常由同时使用单胺氧化酶抑制剂和其他5 -羟色胺能药物引起(Sternbach, 1991)，但最近的报道表明，选择性5 -羟色胺再摄取抑制剂(SSRI)单一疗法可诱导该综合征(Bastani等人，1996;费舍尔,1995;Gill et al.， 1999;Lenzi et al.， 1993)。对于SSRI类药物帕罗西汀，仅有一例与单独使用有关的血清素综合征报告(Cavallazzi和Grezesiuk, 1999)。我们在这里报告的罕见病例的病人谁发展的综合征后接受单剂量帕罗西汀。
{"title":"Serotonin syndrome - 'potential' role of the CYP2D6 genetic polymorphism in Asians.","authors":"Y. Kaneda, I. Kawamura, A. Fujii, T. Ohmori","doi":"10.1017/S1461145701002723","DOIUrl":"https://doi.org/10.1017/S1461145701002723","url":null,"abstract":"The serotonin syndrome is thought to be caused by excess serotonin availability in the CNS, especially at the 5-HT-1A receptor (Sternbach, 1991). Although the syndrome is produced most often by the concurrent use of monoamine oxidase inhibitors and other serotonergic agents (Sternbach, 1991), more recent reports suggest that selective serotonin reuptake inhibitor (SSRI) monotherapy induces the syndrome (Bastani et al., 1996; Fischer, 1995; Gill et al., 1999; Lenzi et al., 1993). For the SSRI paroxetine, there is only one case report of serotonin syndrome connected with its sole use (Cavallazzi and Grezesiuk, 1999). We report here on the rare case of a patient who developed the syndrome after receiving a single dose of paroxetine.","PeriodicalId":394244,"journal":{"name":"The International Journal of Neuropsychopharmacology","volume":"1 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2002-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"131337811","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}
京公网安备 11010802042870号
京ICP备2023020795号-1
扫码关注我们
求助内容：
应助结果提醒方式：