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Cohrs, Stefan
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Cohrs, Stefan
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Cohrs, Stefan
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Cohrs, S.
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2005Conference Abstract [["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Pharmacopsychiatry"],["dc.bibliographiccitation.volume","38"],["dc.contributor.author","Meier, A."],["dc.contributor.author","Neumann, A. C."],["dc.contributor.author","Jordan, W."],["dc.contributor.author","Huther, G."],["dc.contributor.author","Rodenbeck, Andrea"],["dc.contributor.author","Ruther, Eckart"],["dc.contributor.author","Cohrs, Stefan"],["dc.date.accessioned","2018-11-07T10:56:36Z"],["dc.date.available","2018-11-07T10:56:36Z"],["dc.date.issued","2005"],["dc.format.extent","263"],["dc.identifier.isi","000232591900169"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/50052"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Georg Thieme Verlag Kg"],["dc.publisher.place","Stuttgart"],["dc.relation.conference","24th Symposium of the Arbeitsgemeinschaft-fur-Neuropsychopharmakologie-und-Pharmakopsychiatrie (AGNP)"],["dc.relation.eventlocation","Munich, GERMANY"],["dc.relation.issn","0176-3679"],["dc.title","Reduced cortisol excretion in healthy subjects under treatment with ziprasidone"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]Details WOS2004Journal Article [["dc.bibliographiccitation.firstpage","414"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Psychopharmacology"],["dc.bibliographiccitation.lastpage","420"],["dc.bibliographiccitation.volume","174"],["dc.contributor.author","Cohrs, Stefan"],["dc.contributor.author","Pohlmann, K."],["dc.contributor.author","Guan, Zhenghua"],["dc.contributor.author","Jordan, W."],["dc.contributor.author","Meier, A."],["dc.contributor.author","Huether, Gerald"],["dc.contributor.author","Ruther, Eckart"],["dc.contributor.author","Rodenbeck, Andrea"],["dc.date.accessioned","2018-11-07T10:47:56Z"],["dc.date.available","2018-11-07T10:47:56Z"],["dc.date.issued","2004"],["dc.description.abstract","Rationale. Hypothalamic-pituitary-adrenal (HPA) axis dysfunction is a frequent finding in psychiatric disorders, including psychotic depression and schizophrenia. Conflicting results exist concerning the influence of antipsychotics on the HPA-axis. Objective. Therefore, this double-blind, placebo-controlled, randomized cross-over study investigated the effect of quetiapine on nocturnal urinary cortisol and melatonin excretion in 13 healthy male subjects under conditions of undisturbed and experimentally disturbed sleep. Methods. Volunteers were studied 3 times for 3 consecutive nights (N0, adaptation; N1, standard sleep conditions; N2, acoustic stress) 4 days apart. Placebo, quetiapine 25 mg or quetiapine 100 mg was administered orally 1 h before bedtime on nights 1 and 2. Urine produced during the 8-h bedtime period was collected for later determination of cortisol and melatonin concentrations by standard radioimmunoassays. Results. MANOVA showed a significant effect for N1 vs. N2 with elevated total amount of cortisol (p<0.005) and melatonin (p<0.05) excretion after acoustic stress. Both quetiapine 25 mg and 100 mg significantly (p<0.0005) reduced the total amount of cortisol excretion in comparison to placebo. No interaction effect of stress condition was observed. There was no effect of quetiapine on melatonin levels. Conclusion. The significant reduction of nocturnal cortisol excretion following quetiapine reflects a decreased activity of the HPA-axis in healthy subjects. This finding may be an important aspect in quetiapine's mode of action in different patient populations."],["dc.identifier.doi","10.1007/s00213-003-1766-6"],["dc.identifier.isi","000222646700013"],["dc.identifier.pmid","14735295"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/48081"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.relation.issn","0033-3158"],["dc.title","Quetiapine reduces nocturnal urinary cortisol excretion in healthy subjects"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]Details DOI PMID PMC WOS2004Journal Article [["dc.bibliographiccitation.firstpage","867"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","SLEEP"],["dc.bibliographiccitation.lastpage","874"],["dc.bibliographiccitation.volume","27"],["dc.contributor.author","Jordan, W."],["dc.contributor.author","Tumani, Hayrettin"],["dc.contributor.author","Cohrs, Stefan"],["dc.contributor.author","Eggert, S."],["dc.contributor.author","Rodenbeck, Andrea"],["dc.contributor.author","Brunner, E."],["dc.contributor.author","Ruther, Eckart"],["dc.contributor.author","Hajak, Goran"],["dc.date.accessioned","2018-11-07T10:47:06Z"],["dc.date.available","2018-11-07T10:47:06Z"],["dc.date.issued","2004"],["dc.description.abstract","Study Objectives: The prostaglandin D system plays an important role in animal sleep. In humans, alterations in the prostaglandin D system have been found in diseases exhibiting sleep disturbances as a prominent symptom, such as trypanosoma infection, systemic mastocytosis, bacterial meningitis, major depression, or obstructive sleep apnea. Assessment of this system's activity in relation to human physiologic sleep was the target of the present study. Design: Serum concentrations of lipocalin-type prostaglandin D synthase (L-PGDS, former P-trace), and plasma levels of the pineal hormone melatonin were measured in 20 healthy humans (10 women, 10 men; aged: 23.3 +/- 2.39 years) at 4-hour intervals over a period of 5 days and nights, which included physiologic sleep, rapid eye movement sleep deprivation, and total sleep deprivation. In addition, the serum L-PGDS and plasma melatonin levels of 6 subjects were determined under conditions of bright white (10,000 lux) or dark red light (< 50 lux) in a crossover design during total sleep deprivation. Nocturnal blood sampling was performed by a through-the-wall tube system. L-PGDS was measured by an automated immunonephelometric assay, and melatonin was analyzed by direct radioimmunoassay. Results: Serum L-PGDS concentrations showed marked time-dependent changes with evening increases and the highest values at night (P < .0005). This nocturnal increase was suppressed during total sleep deprivation (P < .05), independent of external light conditions and melatonin secretion. Rapid eye movement sleep deprivation had no impact on circulating L-PGDS levels. Conclusions: The circadian L-PGDS pattern and its suppression by total sleep deprivation indicate an interaction of the prostaglandin D system and human sleep regulation. L-PGDS measurements may well provide new insights into physiologic and pathologic sleep regulation in humans."],["dc.identifier.isi","000223451400008"],["dc.identifier.pmid","15453544"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/47897"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Academy Sleep Medicine"],["dc.relation.issn","0161-8105"],["dc.title","Prostaglandin D synthase (beta-trace) in healthy human sleep"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]Details PMID PMC WOS2006Journal Article [["dc.bibliographiccitation.firstpage","11"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Psychopharmacology"],["dc.bibliographiccitation.lastpage","18"],["dc.bibliographiccitation.volume","185"],["dc.contributor.author","Cohrs, Stefan"],["dc.contributor.author","Roher, C."],["dc.contributor.author","Jordan, W."],["dc.contributor.author","Meier, A."],["dc.contributor.author","Huether, Gerald"],["dc.contributor.author","Wuttke, Wolfgang"],["dc.contributor.author","Ruther, Eckart"],["dc.contributor.author","Rodenbeck, Andrea"],["dc.date.accessioned","2018-11-07T10:16:09Z"],["dc.date.available","2018-11-07T10:16:09Z"],["dc.date.issued","2006"],["dc.description.abstract","Rationale: Increased activity of the hypothalamic-pituitary-adrenal (HPA) axis is an important aspect of the pathophysiology of major depression and schizophrenia. Despite the usefulness of atypical antipsychotics in the treatment of depression and their positive influence on cognitive functioning possibly related to their impact on cortisol, little is known about their effect on HPA axis function. Objective: Therefore, this double-blind, placebo-controlled, randomized cross-over study investigated the influence of the atypical antipsychotics quetiapine and olanzapine in comparison with haloperidol and placebo on plasma adrenocorticotropic hormone (ACTH), cortisol, and prolactin levels. Eleven healthy male volunteers were studied during four sessions one week apart, orally receiving placebo, quetiapine (50 mg), olanzapine (5 mg), or haloperidol (3 mg). Blood samples were taken at hourly intervals from 0900 until 1700 hours. For ACTH, cortisol, and prolactin a significant effect of treatment condition (p <= 0.005; p <= 0.035; p <= 0.0001, respectively) for area under the curve (AUC) was found. In comparison to placebo, quetiapine and olanzapine significantly reduced ACTH (p <= 0.002; p <= 0.05, respectively) and cortisol (p <= 0.005; p <= 0.03, respectively). No effect of haloperidol on AUC of ACTH or cortisol levels was observed. In comparison with placebo, haloperidol (p <= 0.0001) and olanzapine (p <= 0.0001) elevated AUC of prolactin plasma levels, whereas no significant effect was observed for quetiapine as a main effect of treatment condition. The atypical antipsychotics' strong influence on HPA-function with pronounced ACTH and cortisol lowering is possibly related to the atypicals' blockade of serotonergic receptors, but blockade of adrenergic or histaminergic receptors may play a role as well. The observed HPA-axis down-regulation may be clinically important for the atypicals' effects on depressive symptomatology and cognitive functioning."],["dc.identifier.doi","10.1007/s00213-005-0279-x"],["dc.identifier.isi","000235547600002"],["dc.identifier.pmid","16432682"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/40980"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","0033-3158"],["dc.title","The atypical antipsychotics olanzapine and quetiapine, but not haloperidol, reduce ACTH and cortisol secretion in healthy subjects"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]Details DOI PMID PMC WOS2003Conference Abstract [["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Pharmacopsychiatry"],["dc.bibliographiccitation.volume","36"],["dc.contributor.author","Jordan, W."],["dc.contributor.author","Berger, C."],["dc.contributor.author","Cohrs, Stefan"],["dc.contributor.author","Rodenbeck, Andrea"],["dc.contributor.author","Mayer, G."],["dc.contributor.author","Niedmann, P."],["dc.contributor.author","Ruther, Eckart"],["dc.contributor.author","Bleich, Stefan"],["dc.date.accessioned","2018-11-07T10:36:46Z"],["dc.date.available","2018-11-07T10:36:46Z"],["dc.date.issued","2003"],["dc.identifier.isi","000186262800150"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/45404"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Georg Thieme Verlag Kg"],["dc.publisher.place","Stuttgart"],["dc.relation.conference","23rd Symposium of the Arbeitsgemeinschaft-Neuropsychopharmakologie-und-Pharmakopsychiatrie (AGNP)"],["dc.relation.eventlocation","MUNICH, GERMANY"],["dc.title","Serum homocysteine in obstructive sleep apnea syndrome can be lowered by CPAP-therapy"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]Details WOS2004Journal Article [["dc.bibliographiccitation.firstpage","161"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Neuroscience Letters"],["dc.bibliographiccitation.lastpage","164"],["dc.bibliographiccitation.volume","360"],["dc.contributor.author","Cohrs, Stefan"],["dc.contributor.author","Guan, Z."],["dc.contributor.author","Pohlmann, K."],["dc.contributor.author","Jordan, W."],["dc.contributor.author","Pilz, J."],["dc.contributor.author","Ruther, Eckart"],["dc.contributor.author","Rodenbeck, Andrea"],["dc.date.accessioned","2018-11-07T10:49:33Z"],["dc.date.available","2018-11-07T10:49:33Z"],["dc.date.issued","2004"],["dc.description.abstract","The pathophysiology of periodic leg movements (PLMs) in sleep remains to be elucidated. Among other hypotheses all alteration of dopaminergic function has been suggested. Nocturnal urinary dopamine and 4-hydroxy-3-methoxyphenylacetic acid excretion in otherwise healthy subjects with PLMs was significantly reduced (P < 0.001 and P < 0.05, respectively) compared to subjects without PLMs. This finding, for the first time, demonstrates a correlate of a functionally relevant hypoactivity of the dopaminergic system in subjects with PLMs. (C) 2004 Elsevier Ireland Ltd. All rights reserved."],["dc.identifier.doi","10.1016/j.neulet.2004.02.056"],["dc.identifier.isi","000221141400013"],["dc.identifier.pmid","15082158"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/48459"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Sci Ireland Ltd"],["dc.relation.issn","0304-3940"],["dc.title","Nocturnal urinary dopamine excretion is reduced in otherwise healthy subjects with periodic leg movements in sleep"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]Details DOI PMID PMC WOS2003Conference Abstract [["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Pharmacopsychiatry"],["dc.bibliographiccitation.volume","36"],["dc.contributor.author","Cohrs, Stefan"],["dc.contributor.author","Rodenbeck, Andrea"],["dc.contributor.author","Guan, Z."],["dc.contributor.author","Pohlmann, K."],["dc.contributor.author","Jordan, W."],["dc.contributor.author","Meier, A."],["dc.contributor.author","Ruther, Eckart"],["dc.date.accessioned","2018-11-07T10:36:45Z"],["dc.date.available","2018-11-07T10:36:45Z"],["dc.date.issued","2003"],["dc.format.extent","217"],["dc.identifier.isi","000186262800047"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/45399"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Georg Thieme Verlag Kg"],["dc.publisher.place","Stuttgart"],["dc.relation.conference","23rd Symposium of the Arbeitsgemeinschaft-Neuropsychopharmakologie-und-Pharmakopsychiatrie (AGNP)"],["dc.relation.eventlocation","MUNICH, GERMANY"],["dc.relation.issn","0176-3679"],["dc.title","Quetiapine improves sleep quality in healthy subjects"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]Details WOS2003Journal Article [["dc.bibliographiccitation.firstpage","423"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Psychopharmacology"],["dc.bibliographiccitation.lastpage","428"],["dc.bibliographiccitation.volume","170"],["dc.contributor.author","Rodenbeck, Andrea"],["dc.contributor.author","Cohrs, Stefan"],["dc.contributor.author","Jordan, W."],["dc.contributor.author","Huether, Gerald"],["dc.contributor.author","Ruther, Eckart"],["dc.contributor.author","Hajak, Goran"],["dc.date.accessioned","2018-11-07T10:34:33Z"],["dc.date.available","2018-11-07T10:34:33Z"],["dc.date.issued","2003"],["dc.description.abstract","Rationale. In primary care, sedating antidepressants are often used for treating insomnia, although their underlying sleep-promoting mechanisms are only incompletely understood. Since enhanced evening and nocturnal plasma cortisol levels are supposed to maintain insomniac sleep complaints, a functional link between sleep and cortisol secretion in the mode of action of antidepressants in insomnia might be suspected. Objectives. We therefore investigated the effects of the tricyclic antidepressant doxepin on nocturnal sleep and plasma cortisol concentration in ten patients (age 41.3+/-9.5 years) with chronic primary insomnia between 1700 hours and 0800 hours. Methods. Single infusions of placebo and 25 mg doxepin were applied following a double-blind, randomized cross-over design. Afterward, all patients received 25 mg doxepin p.o. for 3 weeks in an open-study design. Results. Both doxepin application forms improved sleep significantly and reduced mean cortisol levels from 9.0+/-1.7 mug/l (single placebo i.v.) to 7.5+/-1.6 mug/l (single doxepin i.v.) or 7.6+/-2.0 mug/l (subchronic doxepin p.o.). The duration of the quiescent period of the cortisol rhythm was significantly prolonged following both doxepin administrations compared with placebo. Conclusions. The results implicate that the sleep-improving effects of doxepin are mediated at least in part by a normalization of hypothalamic-pituitary-adrenal axis functions. Although in some patients rebound insomnia and specific side effects must be considered, our findings give a further rationale for the use of antidepressants in the treatment of primary insomnia."],["dc.identifier.doi","10.1007/s00213-003-1565-0"],["dc.identifier.isi","000186831000011"],["dc.identifier.pmid","13680082"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/44900"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","0033-3158"],["dc.title","The sleep-improving effects of doxepin are paralleled by a normalized plasma cortisol secretion in primary insomnia - A placebo-controlled, double-blind, randomized, cross-over study followed by an open treatment over 3 weeks"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]Details DOI PMID PMC WOS2005Journal Article [["dc.bibliographiccitation.firstpage","1372"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","Journal of Neurology"],["dc.bibliographiccitation.lastpage","1378"],["dc.bibliographiccitation.volume","252"],["dc.contributor.author","Jordan, W."],["dc.contributor.author","Tumani, Hayrettin"],["dc.contributor.author","Cohrs, Stefan"],["dc.contributor.author","Rodenbeck, Andrea"],["dc.contributor.author","Ruther, Eckart"],["dc.contributor.author","Bechthold, J."],["dc.contributor.author","Mayer, G."],["dc.date.accessioned","2018-11-07T10:54:43Z"],["dc.date.available","2018-11-07T10:54:43Z"],["dc.date.issued","2005"],["dc.description.abstract","Objectives Alterations in the prostaglandin-D-system have been found in animal sleep experiments and disorders that present with hypersomnia or sleep disturbances. The recently demonstrated involvement of the leptomeningeal lipocalin-type prostaglandin-D-synthase (L-PGDS) (P-trace) in human physiological sleep encouraged us to investigate its role in the pathophysiology of narcolepsy. Methods In a pilot study, serum L-PGDS and melatonin concentrations were assessed in 14 narcoleptic patients during undisturbed sleep and total sleep deprivation, compared with those from 14 healthy controls during undisturbed sleep. Excessive daytime sleepiness was measured by a standardized questionnaire (Epworth sleepiness scale, ESS). Results In narcoleptic patients, markedly increased baseline L-PGDS levels were significantly correlated with the ESS score, but not with the degree of cataplexy. Serum L-PGDS concentrations in patients as well as in controls followed a time-dependent fluctuation with evening increases, highest values during the night and in the morning. Compared with controls, patients exhibited significant/increased amplitude of circulating L-PGDS without any suppression by total sleep deprivation. Conclusion These findings indicate that the prostaglandin-D-system contributes to the pathophysiology of narcolepsy, e. g. the regulation of excessive daytime sleepiness. Since it has been suggested that L-PGDS is also involved in neurodegenerative disorders, there may be a more specific role of the prostaglandin-D-system in narcoleptic aetiogenesis. Moreover, its linkage with the immune system as well as with human sleep regulation offers a direct access for investigating both systems."],["dc.identifier.doi","10.1007/s00415-005-0870-4"],["dc.identifier.isi","000233543200013"],["dc.identifier.pmid","15944863"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/49628"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Dr Dietrich Steinkopff Verlag"],["dc.relation.issn","0340-5354"],["dc.title","Narcolepsy - Increased L-PGDS (beta-trace) levels correlate with excessive daytime sleepiness but not with cataplexy"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]Details DOI PMID PMC WOS2004Journal Article [["dc.bibliographiccitation.firstpage","421"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Psychopharmacology"],["dc.bibliographiccitation.lastpage","429"],["dc.bibliographiccitation.volume","174"],["dc.contributor.author","Cohrs, Stefan"],["dc.contributor.author","Rodenbeck, Andrea"],["dc.contributor.author","Guan, Zhenghua"],["dc.contributor.author","Pohlmann, K."],["dc.contributor.author","Jordan, W."],["dc.contributor.author","Meier, A."],["dc.contributor.author","Ruther, Eckart"],["dc.date.accessioned","2018-11-07T10:47:56Z"],["dc.date.available","2018-11-07T10:47:56Z"],["dc.date.issued","2004"],["dc.description.abstract","The aim of this study was to investigate the effects of quetiapine, an atypical antipsychotic, on polysomnographic sleep structure and subjective sleep quality. This double-blind, placebo-controlled, randomized cross-over study investigated the polysomnographic sleep structure and subjective sleep quality of 14 healthy male subjects given placebo, quetiapine 25 mg or quetiapine 100 mg. Volunteers were studied 3 times for 3 consecutive nights (N0, adaptation; N1, standard sleep conditions; N2, acoustic stress) 4 days apart. Treatment was administered orally 1 h before bedtime on nights 1 and 2. Quetiapine 25 mg and 100 mg significantly improved sleep induction and continuity under standard and acoustic stress conditions. Increases in total sleep time, sleep efficiency, percentage sleep stage 2 and subjective sleep quality were seen. A significant increase in periodic leg movements during sleep was observed with quetiapine 100 mg. The sleep-improving properties of quetiapine may be important in counteracting different aspects of psychopathology in schizophrenia and other disorders. These sleep-inducing and sleep-modifying properties are probably related to quetiapine's receptor-binding profile, including its antihistaminergic, antidopaminergic and antiadrenergic properties. Other mechanisms might be relevant as well and further investigation is required."],["dc.identifier.doi","10.1007/s00213-003-1759-5"],["dc.identifier.isi","000222646700014"],["dc.identifier.pmid","15029469"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/48082"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.relation.issn","0033-3158"],["dc.title","Sleep-promoting properties of quetiapine in healthy subjects"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]Details DOI PMID PMC WOS