Hüther, Gerald

[["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"]]

[["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"]]

[["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"]]

[["dc.bibliographiccitation.firstpage","201"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Journal of Pineal Research"],["dc.bibliographiccitation.lastpage","210"],["dc.bibliographiccitation.volume","25"],["dc.contributor.author","Rodenbeck, Andrea"],["dc.contributor.author","Huether, Gerald"],["dc.contributor.author","Rüther, Eckart"],["dc.contributor.author","Hajak, Goran"],["dc.date.accessioned","2021-12-08T12:27:55Z"],["dc.date.available","2021-12-08T12:27:55Z"],["dc.date.issued","1998"],["dc.identifier.doi","10.1111/j.1600-079X.1998.tb00389.x"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/95496"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-476"],["dc.relation.eissn","1600-079X"],["dc.relation.issn","0742-3098"],["dc.rights.uri","http://doi.wiley.com/10.1002/tdm_license_1.1"],["dc.title","Altered circadian melatonin secretion patterns in relation to sleep in patients with chronic sleep-wake rhythm disorders"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","PII S0304-3940(02)00192-1"],["dc.bibliographiccitation.firstpage","159"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Neuroscience Letters"],["dc.bibliographiccitation.lastpage","163"],["dc.bibliographiccitation.volume","324"],["dc.contributor.author","Rodenbeck, Andrea"],["dc.contributor.author","Huether, Gerald"],["dc.contributor.author","Rüther, Eckart"],["dc.contributor.author","Hajak, Göran"],["dc.date.accessioned","2021-06-01T10:50:14Z"],["dc.date.available","2021-06-01T10:50:14Z"],["dc.date.issued","2002"],["dc.description.abstract","Recent research provides evidence for an interaction between sleep and the activation of the hypothalamic-pituitary-adrenal (HPA)-axis, but detailed studies in patients are still missing. We investigated hourly evening and nocturnal plasma cortisol secretion and sleep in seven male patients with severe chronic primary insomnia and age- and gender-matched controls. Evening and nocturnal cortisol levels were significantly increased in patients. Evening cortisol correlated with the number of nocturnal awakenings in patients and controls. Additionally, patients showed significant correlations between sleep parameters and the first 4 h of nocturnal cortisol secretion. These results are indicative of changes in the HPA system in insomnia and may reflect a path of physiological mechanism of chronic insomnia resulting in a vicious cycle of both disturbed HPA functions and chronic insomnia according to the arousal hypothesis of insomnia. (C) 2002 Elsevier Science Ireland Ltd. All rights reserved."],["dc.identifier.doi","10.1016/S0304-3940(02)00192-1"],["dc.identifier.isi","000175793100018"],["dc.identifier.pmid","11988351"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/86583"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Sci Ireland Ltd"],["dc.relation.issn","0304-3940"],["dc.title","Interactions between evening and nocturnal cortisol secretion and sleep parameters in patients with severe chronic primary insomnia"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","251"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","DEVELOPMENTAL BRAIN RESEARCH"],["dc.bibliographiccitation.lastpage","257"],["dc.bibliographiccitation.volume","119"],["dc.contributor.author","Moll, Gunther H."],["dc.contributor.author","Mehnert, C."],["dc.contributor.author","Wicker, M."],["dc.contributor.author","Bock, Nathalie"],["dc.contributor.author","Rothenberger, A."],["dc.contributor.author","Ruther, Eckart"],["dc.contributor.author","Huether, Gerald"],["dc.date.accessioned","2018-11-07T10:03:27Z"],["dc.date.available","2018-11-07T10:03:27Z"],["dc.date.issued","2000"],["dc.description.abstract","The binding parameters of highly selective ligands of serotonin (5-HT) transporters ([H-3]paroxetine), noradrenaline (NE) transporters ([H-3]nisoxetine), and of dopamine (DA) transporters ([H-3]GBR-12935) were determined on membrane preparations from frontal cortex, striatum, midbrain and brain stem of Wistar rats on postnatal days 25, 50, 90 and 240, i.e., from the time of weaning till late adulthood. No age-dependent alterations in the affinity-parameters (K-D-values) of all three monoamine transporters were observed. Age-associated changes in B-max-values of the binding of all three specific ligands were most pronounced in the phylogenetically younger, late maturing brain regions (frontal cortex, striatum). Most likely, these changes reflect age-related changes in 5-HT, NE and DA-innervation densities. In the frontal cortex, 5-HT-transporter density increased steadily from weaning (day 25) till late adulthood, whereas the density of NE-transporters was highest at weaning, declined till puberty (day 50) and remained at this level until old age. DA-transporter density in the frontal cortex was not reliably measurable by [H-3]GBR-binding assays. In the striatum, DA-transporter density increased till puberty and declined thereafter considerably and steadily to about one-fourth of the pubertal values at old age. No such age-associated changes in DA-transporter density were seen in the midbrain. Densities of 5-HT and NE remained at the level reached already at weaning until old age in the striatum, midbrain and brain stem. These findings provide the first comprehensive description of the normally occurring changes in the densities of all three presynaptically located monoamine transporters in the rat brain throughout the life span from weaning to late adulthood. (C) 2000 Elsevier Science B.V. All rights reserved."],["dc.identifier.doi","10.1016/S0165-3806(99)00182-0"],["dc.identifier.isi","000085355100011"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/38469"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.relation.issn","0165-3806"],["dc.title","Age-associated changes in the densities of presynaptic monoamine transporters in different regions of the rat brain from early juvenile life to late adulthood"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","119"],["dc.bibliographiccitation.issue","2-3"],["dc.bibliographiccitation.journal","Neuropsychobiology"],["dc.bibliographiccitation.lastpage","122"],["dc.bibliographiccitation.volume","56"],["dc.contributor.author","Wedekind, Dirk"],["dc.contributor.author","Preiss, Birgit"],["dc.contributor.author","Cohrs, Stefan"],["dc.contributor.author","Ruether, Eckart"],["dc.contributor.author","Huether, Gerald"],["dc.contributor.author","Adler, Lothar"],["dc.date.accessioned","2018-11-07T11:07:14Z"],["dc.date.available","2018-11-07T11:07:14Z"],["dc.date.issued","2007"],["dc.description.abstract","Introduction: The aim of this naturalistic study was to gain more information about the elevation of basal hypothalamic-pituitary- adrenal (HPA) activity in relationship to symptom severity in specific subtypes of depressive episodes. Method: Hamilton Depression Rating Scale scores and aggregated nocturnal urinary cortisol excretion were measured in 4 groups of inpatients with depressive episodes (n = 48; monopolar nonpsychotic, monopolar psychotic, bipolar nonpsychotic and bipolar psychotic) at the beginning and at the end of inpatient treatment. Results: The initial elevation of nocturnal urinary cortisol excretion was most pronounced in psychotic patients. At the end of treatment, the Hamilton Depression Rating Scale scores had decreased significantly in all patients to comparable levels, whereas the nocturnal cortisol excretion values were still relatively elevated in mono- and bipolar psychotic patients compared to mono- and bipolar nonpsychotic ones. Conclusion: The observation that the basal HPA activity remains elevated even after remission of symptoms in patients with psychotic depression supports the concept that a dysfunctional regulation of the HPA system is possibly a trait- rather than a state-related feature. Copyright (c) 2008 S. Karger AG, Basel."],["dc.identifier.doi","10.1159/000112953"],["dc.identifier.isi","000253014500009"],["dc.identifier.pmid","18182828"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/52509"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Karger"],["dc.relation.issn","0302-282X"],["dc.title","Relationship between nocturnal urinary cortisol excretion and symptom severity in subgroups of patients with depressive episodes"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["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"]]

[["dc.bibliographiccitation.firstpage","15"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Journal of Child and Adolescent Psychopharmacology"],["dc.bibliographiccitation.lastpage","24"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Moll, Gunther H."],["dc.contributor.author","Hause, S."],["dc.contributor.author","Ruther, Eckart"],["dc.contributor.author","Rothenberger, A."],["dc.contributor.author","Huether, Gerald"],["dc.date.accessioned","2018-11-07T09:19:58Z"],["dc.date.available","2018-11-07T09:19:58Z"],["dc.date.issued","2001"],["dc.description.abstract","Methylphenidate is widely and effectively used for the treatment of attention deficit hyperactivity disorder during early childhood and adolescence, but until now possible effects of this treatment on brain development and the maturation of monoaminergic systems have not been investigated systematically. This experimental animal study describes the effects of methylphenidate administration (2 mg/kg/day) for 2 weeks to very young (prepubertal) and somewhat older (postpubertal) rats on the densities of dopamine, serotonin, and norepinephrine transporters in the striatum and in the midbrain. As shown by ligand-binding-assays, the KD values of all three transporters were unaffected by this treatment. No alterations were found for the B-max values of [H-3]-paroxetine and [H-3]-nisoxetine binding, but the density of dopamine transporters (B-max values of [H-3]-GBR binding) in the striatum (but not in the midbrain) was significantly reduced after early methylphenidate administration (by 25% at day 45), and this decline reached almost 50% at adulthood (day 70), that is, long after termination of the treatment. This is the first empirical demonstration of long-lasting changes in the development of the central dopaminergic system caused by the administration of methylphenidate during early juvenile life."],["dc.identifier.doi","10.1089/104454601750143366"],["dc.identifier.isi","000168087000003"],["dc.identifier.pmid","11322741"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/28764"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Mary Ann Liebert Inc Publ"],["dc.relation.issn","1044-5463"],["dc.title","Early methylphenidate administration to young rats causes a persistent reduction in the density of striatal dopamine transporters"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","85"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Neuroscience Letters"],["dc.bibliographiccitation.lastpage","88"],["dc.bibliographiccitation.volume","347"],["dc.contributor.author","Maler, J. M."],["dc.contributor.author","Seifert, W."],["dc.contributor.author","Hüther, G."],["dc.contributor.author","Wiltfang, J."],["dc.contributor.author","Rüther, E."],["dc.contributor.author","Kornhuber, J."],["dc.contributor.author","Bleich, Stefan"],["dc.date.accessioned","2017-09-07T11:44:38Z"],["dc.date.available","2017-09-07T11:44:38Z"],["dc.date.issued","2003"],["dc.description.abstract","From several disease states as well as from animal models homocysteine is known to be toxic to the central nervous system. Homocysteine is an excitatory amino acid which markedly enhances the vulnerability of neuronal cells to excitotoxic, apoptotic, and oxidative injury in vitro and in vivo. Both beneficent and deleterious effects of astrocytes in the pathogenesis of different neurodegenerative disorders have been described. However, data about the neurotoxic effect of homocysteine on astrocytes are lacking. The present study therefore was undertaken to investigate a possible cytotoxic effect of homocysteine on cortical astrocytes in vitro. Exposure to d,l-homocysteine resulted in a time and dose-dependent gliotoxic effect at doses of 2 mM and above (P<0.001). This is comparable to homocysteine toxicity observed in other cell culture models and implies that a participation of astrocytes in homocysteine-induced neurodegeneration may be considered. The results of the present in vitro studies may therefore have implications for understanding the pathogenesis of neurotoxicity linked to neurodegenerative disorders (e.g. Alzheimer's disease, glaucomatous optic neuropathy). This is the first study to report that homocysteine induces cell death of astrocytes. The mechanisms by which homocysteine induces cell death of astrocytes warrant further study."],["dc.identifier.doi","10.1016/s0304-3940(03)00655-4"],["dc.identifier.gro","3151710"],["dc.identifier.pmid","12873734"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/8530"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.notes.submitter","chake"],["dc.relation.issn","0304-3940"],["dc.title","Homocysteine induces cell death of rat astrocytes in vitro"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]