Michaelis, Thomas

[["dc.bibliographiccitation.firstpage","209"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Magnetic Resonance Imaging"],["dc.bibliographiccitation.lastpage","215"],["dc.bibliographiccitation.volume","24"],["dc.contributor.author","Watanabe, Takashi"],["dc.contributor.author","Radulovic, Jelena"],["dc.contributor.author","Boretius, Susann"],["dc.contributor.author","Frahm, Jens"],["dc.contributor.author","Michaelis, Thomas"],["dc.date.accessioned","2017-09-07T11:45:27Z"],["dc.date.available","2017-09-07T11:45:27Z"],["dc.date.issued","2006"],["dc.description.abstract","This magnetic resonance imaging (MRI) study describes mapping of the habenulo-interpeduncular pathway in living mice based on manganese-induced contrast. Six hours after intracerebroventricular microinjection of MnCl2, T1-weighted 3D MRI (2.35 T) at 117 μm isotropic resolution revealed a continuous pattern of anterograde labeling from the habenula via the fasciculus retroflexus to the interpeduncular nucleus. Alternatively, the less invasive systemic administration of MnCl2 allowed for monitoring of the dynamic uptake pattern of respective neural components with even higher reproducibility across animals. Time courses covered the range from 42 min to 24 h after injection. In conclusion, manganese-enhanced MRI may open new ways for functional assessments of the habenulo-interpeduncular system in animal models with cognitive impairment."],["dc.identifier.doi","10.1016/j.mri.2005.10.034"],["dc.identifier.gro","3150377"],["dc.identifier.pmid","16563949"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7135"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.relation.issn","0730-725X"],["dc.subject","Habenula; Magnetic resonance imaging; Manganese; Mice; Neural pathways"],["dc.title","Mapping of the habenulo-interpeduncular pathway in living mice using manganese-enhanced 3D MRI"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","596"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","NeuroImage"],["dc.bibliographiccitation.lastpage","602"],["dc.bibliographiccitation.volume","24"],["dc.contributor.author","Michaelis, Thomas"],["dc.contributor.author","Watanabe, Takashi"],["dc.contributor.author","Natt, Oliver"],["dc.contributor.author","Boretius, Susann"],["dc.contributor.author","Frahm, Jens"],["dc.contributor.author","Utz, Sandra"],["dc.contributor.author","Schachtner, Joachim"],["dc.date.accessioned","2017-09-07T11:45:31Z"],["dc.date.available","2017-09-07T11:45:31Z"],["dc.date.issued","2005"],["dc.description.abstract","High-resolution 3D MRI of male pupae of Manduca sexta was performed at 2.35 T in order to evaluate its potential for an in vivo characterization of insect brain during metamorphosis. T1-weighted 3D FLASH (TR/TE = 20/7.8 ms, 25° flip angle) and T2-weighted 3D fast SE MRI data sets (TR/TEeff = 3000/100 ms) were acquired at different developmental stages with an isotropic resolution of 100 μm. Both T1- and T2-weighted 3D MRI allowed for the identification of cerebral structures such as the antennal nerve, antennal and optical lobe, and central brain. Pronounced developmental alterations of the morphology were observed during metamorphosis. The results demonstrate the feasibility of 3D MRI at nanoliter resolution to identify major brain systems of M. sexta and respective changes during pupal development from caterpillar to sphinx moth. Together with the use of suitable contrast agents, this approach may provide new ways for studying the axonal connectivity and neural function of the developing insect brain."],["dc.identifier.doi","10.1016/j.neuroimage.2004.08.048"],["dc.identifier.gro","3150381"],["dc.identifier.pmid","15627604"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7139"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.relation.issn","1053-8119"],["dc.subject","Magnetic resonance imaging; Metamorphosis; Brain development; Manduca sexta; Entomology"],["dc.title","In vivo 3D MRI of insect brain: cerebral development during metamorphosis of Manduca sexta"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","213"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Journal of Medical Primatology"],["dc.bibliographiccitation.lastpage","218"],["dc.bibliographiccitation.volume","38"],["dc.contributor.author","Michaelis, Thomas"],["dc.contributor.author","Abaei, A."],["dc.contributor.author","Boretius, Susann"],["dc.contributor.author","Tammer, Roland"],["dc.contributor.author","Frahm, Jens"],["dc.contributor.author","Schlumbohm, C."],["dc.contributor.author","Fuchs, E."],["dc.date.accessioned","2017-09-07T11:45:28Z"],["dc.date.available","2017-09-07T11:45:28Z"],["dc.date.issued","2009"],["dc.description.abstract","BACKGROUND: Animal models of human brain disorders often have to rely on non-human primates because of their immunological, physiological, and cognitive similarities to humans. METHODS: Localized proton magnetic resonance spectroscopy was performed to assess cerebral metabolite profiles of male common marmoset monkeys in vivo and to determine putative alterations of adult brain metabolism in response to intrauterine hyperexposure to the synthetic glucocorticoid hormone dexamethasone. RESULTS: Excellent spectral quality allowed for absolute quantification of the concentrations of major metabolites in predominantly white matter, gray matter, and thalamus. Marmoset monkeys intrauterinely hyperexposed to dexamethasone revealed normal neurochemical profiles at adulthood. CONCLUSIONS: Prenatally applied dexamethasone does not lead to persistent metabolic alterations affecting adult brain integrity."],["dc.identifier.doi","10.1111/j.1600-0684.2009.00342.x"],["dc.identifier.gro","3150368"],["dc.identifier.pmid","19374665"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7125"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.relation.issn","0047-2565"],["dc.subject","Brain metabolism; Callithrix jacchus; glucocorticoids; prenatal; preterm birth; proton magnetic resonance spectroscopy"],["dc.title","Intrauterine hyperexposure to dexamethasone of the common marmoset monkey revealed normal cerebral metabolite concentrations in adulthood as assessed by quantitative proton magnetic resonance spectroscopy in vivo"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","480"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Brain"],["dc.bibliographiccitation.lastpage","489"],["dc.bibliographiccitation.volume","129"],["dc.contributor.author","Sirén, Anna-Leena"],["dc.contributor.author","Radyushkin, Konstantin"],["dc.contributor.author","Boretius, Susann"],["dc.contributor.author","Kämmer, Daniel"],["dc.contributor.author","Riechers, Claas-Christian"],["dc.contributor.author","Natt, Oliver"],["dc.contributor.author","Sargin, Derya"],["dc.contributor.author","Watanabe, Takashi"],["dc.contributor.author","Sperling, Swetlana"],["dc.contributor.author","Michaelis, Thomas"],["dc.contributor.author","Price, Jack"],["dc.contributor.author","Meyer, Barbara"],["dc.contributor.author","Frahm, Jens"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.date.accessioned","2017-09-07T11:45:33Z"],["dc.date.available","2017-09-07T11:45:33Z"],["dc.date.issued","2006"],["dc.description.abstract","In humans, neurotrauma is suspected to cause brain atrophy and accelerate slowly progressive neurodegenerative disorders, such as Alzheimer's disease or schizophrenia. However, a direct link between brain injury and subsequent delayed global neurodegeneration has remained elusive. Here we show that juvenile (4-week-old) mice that are given a discrete unilateral lesion of the parietal cortex, develop to adulthood without obvious clinical symptoms. However, when monitored 3 and 9 months after lesioning, using high-resolution three-dimensional MRI and behavioural testing, the same mice display global neurodegenerative changes. Surprisingly, erythropoietin, a haematopoietic growth factor with potent neuroprotective activity, prevents behavioural abnormalities, cognitive dysfunction and brain atrophy when given for 2 weeks after acute brain injury. This demonstrates that a localized brain lesion is a primary cause of delayed global neurodegeneration that can be efficiently counteracted by neuroprotection."],["dc.identifier.doi","10.1093/brain/awh703"],["dc.identifier.doi","10.1093/brain/awh703"],["dc.identifier.gro","3150392"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7151"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.relation.issn","0006-8950"],["dc.subject","EPO; MRI; neuroprotection; neurodegeneration; neurotrauma; schizophrenia"],["dc.title","Global brain atrophy after unilateral parietal lesion and its prevention by erythropoietin"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","860"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","NeuroImage"],["dc.bibliographiccitation.lastpage","867"],["dc.bibliographiccitation.volume","22"],["dc.contributor.author","Watanabe, Takashi"],["dc.contributor.author","Radulovic, Jelena"],["dc.contributor.author","Spiess, Joachim"],["dc.contributor.author","Natt, Oliver"],["dc.contributor.author","Boretius, Susann"],["dc.contributor.author","Frahm, Jens"],["dc.contributor.author","Michaelis, Thomas"],["dc.date.accessioned","2017-09-07T11:45:29Z"],["dc.date.available","2017-09-07T11:45:29Z"],["dc.date.issued","2004"],["dc.description.abstract","The morphology and function of the hippocampal system of C57BL/6J mice (n = 8) was studied in vivo using T1-weighted 3D magnetic resonance imaging (MRI) (117 μm isotropic resolution) after bilateral injection of MnCl2 (0.25 μl, 5 or 200 mM) into the posterior hippocampal formation. The neuronal uptake of the T1-shortening Mn2+ ions resulted in a pronounced MRI signal enhancement within the CA3 subfield and dentate gyrus with milder increases in CA1 and subiculum. This finding is in line with differences in the excitability of hippocampal neurons previously reported using electrophysiologic recordings. The subsequent axonal transport of Mn2+ highlighted the principal extrinsic projections from the posterior hippocampal formation via the fimbria and the precommissural fornix to the dorsal part of the lateral septal nucleus. A strong MRI signal enhancement was also observed in the ventral hippocampal commissure. A time-course analysis revealed unsaturated conditions of Mn2+ accumulation at about 2 h after injection and optimal contrast-to-noise ratios at about 6 h after injection. The present results using Mn2+-enhanced 3D MRI open new ways for studying the role of the hippocampal system in specific aspects of learning and memory in normal and mutant mice."],["dc.identifier.doi","10.1016/j.neuroimage.2004.01.028"],["dc.identifier.gro","3150384"],["dc.identifier.pmid","15193616"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7143"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.relation.issn","1053-8119"],["dc.subject","Hippocampus; Efferent pathways; Fornix; Manganese-enhanced MRI; Neuroanatomic tracing"],["dc.title","In vivo 3D MRI staining of the mouse hippocampal system using intracerebral injection of MnCl2"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Multiple Sclerosis Journal"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Nessler, S."],["dc.contributor.author","Boretius, Susann"],["dc.contributor.author","Stadelmann, C."],["dc.contributor.author","Bittner, A."],["dc.contributor.author","Merkler, Doron"],["dc.contributor.author","Michaelis, Thomas"],["dc.contributor.author","Bruck, Wolfgang W."],["dc.contributor.author","Frahm, Jens"],["dc.contributor.author","Sommer, N."],["dc.contributor.author","Hemmer, Bernhard"],["dc.date.accessioned","2018-11-07T10:56:29Z"],["dc.date.available","2018-11-07T10:56:29Z"],["dc.date.issued","2005"],["dc.identifier.isi","000232249900170"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/50022"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Hodder Arnold, Hodder Headline Plc"],["dc.publisher.place","London"],["dc.relation.conference","21st Congress of the European-Committee-for-Treatment-and-Research-in-Multiple-Sclerosis/10th Annual Meeting of Rehabilitation in MS"],["dc.relation.eventlocation","Thessaloniki, GREECE"],["dc.title","MRI-histopathology correlation in a clonal mouse EAE model"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","81"],["dc.bibliographiccitation.journal","Annals of Neurology"],["dc.bibliographiccitation.lastpage","93"],["dc.bibliographiccitation.volume","66"],["dc.contributor.author","Gadjanski, Ivana"],["dc.contributor.author","Boretius, Susann"],["dc.contributor.author","Williams, Sarah K."],["dc.contributor.author","Lingor, Paul"],["dc.contributor.author","Knöferle, Johanna"],["dc.contributor.author","Sättler, Muriel B."],["dc.contributor.author","Fairless, Richard"],["dc.contributor.author","Hochmeister, Sonja"],["dc.contributor.author","Sühs, Kurt-Wolfram"],["dc.contributor.author","Michaelis, Thomas"],["dc.contributor.author","Frahm, Jens"],["dc.contributor.author","Storch, Maria K."],["dc.contributor.author","Bähr, Mathias"],["dc.contributor.author","Diem, Ricarda"],["dc.date.accessioned","2019-07-09T11:52:52Z"],["dc.date.available","2019-07-09T11:52:52Z"],["dc.date.issued","2009"],["dc.description.abstract","Objective: The aim of this study was to investigate the role of voltage-dependent calcium channels (VDCCs) in axon degeneration during autoimmune optic neuritis. Methods: Calcium ion (Ca2 ) influx into the optic nerve (ON) through VDCCs was investigated in a rat model of optic neuritis using manganese-enhanced magnetic resonance imaging and in vivo calcium imaging. After having identified the most relevant channel subtype (N-type VDCCs), we correlated immunohistochemistry of channel expression with ON histopathology. In the confirmatory part of this work, we performed a treatment study using -conotoxin GVIA, an N-type specific blocker. Results: We observed that pathological Ca2 influx into ONs during optic neuritis is mediated via N-type VDCCs. By analyzing the expression of VDCCs in the inflamed ONs, we detected an upregulation of 1B, the pore-forming subunit of N-type VDCCs, in demyelinated axons. However, high expression levels were also found on macrophages/activated microglia, and lower levels were detected on astrocytes. The relevance of N-type VDCCs for inflammation-induced axonal degeneration and the severity of optic neuritis was corroborated by treatment with -conotoxin GVIA. This blocker led to decreased axon and myelin degeneration in the ONs together with a reduced number of macrophages/activated microglia. These protective effects were confirmed by analyzing the spinal cords of the same animals. Interpretation: We conclude that N-type VDCCs play an important role in inflammation-induced axon degeneration via two mechanisms: First, they directly mediate toxic Ca2 influx into the axons; and second, they contribute to macrophage/microglia function, thereby promoting secondary axonal damage."],["dc.identifier.doi","10.1002/ ana.21668"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6088"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/60296"],["dc.language.iso","en"],["dc.subject.ddc","610"],["dc.title","Role of N-Type Voltage-Dependent Calcium Channels in Autoimmune Optic Neuritis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","244"],["dc.bibliographiccitation.journal","NeuroImage"],["dc.bibliographiccitation.lastpage","255"],["dc.bibliographiccitation.volume","69"],["dc.contributor.author","Boretius, Susann"],["dc.contributor.author","Tammer, Roland"],["dc.contributor.author","Michaelis, Thomas"],["dc.contributor.author","Brockmöller, Jürgen"],["dc.contributor.author","Frahm, Jens"],["dc.date.accessioned","2017-09-07T11:44:52Z"],["dc.date.available","2017-09-07T11:44:52Z"],["dc.date.issued","2012"],["dc.description.abstract","Halogenated volatile anesthetics (HVA) are widely used in medicine and research but their effects on brain metabolism in intact organisms are still largely unknown. Here, localized proton magnetic resonance spectroscopy (MRS) of anesthetized mice was applied to evaluate HVA effects on cerebral metabolites in vivo. Experimental protocols combined different concentrations of isoflurane, halothane, sevoflurane, and desflurane with known modulators of adrenergic, GABAergic, and glutamatergic neurotransmission. As a most striking finding, brain lactate increased in individual mice from 1.0 ± 0.6 mM (awake state) to 6.2 ± 1.5 mM (1.75% isoflurane). In addition, relative to total creatine, there were significant isoflurane-induced increases of alanine by 111%, GABA by 20%, choline-containing compounds by 20%, and myo-inositol by 10% which were accompanied by significant decreases of glucose by 51% and phosphocreatine by 9%. The elevation of lactate was most pronounced in the striatum. The HVA effects correlated with the respective minimal alveolar concentrations and were mostly reversible within minutes. The observed alterations are best explained by an HVA-induced stimulation of adrenergic pathways in conjunction with an inhibition of the respiratory chain. Apart from casting new light on cerebral energy metabolism, the present results challenge brain studies of HVA-anesthetized animals."],["dc.identifier.doi","10.1016/j.neuroimage.2012.12.020"],["dc.identifier.gro","3150358"],["dc.identifier.pmid","23266699"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7113"],["dc.language.iso","en"],["dc.notes.status","public"],["dc.relation.issn","1053-8119"],["dc.title","Halogenated volatile anesthetics alter brain metabolism as revealed by proton magnetic resonance spectroscopy of mice in vivo"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","203"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Journal of Neuroscience Methods"],["dc.bibliographiccitation.lastpage","209"],["dc.bibliographiccitation.volume","120"],["dc.contributor.author","Natt, Oliver"],["dc.contributor.author","Watanabe, Takashi"],["dc.contributor.author","Boretius, Susann"],["dc.contributor.author","Radulovic, Jelena"],["dc.contributor.author","Frahm, Jens"],["dc.contributor.author","Michaelis, Thomas"],["dc.date.accessioned","2017-09-07T11:45:33Z"],["dc.date.available","2017-09-07T11:45:33Z"],["dc.date.issued","2002"],["dc.description.abstract","This work demonstrates technical approaches to high-quality magnetic resonance imaging (MRI) of small structures of the mouse brain in vivo. It turns out that excellent soft-tissue contrast requires the reduction of partial volume effects by using 3D MRI at high (isotropic) resolution with linear voxel dimensions of about 100–150 μm. The long T2 relaxation times at relatively low magnetic fields (2.35 T) offer the benefit of a small receiver bandwidth (increased signal-to-noise) at a moderate echo time which together with the small voxel size avoids visual susceptibility artifacts. For measuring times of 1–1.5 h both T1-weighted (FLASH) and T2-weighted (Fast Spin-Echo) 3D MRI acquisitions exhibit detailed anatomical insights in accordance with histological sections from a mouse brain atlas. Preliminary applications address the identification of neuroanatomical variations in different mouse strains and the use of Mn2+ as a T1 contrast agent for neuroaxonal tracing of fiber tracts within the mouse visual pathway."],["dc.identifier.doi","10.1016/s0165-0270(02)00211-x"],["dc.identifier.gro","3150389"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7148"],["dc.language.iso","en"],["dc.notes.status","zu prüfen"],["dc.relation.issn","0165-0270"],["dc.title","High-resolution 3D MRI of mouse brain reveals small cerebral structures in vivo"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","412"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","Disease Models & Mechanisms"],["dc.bibliographiccitation.lastpage","418"],["dc.bibliographiccitation.volume","2"],["dc.contributor.author","Miró, Xavier"],["dc.contributor.author","Zhou, Xunlei"],["dc.contributor.author","Boretius, Susann"],["dc.contributor.author","Michaelis, Thomas"],["dc.contributor.author","Kubisch, Christian"],["dc.contributor.author","Alvarez-Bolado, Gonzalo"],["dc.contributor.author","Gruss, Peter"],["dc.date.accessioned","2017-09-07T11:45:25Z"],["dc.date.available","2017-09-07T11:45:25Z"],["dc.date.issued","2009"],["dc.description.abstract","Polycomb proteins are epigenetic regulators of gene expression. Human central nervous system (CNS) malformations are congenital defects of the brain and spinal cord. One example of a human CNS malformation is Chiari malformation (CM), which presents as abnormal brainstem growth and cerebellar herniation, sometimes accompanied by spina bifida and cortical defects; it can occur in families. Clinically, CM ranges from an asymptomatic condition to one with incapacitating or lethal symptoms, including neural tube defects and hydrocephalus. However, no genes that are causally involved in any manifestation of CM or similar malformations have been identified. Here, we show that a pathway that involves Zac1 (also known as Plagl1 or Lot1) and controls neuronal proliferation is altered in mice that are heterozygous for the polycomb gene Suz12, resulting in a phenotype that overlaps with some clinical manifestations of the CM spectrum. Suz12 heterozygotes show cerebellar herniation and an enlarged brainstem, accompanied by occipital cortical alterations and spina bifida. Downward displacement of the cerebellum causes hydrocephalus in the most severely impaired cases. Although the involvement of polycomb genes in human disease is starting to be recognized, this is the first demonstration of their role in nervous system malformations. Our work strongly suggests that brain malformations such as CM can result from altered epigenetic regulation of genes involved in cell proliferation in the brain."],["dc.identifier.doi","10.1242/dmm.001602"],["dc.identifier.gro","3150365"],["dc.identifier.pmid","19535498"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7122"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.relation.issn","1754-8403"],["dc.title","Haploinsufficiency of the murine polycomb gene Suz12 results in diverse malformations of the brain and neural tube"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]