Woldt, Helge

[["dc.bibliographiccitation.firstpage","1305"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","Neurochemical Research"],["dc.bibliographiccitation.lastpage","1309"],["dc.bibliographiccitation.volume","30"],["dc.contributor.author","Unzicker, Christian"],["dc.contributor.author","Erberich, Heike"],["dc.contributor.author","Moldrich, Gabriella"],["dc.contributor.author","Woldt, Helge"],["dc.contributor.author","Bulla, Jan"],["dc.contributor.author","Mechoulam, Raphael"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.contributor.author","Sirén, Anna-Leena"],["dc.date.accessioned","2017-09-07T11:46:33Z"],["dc.date.available","2017-09-07T11:46:33Z"],["dc.date.issued","2005"],["dc.description.abstract","Endothelin (ETB)-receptors mediate anti-apoptotic actions. Lack of functional ETB-receptors leads to increased neuronal apoptosis in the hippocampus. The increased apoptosis must be compensated by other mechanisms, however, as ETB-deficient rats display normal overall brain morphology. To illuminate on brain plasticity in ETB-receptor deficiency, we studied the expression and function of another neuroprotective system, the cannabinoid CB1-receptors, in ETB-deficient hippocampus. We show that CB1 expression in hippocampus increases postnatally in all rats but that the increase in CB1-receptor expression is significantly higher in ETB-deficient compared to wildtype littermates. Neuronal apoptosis decreases during brain maturation but remains on a significantly higher level in the ETB-deficient compared to wildtype dentate. When investigating survival of hippocampal neurons in culture, we found significant protection against hypoxia-induced cell death with CB1-analogs (noladin, (9-tetrahydrocannabinol) only in ETB-deficient neurons. We suggest that CB1-receptor upregulation in the ETB-mutant hippocampus reflects an attempt to compensate for the lack of ETB-receptors."],["dc.identifier.doi","10.1007/s11064-005-8802-3"],["dc.identifier.gro","3150522"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7294"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.subject","Cannabis; CB1; endocannabinoid system; noladin; tetrahydrocannabinol; THC; endothelin; ETB; apoptosis; hippocampus; dentate gyrus; neuronal culture; Wistar-Imamichi rat; spotting lethal rat; hypoxia; neuroprotection; immunohistochemistry; Western blot"],["dc.title","Hippocampal cannabinoid-1 receptor upregulation upon endothelin-B receptor deficiency: A neuroprotective substitution effect?"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1219"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","Neurochemical Research"],["dc.bibliographiccitation.lastpage","1230"],["dc.contributor.author","Byts, Nadiya"],["dc.contributor.author","Samoylenko, Anatoly"],["dc.contributor.author","Woldt, Helge"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.contributor.author","Sirén, Anna-Leena"],["dc.date.accessioned","2017-09-07T11:46:18Z"],["dc.date.available","2017-09-07T11:46:18Z"],["dc.date.issued","2006"],["dc.description.abstract","Correct timing and spatial location of growth factor expression is critical for undisturbed brain development and functioning. In terminally differentiated cells distinct biological responses to growth factors may depend on cell type specific activation of signalling cascades. We show that the hematopoietic growth factors thrombopoietin (TPO) and granulocyte colony-stimulating factor (GCSF) exert cell type specific effects on survival, proliferation and the degree of phosphorylation of Akt1, ERK1/2 and STAT3 in rat hippocampal neurons and cortical astrocytes. In neurons, TPO induced cell death and selectively activated ERK1/2. GCSF protected neurons from TPO- and hypoxia-induced cell death via selective activation of Akt1. In astrocytes, neither TPO nor GCSF had any effect on cell viability but inhibited proliferation. This effect was accompanied by activation of ERK1/2 and inhibition of STAT3 activity. A balance between growth factors, their receptors and signalling proteins may play an important role in regulation of neural cell survival."],["dc.identifier.gro","3150471"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7239"],["dc.language.iso","en"],["dc.notes.status","zu prüfen"],["dc.relation.issn","0364-3190"],["dc.title","Cell type specific signalling by hematopoietic growth factors in neural cells"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","42"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Molecular Psychiatry"],["dc.bibliographiccitation.lastpage","54"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.contributor.author","Degner, D."],["dc.contributor.author","Meller, Johannes"],["dc.contributor.author","Brines, Michael"],["dc.contributor.author","Behe, M."],["dc.contributor.author","Hasselblatt, Martin"],["dc.contributor.author","Woldt, Helge"],["dc.contributor.author","Falkai, Peter"],["dc.contributor.author","Knerlich, Friederike"],["dc.contributor.author","Jacob, Silke"],["dc.contributor.author","von Ahsen, Nicolas"],["dc.contributor.author","Maier, Wolfgang"],["dc.contributor.author","Brück, W."],["dc.contributor.author","Rüther, Eckart"],["dc.contributor.author","Cerami, A."],["dc.contributor.author","Becker, Wolfgang"],["dc.contributor.author","Sirén, Anna-Leena"],["dc.date.accessioned","2017-09-07T11:46:26Z"],["dc.date.available","2017-09-07T11:46:26Z"],["dc.date.issued","2004"],["dc.description.abstract","Erythropoietin (EPO) is a candidate compound for neuroprotection in human brain disease capable of combating a spectrum of pathophysiological processes operational during the progression of schizophrenic psychosis. The purpose of the present study was to prepare the ground for its application in a first neuroprotective add-on strategy in schizophrenia, aiming at improvement of cognitive brain function as well as prevention/slowing of degenerative processes. Using rodent studies, primary hippocampal neurons in culture, immunohistochemical analysis of human post-mortem brain tissue and nuclear imaging technology in man, we demonstrate that: (1) peripherally applied recombinant human (rh) EPO penetrates into the brain efficiently both in rat and humans, (2) rhEPO is enriched intracranially in healthy men and more distinctly in schizophrenic patients, (3) EPO receptors are densely expressed in hippocampus and cortex of schizophrenic subjects but distinctly less in controls, (4) rhEPO attenuates the haloperidol-induced neuronal death in vitro, and (4) peripherally administered rhEPO enhances cognitive functioning in mice in the context of an aversion task involving cortical and subcortical pathways presumably affected in schizophrenia. These observations, together with the known safety of rhEPO, render it an interesting compound for neuroprotective add-on strategies in schizophrenia and other human diseases characterized by a progressive decline in cognitive performance."],["dc.identifier.doi","10.1038/sj.mp.4001442"],["dc.identifier.gro","3150503"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7274"],["dc.language.iso","en"],["dc.notes.status","zu prüfen"],["dc.relation.issn","1359-4184"],["dc.subject","recombinant human erythropoietin; EPO; schizophrenia; clinical; rodent; SPECT"],["dc.title","Erythropoietin: a candidate compound for neuroprotection in schizophrenia"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","862"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Proceedings of the National Academy of Sciences of the United States of America"],["dc.bibliographiccitation.lastpage","867"],["dc.bibliographiccitation.volume","102"],["dc.contributor.author","Hasselblatt, Martin"],["dc.contributor.author","Knerlich, Friederike"],["dc.contributor.author","von Ahsen, N."],["dc.contributor.author","Jacob, Sonja"],["dc.contributor.author","Sperling, S."],["dc.contributor.author","Woldt, H."],["dc.contributor.author","Vehmeyer, K."],["dc.contributor.author","Nave, Klaus-Armin"],["dc.contributor.author","Sirén, A.-L."],["dc.contributor.author","Ehrenreich, H."],["dc.date.accessioned","2017-09-07T11:46:36Z"],["dc.date.available","2017-09-07T11:46:36Z"],["dc.date.issued","2005"],["dc.description.abstract","Central nervous and hematopoietic systems share developmental features. We report that thrombopoietin (TPO), a stimulator of platelet formation, acts in the brain as a counterpart of erythropoietin (EPO), a hematopoietic growth factor with neuroprotective properties. TPO is most prominent in postnatal brain, whereas EPO is abundant in embryonic brain and decreases postnatally. Upon hypoxia, EPO and its receptor are rapidly reexpressed, whereas neuronal TPO and its receptor are down-regulated. Unexpectedly, TPO is strongly proapoptotic in the brain, causing death of newly generated neurons through the Ras-extracellular signal-regulated kinase 1/2 pathway. This effect is not only inhibited by EPO but also by neurotrophins. We suggest that the proapoptotic function of TPO helps to select for neurons that have acquired target-derived neurotrophic support."],["dc.identifier.doi","10.1073/pnas.0406008102"],["dc.identifier.gro","3150545"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7318"],["dc.language.iso","en"],["dc.notes.status","zu prüfen"],["dc.relation.issn","0027-8424"],["dc.subject","astrocytes; erythropoietin; neurons; differentiation; development"],["dc.title","A hematopoietic growth factor, thrombopoietin, has a proapoptotic role in the brain"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]