Klinker, Florian

[["dc.bibliographiccitation.firstpage","10701"],["dc.bibliographiccitation.issue","32"],["dc.bibliographiccitation.journal","Journal of Neuroscience"],["dc.bibliographiccitation.lastpage","10709"],["dc.bibliographiccitation.volume","34"],["dc.contributor.author","Fresnoza, Shane"],["dc.contributor.author","Stiksrud, Elisabeth"],["dc.contributor.author","Klinker, Florian"],["dc.contributor.author","Liebetanz, David"],["dc.contributor.author","Paulus, Walter J."],["dc.contributor.author","Kuo, Min-Fang"],["dc.contributor.author","Nitsche, Michael A."],["dc.date.accessioned","2018-11-07T09:36:45Z"],["dc.date.available","2018-11-07T09:36:45Z"],["dc.date.issued","2014"],["dc.description.abstract","The neuromodulator dopamine plays an important role in synaptic plasticity. The effects depend on receptor subtypes, affinity, concentration level, and the kind of neuroplasticity induced. In animal experiments, dopamine D-2-like receptor stimulation revealed partially antagonistic effects on plasticity, which might be explained by dosage dependency. In humans, D-2 receptor block abolishes plasticity, and the D-2/D-3, but predominantly D-3, receptor agonist ropinirol has a dosage-dependent nonlinear affect on plasticity. Here we aimed to determine the specific affect of D-2 receptor activation on neuroplasticity in humans, because physiological effects of D-2 and D-3 receptors might differ. Therefore, we combined application of the selective D-2 receptor agonist bromocriptine (2.5, 10, and 20 mg or placebo medication) with anodal and cathodal transcranial direct current stimulation (tDCS), which induces nonfocal plasticity, and with paired associative stimulation (PAS) generating a more focal kind of plasticity in the motor cortex of healthy humans. Plasticity was monitored by transcranial magnetic stimulation-induced motor-evoked potential amplitudes. For facilitatory tDCS, bromocriptine prevented plasticity induction independent from drug dosage. However, its application resulted in an inverted U-shaped dose-response curve on inhibitory tDCS, excitability-diminishing PAS, and to a minor degree on excitability-enhancing PAS. These data support the assumption that modulation of D-2-like receptor activity exerts a nonlinear dose-dependent effect on neuroplasticity in the human motor cortex that differs from predominantly D-3 receptor activation and that the kind of plasticity-induction procedure is relevant for its specific impact."],["dc.description.sponsorship","German Research Foundation [NI 683/6-1]"],["dc.identifier.doi","10.1523/JNEUROSCI.0832-14.2014"],["dc.identifier.isi","000341017300023"],["dc.identifier.pmid","25100602"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/32687"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Soc Neuroscience"],["dc.relation.issn","0270-6474"],["dc.title","Dosage-Dependent Effect of Dopamine D-2 Receptor Activation on Motor Cortex Plasticity in Humans"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","55"],["dc.bibliographiccitation.journal","Epilepsia"],["dc.bibliographiccitation.lastpage","56"],["dc.bibliographiccitation.volume","48"],["dc.contributor.author","Klinker, Florian"],["dc.contributor.author","Hering, Diana"],["dc.contributor.author","Koch, R."],["dc.contributor.author","Nitsche, M. A."],["dc.contributor.author","Potschka, Heidrun"],["dc.contributor.author","Loscher, W."],["dc.contributor.author","Paulus, Walter J."],["dc.contributor.author","Tergau, Frithjof"],["dc.contributor.author","Liebetanz, David"],["dc.date.accessioned","2018-11-07T11:06:29Z"],["dc.date.available","2018-11-07T11:06:29Z"],["dc.date.issued","2007"],["dc.identifier.isi","000246578400172"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/52321"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Blackwell Publishing"],["dc.publisher.place","Oxford"],["dc.relation.conference","5th Joint Meeting of the German, Austrian, and Swiss Sections of the International League Against Epilepsy"],["dc.relation.eventlocation","Basle, SWITZERLAND"],["dc.relation.issn","0013-9580"],["dc.title","Anticonvulsive aftereffects of cathodal transcranial direct current stimulation (tDCS) in the rat transcranial ramp model of focal epilepsy"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","235"],["dc.bibliographiccitation.journal","Behavioural Brain Research"],["dc.bibliographiccitation.lastpage","241"],["dc.bibliographiccitation.volume","333"],["dc.contributor.author","Klinker, Florian"],["dc.contributor.author","Köhnemann, Kathrin"],["dc.contributor.author","Paulus, Walter"],["dc.contributor.author","Liebetanz, David"],["dc.date.accessioned","2020-12-10T14:22:35Z"],["dc.date.available","2020-12-10T14:22:35Z"],["dc.date.issued","2017"],["dc.identifier.doi","10.1016/j.bbr.2017.06.043"],["dc.identifier.issn","0166-4328"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/71658"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Dopamine D3 receptor status modulates sexual dimorphism in voluntary wheel running behavior in mice"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","MULTIPLE SCLEROSIS"],["dc.bibliographiccitation.volume","15"],["dc.contributor.author","Merkler, Doron"],["dc.contributor.author","Klinker, Florian"],["dc.contributor.author","Juergens, T."],["dc.contributor.author","Glaser, Raoul"],["dc.contributor.author","Paulus, Walter J."],["dc.contributor.author","Brinkmann, Bastian G."],["dc.contributor.author","Sereda, Michael W."],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Liebetanz, David"],["dc.date.accessioned","2018-11-07T11:25:14Z"],["dc.date.available","2018-11-07T11:25:14Z"],["dc.date.issued","2009"],["dc.format.extent","S180"],["dc.identifier.isi","000269652500538"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/56580"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Sage Publications Ltd"],["dc.publisher.place","London"],["dc.relation.conference","25th Congress of the European-Committee-for-Treatment-and-Research-in-Multiple-Sclerosis"],["dc.relation.eventlocation","Dusseldorf, GERMANY"],["dc.relation.issn","1352-4585"],["dc.title","Propagation of cortical spreading depression inversely correlates with cortical myelin content"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1914"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Brain"],["dc.bibliographiccitation.lastpage","1925"],["dc.bibliographiccitation.volume","135"],["dc.contributor.author","Frank, T."],["dc.contributor.author","Klinker, F."],["dc.contributor.author","Falkenburger, B. H."],["dc.contributor.author","Laage, R."],["dc.contributor.author","Lühder, F."],["dc.contributor.author","Göricke, B."],["dc.contributor.author","Schneider, A."],["dc.contributor.author","Neurath, H."],["dc.contributor.author","Desel, H."],["dc.contributor.author","Liebetanz, D."],["dc.contributor.author","Bähr, M."],["dc.contributor.author","Weishaupt, J. H."],["dc.date.accessioned","2017-09-07T11:48:52Z"],["dc.date.available","2017-09-07T11:48:52Z"],["dc.date.issued","2012"],["dc.description.abstract","Recent proof-of-principle data showed that the haematopoietic growth factor granulocyte colony-stimulating factor (filgrastim) mediates neuroprotection in rodent models of Parkinson's disease. In preparation for future clinical trials, we performed a preclinical characterization of a pegylated derivative of granulocyte colony-stimulating factor (pegfilgrastim) in the mouse 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine model of Parkinson's disease. We determined serum and cerebrospinal fluid drug levels after subcutaneous injection. A single injection of pegfilgrastim was shown to achieve stable levels of granulocyte colony-stimulating factor in both serum and cerebrospinal fluid with substantially higher levels compared to repetitive filgrastim injections. Leucocyte blood counts were only transiently increased after repeated injections. We demonstrated substantial dose-dependent long-term neuroprotection by pegfilgrastim in both young and aged mice, using bodyweight-adjusted doses that are applicable in clinical settings. Importantly, we found evidence for the functionally relevant preservation of nigrostriatal projections by pegfilgrastim in our model of Parkinson's disease, which resulted in improved motor performance. The more stable levels of pegylated neuroprotective proteins in serum and cerebrospinal fluid may represent a general advantage in the treatment of chronic neurodegenerative diseases and the resulting longer injection intervals are likely to improve patient compliance. In summary, we found that pegylation of a neuroprotective growth factor improved its pharmacokinetic profile over its non-modified counterpart in an in vivo model of Parkinson's disease. As the clinical safety profile of pegfilgrastim is already established, these data suggest that evaluation of pegfilgrastim in further Parkinson's disease models and ultimately clinical feasibility studies are warranted."],["dc.identifier.doi","10.1093/brain/aws054"],["dc.identifier.gro","3142529"],["dc.identifier.isi","000304538900022"],["dc.identifier.pmid","22427327"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/8890"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10 / Funder: Michael J. Fox Foundation"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","0006-8950"],["dc.subject","granulocyte colony-stimulating factor; 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine; neuroprotection; Parkinson’s disease"],["dc.title","Pegylated granulocyte colony-stimulating factor conveys long-term neuroprotection and improves functional outcome in a model of Parkinson's disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","930"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Muscle & Nerve"],["dc.bibliographiccitation.lastpage","936"],["dc.bibliographiccitation.volume","44"],["dc.contributor.author","Kutschenko, Anna"],["dc.contributor.author","Reinert, Marie-Christine"],["dc.contributor.author","Klinker, Florian"],["dc.contributor.author","Paulus, Walter J."],["dc.contributor.author","Hesse, Stefan"],["dc.contributor.author","Liebetanz, David"],["dc.date.accessioned","2018-11-07T08:49:18Z"],["dc.date.available","2018-11-07T08:49:18Z"],["dc.date.issued","2011"],["dc.description.abstract","Introduction: To test the hypothesis that the efficacy of botulinum toxin depends on the activity of the neuromuscular junction, we developed an in vivo paradigm to determine the degree and duration of low-dose botulinum toxin-induced focal paresis in mice. Methods: We combined an automated wheel-running paradigm with low-dose botulinum toxin injections into the calf muscles of wild-type mice. Half of the mice were injected either before the nightly running or before the daily resting period. Results: After botulinum toxin injections, running distance and maximum velocity decreased dose-dependently. The degree and duration of decrease between the respective groups with regard to the time-points of injection were identical. Conclusions: This in vivo paradigm quantifies the degree of otherwise clinically inapparent botulinum toxin-induced focal calf muscle paresis. Increased muscle activity after low-dose injections does not influence the efficacy of botulinum toxin in normal muscles. Muscle Nerve 44: 930-936, 2011"],["dc.identifier.doi","10.1002/mus.22210"],["dc.identifier.isi","000297938800015"],["dc.identifier.pmid","22102464"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/21429"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","0148-639X"],["dc.title","BOTULINUM TOXIN-INDUCED FOCAL PARESIS IN MICE IS UNAFFECTED BY MUSCLE ACTIVITY"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","89"],["dc.bibliographiccitation.journal","Toxicon"],["dc.bibliographiccitation.lastpage","90"],["dc.bibliographiccitation.volume","68"],["dc.contributor.author","Kutschenko, Anna"],["dc.contributor.author","Reinert, M. C."],["dc.contributor.author","Klinker, Florian"],["dc.contributor.author","Paulus, Walter J."],["dc.contributor.author","Hesse, Stefan"],["dc.contributor.author","Liebetanz, David"],["dc.date.accessioned","2018-11-07T09:23:39Z"],["dc.date.available","2018-11-07T09:23:39Z"],["dc.date.issued","2013"],["dc.identifier.doi","10.1016/j.toxicon.2012.07.089"],["dc.identifier.isi","000320075500077"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/29632"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Pergamon-elsevier Science Ltd"],["dc.publisher.place","Oxford"],["dc.relation.eventlocation","Santa Fe, NM"],["dc.relation.issn","0041-0101"],["dc.title","Novel in vivo test shows low-dosage botulinum toxin-induced focal calf muscle paresis is independent of increased muscle activity in wild-type mice"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","374"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Experimental Neurology"],["dc.bibliographiccitation.lastpage","379"],["dc.bibliographiccitation.volume","235"],["dc.contributor.author","Schmitz, Thomas"],["dc.contributor.author","Endesfelder, Stefanie"],["dc.contributor.author","Reinert, Marie-Christine"],["dc.contributor.author","Klinker, Florian"],["dc.contributor.author","Müller, Susann"],["dc.contributor.author","Bührer, Christoph"],["dc.contributor.author","Liebetanz, David"],["dc.date.accessioned","2018-11-07T09:10:49Z"],["dc.date.available","2018-11-07T09:10:49Z"],["dc.date.issued","2012"],["dc.description.abstract","In preterm infants, the risk to develop attention-deficit/hyperactivity disorder is 3 to 4-fold higher than in term infants. Moreover, preterm infants exhibit deficits in motor coordination and balance. Based on clinical data, higher oxygen levels in preterm infants lead to worse neurological outcome, and experimental hyperoxia causes wide-ranging cerebral changes in neonatal rodents. We hypothesize that hyperoxia in the immature brain may affect motor activity in preterm infants. We subjected newborn mice from P6 to P8 to 48 h of hyperoxia (80% O-2) and tested motor activity in running wheels starting at adolescent age P30. Subsequently, from P44 to P53, regular wheels were replaced by complex wheels with variable crossbar positions to assess motor coordination deficits. MRI with diffusion tensor imaging was performed in the corpus callosum to determine white matter diffusivity in mice after hyperoxia at ages P30 and P53 in comparison to control animals. Adolescent mice after neonatal hyperoxia revealed significantly higher values for maximum velocity and mean velocity in regular wheels than controls (P<0.05). In the complex running wheels, however, maximum velocity was decreased in animals after hyperoxia, as compared to controls (P<0.05). Decreased fractional anisotropy and increased radial diffusion coefficient were observed in the corpus callosum of P30 and P53 mice after neonatal hyperoxia compared to control mice. Hyperoxia in the immature brain causes hyperactivity, motor coordination deficits, and impaired white matter diffusivity in adolescent and young adult mice. (C) 2012 Elsevier Inc. All rights reserved."],["dc.description.sponsorship","Medical Faculty, University of Gottingen"],["dc.identifier.doi","10.1016/j.expneurol.2012.03.002"],["dc.identifier.isi","000303430400039"],["dc.identifier.pmid","22449476"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/26581"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.notes.submitter","Najko"],["dc.relation.issn","0014-4886"],["dc.title","Adolescent hyperactivity and impaired coordination after neonatal hyperoxia"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","70"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Journal of Neuroscience"],["dc.bibliographiccitation.lastpage","77"],["dc.bibliographiccitation.volume","31"],["dc.contributor.author","Dowling, Pascal"],["dc.contributor.author","Klinker, Florian"],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Hasan, Kenan"],["dc.contributor.author","Paulus, Walter J."],["dc.contributor.author","Liebetanz, David"],["dc.date.accessioned","2018-11-07T09:00:08Z"],["dc.date.available","2018-11-07T09:00:08Z"],["dc.date.issued","2011"],["dc.description.abstract","Restless legs syndrome (RLS) is a common neurological disorder whose exact pathophysiological mechanism remains unclear despite the successful use of dopaminergic treatment and recent discovery of predisposing genetic factors. As iron deficiency has been associated with RLS for some patients and there is evidence for decreased spinal dopamine D-3-receptor (D3R) signaling in RLS, we aimed at establishing whether D3R activity and iron deficiency share common pathways within the pathophysiology of RLS sensory and motor symptoms. Using a combined mouse model of iron deficiency and dopamine D-3-receptor deficiency (D3R-/-), circadian motor symptoms were evaluated by continuous recording of spontaneous wheel running activity. Testing the acute and persistent pain responses with the hot-plate test and formalin test, respectively, assessed sensory symptoms. A 15 week iron-deficient (ID) diet alone increased acute and persistent pain responses as compared to control diet. As compared to C57BL/6 (WT), homozygous D3R-/- mice already exhibited elevated responses to acute and persistent pain stimuli, where the latter was further elevated by concurrent iron deficiency. ID changed the circadian activity pattern toward an increased running wheel usage before the resting period, which resembled the RLS symptom of restlessness before sleep. Interestingly, D3R-/- shifted this effect of iron deficiency to a time point 3-4 h earlier. The results confirm the ability of iron deficiency and D3R-/- to evoke sensory and motor symptoms in mice resembling those observed in RLS patients. Furthermore this study suggests an increase of ID-related sensory symptoms and modification of ID-related motor symptoms by D3R-/-."],["dc.identifier.doi","10.1523/JNEUROSCI.0959-10.2011"],["dc.identifier.isi","000285915100009"],["dc.identifier.pmid","21209191"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/24076"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Soc Neuroscience"],["dc.relation.issn","0270-6474"],["dc.title","Dopamine D-3 Receptor Specifically Modulates Motor and Sensory Symptoms in Iron-Deficient Mice"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","358"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Behavioural Brain Research"],["dc.bibliographiccitation.lastpage","361"],["dc.bibliographiccitation.volume","220"],["dc.contributor.author","Klinker, Florian"],["dc.contributor.author","Hasan, Kenan"],["dc.contributor.author","Dowling, Pascal"],["dc.contributor.author","Paulus, Walter J."],["dc.contributor.author","Liebetanz, David"],["dc.date.accessioned","2018-11-07T08:54:22Z"],["dc.date.available","2018-11-07T08:54:22Z"],["dc.date.issued","2011"],["dc.description.abstract","Iron deficiency is a widespread form of malnutrition and is known to interfere with cognitive performance and development. To elucidate the role of dopamine D3 and iron deficiency (ID) in inducing cognitive deficits, we studied wildtype and D3 knockout mice on normal or iron-deficient diets subjected to a running wheel-based motor skill sequence. Surprisingly, ID alone had no effect on motor learning in this study, whereas combined ID and dopamine D(3) receptor (D3R)-deficiency significantly interfered with the acquisition of motor skills. Reduced D3R function may serve as a predisposing factor towards ID-related effects on motor learning. (C) 2011 Elsevier B.V. All rights reserved."],["dc.identifier.doi","10.1016/j.bbr.2011.02.022"],["dc.identifier.isi","000289958300015"],["dc.identifier.pmid","21354213"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/22653"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.relation.issn","0166-4328"],["dc.title","Dopamine D(3) receptor deficiency sensitizes mice to iron deficiency-related deficits in motor learning"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]