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Manzke, Till U.
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Manzke, Till U.
Official Name
Manzke, Till U.
Alternative Name
Manzke, T. U.
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2005Conference Abstract [["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","The FASEB Journal"],["dc.bibliographiccitation.volume","19"],["dc.contributor.author","Manzke, Till"],["dc.contributor.author","Kron, Martina"],["dc.contributor.author","Dutschmann, Mathias"],["dc.contributor.author","Richter, D."],["dc.date.accessioned","2018-11-07T11:17:10Z"],["dc.date.available","2018-11-07T11:17:10Z"],["dc.date.issued","2005"],["dc.format.extent","A657"],["dc.identifier.isi","000227610704502"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/54748"],["dc.notes.status","zu prĂĽfen"],["dc.notes.submitter","Najko"],["dc.publisher","Federation Amer Soc Exp Biol"],["dc.publisher.place","Bethesda"],["dc.relation.conference","Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences"],["dc.relation.eventlocation","San Diego, CA"],["dc.relation.issn","0892-6638"],["dc.title","Expression patterns of 5-HT1A, 2A, 2B, 4(a) and 7 receptor isoforms in the respiratory network of rat"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]Details WOS2010Journal Article [["dc.bibliographiccitation.firstpage","4118"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","Journal of Clinical Investigation"],["dc.bibliographiccitation.lastpage","4128"],["dc.bibliographiccitation.volume","120"],["dc.contributor.author","Manzke, Till"],["dc.contributor.author","Niebert, Marcus"],["dc.contributor.author","Koch, Uwe R."],["dc.contributor.author","Caley, Alex"],["dc.contributor.author","Vogelgesang, Steffen"],["dc.contributor.author","Huelsmann, Swen"],["dc.contributor.author","Ponimaskin, Evgeni G."],["dc.contributor.author","Mueller, Ulrike"],["dc.contributor.author","Smart, Trevor G."],["dc.contributor.author","Harvey, Robert J."],["dc.contributor.author","Richter, Diethelm W."],["dc.date.accessioned","2018-11-07T08:37:37Z"],["dc.date.available","2018-11-07T08:37:37Z"],["dc.date.issued","2010"],["dc.description.abstract","Rhythmic breathing movements originate from a dispersed neuronal network in the medulla and pons. Here, we demonstrate that rhythmic activity of this respiratory network is affected by the phosphorylation status of the inhibitory glycine receptor alpha 3 subtype (GlyR alpha 3), which controls glutamatergic and glycinergic neuronal discharges, subject to serotonergic modulation. Serotonin receptor type 1A-specific (5-HTR(1A)-specific) modulation directly induced dephosphorylation of GlyR alpha 3 receptors, which augmented inhibitory glycine-activated chloride currents in HEK293 cells coexpressing 5-HTR(1A) and GlyR alpha 3. The 5-HTR(1A)-GlyR alpha 3 signaling pathway was distinct from opioid receptor signaling and efficiently counteracted opioid-induced depression of breathing and consequential apnea in mice. Paradoxically, this rescue of breathing originated from enhanced glycinergic synaptic inhibition of glutamatergic and glycinergic neurons and caused disinhibition of their target neurons. Together, these effects changed respiratory phase alternations and ensured rhythmic breathing in vivo. GlyR alpha 3-deficient mice had an irregular respiratory rhythm under baseline conditions, and systemic 5-HTR(1A) activation failed to remedy opioid-induced respiratory depression in these mice. Delineation of this 5-HTR(1A)-GlyR alpha 3 signaling pathway offers a mechanistic basis for pharmacological treatment of opioid-induced apnea and other breathing disturbances caused by disorders of inhibitory synaptic transmission, such as hyperekplexia, hypoxia/ischemia, and brainstem infarction."],["dc.identifier.doi","10.1172/JCI43029"],["dc.identifier.isi","000283621800043"],["dc.identifier.pmid","20978350"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6108"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/18577"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prĂĽfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Soc Clinical Investigation Inc"],["dc.relation.issn","0021-9738"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Serotonin receptor 1A-modulated phosphorylation of glycine receptor alpha 3 controls breathing in mice"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]Details DOI PMID PMC WOS2003Journal Article [["dc.bibliographiccitation.firstpage","226"],["dc.bibliographiccitation.issue","5630"],["dc.bibliographiccitation.journal","Science"],["dc.bibliographiccitation.lastpage","229"],["dc.bibliographiccitation.volume","301"],["dc.contributor.author","Manzke, Till"],["dc.contributor.author","Guenther, U."],["dc.contributor.author","Ponimaskin, Evgeni G."],["dc.contributor.author","Haller, M."],["dc.contributor.author","Dutschmann, Mathias"],["dc.contributor.author","Schwarzacher, S."],["dc.contributor.author","Richter, Diethelm W."],["dc.date.accessioned","2018-11-07T10:37:41Z"],["dc.date.available","2018-11-07T10:37:41Z"],["dc.date.issued","2003"],["dc.description.abstract","Opiates are widely used analgesics in anesthesiology, but they have serious adverse effects such as depression of breathing. This is caused by direct inhibition of rhythm-generating respiratory neurons in the Pre-Boetzinger complex (PBC) of the brainstem. We report that serotonin 4(a) [5-HT4(a)] receptors are strongly expressed in respiratory PBC neurons and that their selective activation protects spontaneous respiratory activity. Treatment of rats with a 5-HT4 receptor specific agonist overcame fentanyl-induced respiratory depression and reestablished stable respiratory rhythm without loss of fentanyl's analgesic effect. These findings imply the prospect of a fine-tuned recovery from opioid-induced respiratory depression, through adjustment of intracellular adenosine 3', 5'-monophosphate levels through the convergent signaling pathways in neurons."],["dc.identifier.doi","10.1126/science.1084674"],["dc.identifier.isi","000184056200047"],["dc.identifier.pmid","12855812"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/45628"],["dc.notes.status","zu prĂĽfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Assoc Advancement Science"],["dc.relation.issn","0036-8075"],["dc.title","5-HT4(a) receptors avert opioid-induced breathing depression without loss of analgesia"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]Details DOI PMID PMC WOS2003Review [["dc.bibliographiccitation.firstpage","542"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","Trends in Molecular Medicine"],["dc.bibliographiccitation.lastpage","548"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Richter, Diethelm W."],["dc.contributor.author","Manzke, Till"],["dc.contributor.author","Wilken, Barbara"],["dc.contributor.author","Ponimaskin, Evgeni G."],["dc.date.accessioned","2018-11-07T10:34:35Z"],["dc.date.available","2018-11-07T10:34:35Z"],["dc.date.issued","2003"],["dc.description.abstract","Disturbances of breathing arising from failures of the respiratory center are not uncommon. Among them, breath holding and apnea occur most frequently as consequences of pulmonary and cardiac diseases, hypoxia, head trauma, cerebral inflammatory processes, genetic defects, degenerative brain diseases, alcoholism, deep anesthesia and drug overdose. They are often life-threatening and fail to respond to existing pharmacotherapies. After extensive research, there is now a reliable basis for new strategies to treat respiratory disturbances by pharmacological manipulation of intracellular signaling pathways, particularly those involving the serotonin receptor family. Specific activation of these pathways effectively prevails respiratory disturbances and can be extended to treatment of life-threatening respiratory disorders in patients."],["dc.identifier.doi","10.1016/j.molmed.2003.10.010"],["dc.identifier.isi","000187575100008"],["dc.identifier.pmid","14659469"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/44908"],["dc.notes.status","zu prĂĽfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Sci Ltd"],["dc.relation.issn","1471-4914"],["dc.title","Serotonin receptors: guardians of stable breathing"],["dc.type","review"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]Details DOI PMID PMC WOS2008Journal Article [["dc.bibliographiccitation.firstpage","775"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","The Journal of Comparative Neurology"],["dc.bibliographiccitation.lastpage","790"],["dc.bibliographiccitation.volume","506"],["dc.contributor.author","Manzke, Till"],["dc.contributor.author","Preusse, Stefan"],["dc.contributor.author","Huelsmann, Swen"],["dc.contributor.author","Richter, Diethelm W."],["dc.date.accessioned","2018-11-07T11:18:20Z"],["dc.date.available","2018-11-07T11:18:20Z"],["dc.date.issued","2008"],["dc.description.abstract","Serotonin receptors (5-HTRs) are known to be involved in the regulation of breathing behavior and to mediate neurotrophic actions that exert a significant function in network formation during development. We studied neuronal 5-HT4(a)R-immunoreactivity (-IR) at developmental ages from E14 to P10. Within the pre-Botzinger complex (pre-BotC), a part of the respiratory network important for rhythmogenesis, 5-HT4(a)R-IR was most extensive in rats at an age of E18. The 5-HT4(a)-IR was found predominantly in the neuropil, whereas somatic staining was sporadic at late embryonic (E18-E20) stages. At birth, we observed a dramatic change to a predominantly somatic staining, and neuropil staining was greatly reduced and disappeared at an age of P4. In all developmental stages, 5-HT4(a) and mu-opioid receptors were strongly coexpressed in neurons of the pre-BotC, whereas 5-HT4(a)R expression was absent in neurons within the dorsal horn. Nestin, a marker for CNS progenitor cells, was used to obtain information about the degree of pre-BotC differentiation. Nestin-positive cells did not appear within the pre-BotC before age E20. At E16, nestin-expressing cells were absent in the nucleus ambiguus (NA) and its ventral periphery. The number of nestin-positive cells increased after birth within and outside the pre-BotC, the majority of cells being glial. Coexpression of nestin and 5-HT4(a)R was localized predominantly within the NA and appeared only sporadically within the pre-BotC. We conclude that 5-HT(4(a))Rs are important not only for neuromodulation of cellular excitability but also for respiratory network formation."],["dc.identifier.doi","10.1002/cne.21581"],["dc.identifier.isi","000252334500003"],["dc.identifier.pmid","18076058"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/55012"],["dc.notes.status","zu prĂĽfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-liss"],["dc.relation.issn","0021-9967"],["dc.title","Developmental changes of serotonin 4(a) receptor expression in the rat pre-Botzinger complex"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]Details DOI PMID PMC WOS2008Journal Article [["dc.bibliographiccitation.firstpage","2331"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","The Journal of Physiology"],["dc.bibliographiccitation.lastpage","2343"],["dc.bibliographiccitation.volume","586"],["dc.contributor.author","Kron, Miriam"],["dc.contributor.author","Reuter, Julia"],["dc.contributor.author","Gerhardt, Ellen"],["dc.contributor.author","Manzke, Till"],["dc.contributor.author","Zhang, W."],["dc.contributor.author","Dutschmann, Mathias"],["dc.date.accessioned","2018-11-07T11:15:39Z"],["dc.date.available","2018-11-07T11:15:39Z"],["dc.date.issued","2008"],["dc.description.abstract","The Kolliker-Fuse nucleus (KF) contributes essentially to respiratory pattern formation and adaptation of breathing to afferent information. Systems physiology suggests that these KF functions depend on NMDA receptors (NMDA-R). Recent investigations revealed postnatal changes in the modulation of glutamatergic neurotransmission by brain-derived neurotrophic factor (BDNF) in the KF. Therefore, we investigated postnatal changes in NMDA-R subunit composition and postsynaptic modulation of NMDA-R-mediated currents by BDNF in KF slice preparations derived from three age groups (neonatal: postnatal day (P) 1-5; intermediate: P6-13; juvenile: P14-21). Immunohistochemistry showed a developmental up-regulation of the NR2D subunit. This correlated with a developmental increase in decay time of NMDA currents and a decline of desensitization in response to repetitive exogenous NMDA applications. Thus, developmental up-regulation of the NR2D subunit, which reduces the Mg2+ block of NMDA-R, causes these specific changes in NMDA current characteristics. This may determine the NMDA-R-dependent function of the mature KF in the control of respiratory phase transition. Subsequent experiments revealed that bath-application of BDNF progressively potentiated these repetitively evoked NMDA currents only in intermediate and juvenile age groups. Pharmacological inhibition of protein kinase C (PKC), as a downstream component of the BDNF-tyrosine kinase B receptor (trkB) signalling, prevented BDNF-induced potentiation of NMDA currents. BDNF-induced potentiation of NMDA currents in later developmental stages might be essential for synaptic plasticity during the adaptation of the breathing pattern in response to peripheral/central commands. The lack of plasticity in neonatal neurones strengthens the hypothesis that the respiratory network becomes permissive for activity-dependent plasticity with ongoing postnatal development."],["dc.identifier.doi","10.1113/jphysiol.2007.148916"],["dc.identifier.isi","000255497900011"],["dc.identifier.pmid","18339694"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/54416"],["dc.notes.status","zu prĂĽfen"],["dc.notes.submitter","Najko"],["dc.publisher","Blackwell Publishing"],["dc.relation.issn","0022-3751"],["dc.title","Emergence of brain-derived neurotrophic factor-induced postsynaptic potentiation of NMDA currents during the postnatal maturation of the Kolliker-Fuse nucleus of rat"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]Details DOI PMID PMC WOS2008Journal Article [["dc.bibliographiccitation.firstpage","425"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Molecular and Cellular Neuroscience"],["dc.bibliographiccitation.lastpage","431"],["dc.bibliographiccitation.volume","37"],["dc.contributor.author","Hartelt, N."],["dc.contributor.author","Skorova, Ekaterina Y."],["dc.contributor.author","Manzke, Till"],["dc.contributor.author","Suhr, M."],["dc.contributor.author","Mironova, L."],["dc.contributor.author","Kuegler, Sebastian"],["dc.contributor.author","Mironov, Sergej L."],["dc.date.accessioned","2018-11-07T11:17:53Z"],["dc.date.available","2018-11-07T11:17:53Z"],["dc.date.issued","2008"],["dc.description.abstract","Topology of neuronal networks contributes to their functioning but the structure-function relationships are not yet understood. In order to reveal the spatial organisation of the respiratory network, we expressed enhanced green fluorescent proteins in neurons in brainstem slices containing the respiratory kernel (pre-Botzinger complex). The expression was neuron specific due to use of adeno-associated viral vector driving transgene expression from synapsin I promoter. Both neuronal cell bodies and their dendrites were labelled with high efficacy. This labelling allowed for enhanced spatial resolution as compared to conventional calcium-sensitive dyes. Neurons occupied about 10% of tissue volume and formed an interconnected network. Using custom-developed software, we quantified the network structure that had a modular structure consisting of clusters having transverse (dorsoventral) orientation. They contained in average seven neurons and connections between the cells in different clusters were less frequent. This novel in situ imaging technique is promising to gain new knowledge about the fine structure and function of neuronal networks in living slice preparations. (c) 2007 Elsevier Inc. All rights reserved."],["dc.identifier.doi","10.1016/j.mcn.2007.10.011"],["dc.identifier.isi","000253928500001"],["dc.identifier.pmid","18203620"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/54917"],["dc.notes.status","zu prĂĽfen"],["dc.notes.submitter","Najko"],["dc.publisher","Academic Press Inc Elsevier Science"],["dc.relation.issn","1044-7431"],["dc.title","Imaging of respiratory network topology in living brainstem slices"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]Details DOI PMID PMC WOS2005Conference Abstract [["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","The FASEB Journal"],["dc.bibliographiccitation.volume","19"],["dc.contributor.author","Dutschmann, Mathias"],["dc.contributor.author","Simms, A."],["dc.contributor.author","Waki, Hidefumi"],["dc.contributor.author","Manzke, Till"],["dc.contributor.author","Pickering, A. E."],["dc.contributor.author","Richter, D."],["dc.contributor.author","Paton, J."],["dc.date.accessioned","2018-11-07T11:16:52Z"],["dc.date.available","2018-11-07T11:16:52Z"],["dc.date.issued","2005"],["dc.format.extent","A603"],["dc.identifier.isi","000227610704253"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/54693"],["dc.notes.status","zu prĂĽfen"],["dc.notes.submitter","Najko"],["dc.publisher","Federation Amer Soc Exp Biol"],["dc.publisher.place","Bethesda"],["dc.relation.conference","Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences"],["dc.relation.eventlocation","San Diego, CA"],["dc.relation.issn","0892-6638"],["dc.title","The role of 5-HT4a and 5-HT1A receptor subtypes for recovery from opioid induced cardiovascular depression"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]Details WOS2011Journal Article [["dc.bibliographiccitation.firstpage","1276"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","European Journal of Neuroscience"],["dc.bibliographiccitation.lastpage","1291"],["dc.bibliographiccitation.volume","34"],["dc.contributor.author","Shevtsova, Natalia A."],["dc.contributor.author","Manzke, Till"],["dc.contributor.author","Molkov, Yaroslav I."],["dc.contributor.author","Bischoff, Anne M."],["dc.contributor.author","Smith, Jeffrey C."],["dc.contributor.author","Rybak, Ilya A."],["dc.contributor.author","Richter, Diethelm W."],["dc.date.accessioned","2018-11-07T08:50:56Z"],["dc.date.available","2018-11-07T08:50:56Z"],["dc.date.issued","2011"],["dc.description.abstract","Brainstem respiratory neurons express the glycine a3 receptor (Glya3R), which is a target of modulation by several serotonin (5-HT) receptor agonists. Application of the 5-HT1A receptor (5-HT1AR) agonist 8-OH-DPAT was shown (i) to depress cellular cAMP, leading to dephosphorylation of Glya3R and augmentation of postsynaptic inhibition of neurons expressing Glya3R (Manzke , 2010) and (ii) to hyperpolarize respiratory neurons through 5-HT-activated potassium channels. These processes counteract opioid-induced depression and restore breathing from apnoeas often accompanying pharmacotherapy of pain. The effect is postulated to rely on the enhanced Glya3R-mediated inhibition of inhibitory neurons causing disinhibition of their target neurons. To evaluate this proposal and investigate the neural mechanisms involved, an established computational model of the brainstem respiratory network (Smith , 2007), was extended by (i) incorporating distinct subpopulations of inhibitory neurons (glycinergic and GABAergic) and their synaptic interconnections within the Botzinger and pre-Botzinger complexes and (ii) assigning the 5-HT1AR-Glya3R complex to some of these inhibitory neuron types in the network. The modified model was used to simulate the effects of 8-OH-DPAT on the respiratory pattern and was able to realistically reproduce a number of experimentally observed responses, including the shift in the onset of post-inspiratory activity to inspiration and conversion of the eupnoeic three-phase rhythmic pattern into a two-phase pattern lacking the post-inspiratory phase. The model shows how 5-HT1AR activation can produce a disinhibition of inspiratory neurons, leading to the recovery of respiratory rhythm from opioid-induced apnoeas."],["dc.identifier.doi","10.1111/j.1460-9568.2011.07825.x"],["dc.identifier.isi","000297014000011"],["dc.identifier.pmid","21899601"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/21810"],["dc.notes.status","zu prĂĽfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","0953-816X"],["dc.title","Computational modelling of 5-HT receptor-mediated reorganization of the brainstem respiratory network"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]Details DOI PMID PMC WOS2018Journal Article [["dc.bibliographiccitation.artnumber","28"],["dc.bibliographiccitation.firstpage","1"],["dc.bibliographiccitation.journal","Frontiers in Molecular Neuroscience"],["dc.bibliographiccitation.lastpage","7"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Vogelgesang, Steffen"],["dc.contributor.author","Niebert, Marcus"],["dc.contributor.author","Bischoff, Anne M."],["dc.contributor.author","HĂĽlsmann, Swen"],["dc.contributor.author","Manzke, Till"],["dc.date.accessioned","2019-07-09T11:45:09Z"],["dc.date.available","2019-07-09T11:45:09Z"],["dc.date.issued","2018"],["dc.description.abstract","Mutations in the transcription factor methyl-CpG-binding protein 2 (MeCP2) cause the neurodevelopmental disorder Rett syndrome (RTT). Besides many other neurological problems, RTT patients show irregular breathing with recurrent apneas or breath-holdings. MeCP2-deficient mice, which recapitulate this breathing phenotype, show a dysregulated, persistent expression of G-protein-coupled serotonin receptor 5-ht5b (Htr5b) in the brainstem. To investigate whether the persistence of 5-ht5b expression is contributing to the respiratory phenotype, we crossbred MeCP2-deficient mice with 5-ht5b-deficient mice to generate double knockout mice (Mecp2-/y ;Htr5b-/-). To compare respiration between wild type (WT), Mecp2-/y and Mecp2-/y ;Htr5b-/- mice, we used unrestrained whole-body plethysmography. While the breathing of MeCP2-deficient male mice (Mecp2-/y ) at postnatal day 40 is characterized by a slow breathing rate and the occurrence of prolonged respiratory pauses, we found that in MeCP2-deficient mice, which also lacked the 5-ht5b receptor, the breathing rate and the number of pauses were indistinguishable from WT mice. To test for a potential mechanism, we also analyzed if the known coupling of 5-ht5b receptors to Gi proteins is altering second messenger signaling. Tissue cAMP levels in the medulla of Mecp2-/y mice were decreased as compared to WT mice. In contrast, cAMP levels in Mecp2-/y ;Htr5b-/- mice were indistinguishable from WT mice. Taken together, our data points towards a role of 5-ht5b receptors within the complex breathing phenotype of MeCP2-deficient mice."],["dc.identifier.doi","10.3389/fnmol.2018.00028"],["dc.identifier.pmid","29515365"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15043"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59167"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.publisher","Frontiers Media S.A."],["dc.relation.eissn","1662-5099"],["dc.relation.issn","1662-5099"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.subject.ddc","610"],["dc.title","Persistent Expression of Serotonin Receptor 5b Alters Breathing Behavior in Male MeCP2 Knockout Mice"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]Details DOI PMID PMC