Langohr, Kersten

[["dc.bibliographiccitation.firstpage","520"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","European Journal of Neuroscience"],["dc.bibliographiccitation.lastpage","526"],["dc.bibliographiccitation.volume","12"],["dc.contributor.author","Mironov, Sergej L."],["dc.contributor.author","Langohr, K."],["dc.contributor.author","Richter, Diethelm W."],["dc.date.accessioned","2018-11-07T10:21:08Z"],["dc.date.available","2018-11-07T10:21:08Z"],["dc.date.issued","2000"],["dc.description.abstract","A hyperpolarization-activated current, I-h, is often implied in pacemaker-like depolarizations during rhythmic oscillatory activity. We describe I-h in the isolated respiratory centre of immature mice (P6-P11). I-h was recorded in 15% (22/146) of all inspiratory neurons examined. The mean half-maximal I-h activation occurred at -78 mV and the reversal potential was -40 mV. I-h was inhibited by Cs+ (1-5 mm) and by organic blockers N-ethyl-1,6-dihydro-1,2-dimethyl-6-(methylimino)-N-phenyl-4-pyrimidinamine (ZD 7288; 0.3-3 mu m) and N,N'-bis-(3,4-dimethylphenylethyl)-N-methylamine (YS 035, 3-30 mu m), but not by Ba2+ (0.5 mm). The organic I-h blockers did not change the inspiratory bursts recorded from the XIIth nerve and synaptic drives in inspiratory neurons. Hypoxia reversibly inhibited I-h but, in the presence of organic blockers, the hypoxic reaction remained unchanged. We conclude that although I-h channels are functional in a minority of inspiratory neurons, I-h does not contribute to respiratory rhythm generation or its modulation by hypoxia."],["dc.identifier.doi","10.1046/j.1460-9568.2000.00928.x"],["dc.identifier.isi","000085927900010"],["dc.identifier.pmid","10712631"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/42035"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Blackwell Science Ltd"],["dc.relation.issn","0953-816X"],["dc.title","Hyperpolarization-activated current, I-h, in inspiratory brainstem neurons and its inhibition by hypoxia"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1056"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","Neuropharmacology"],["dc.bibliographiccitation.lastpage","1065"],["dc.bibliographiccitation.volume","48"],["dc.contributor.author","Mironov, Sergej L."],["dc.contributor.author","Langohr, K."],["dc.date.accessioned","2018-11-07T10:58:13Z"],["dc.date.available","2018-11-07T10:58:13Z"],["dc.date.issued","2005"],["dc.description.abstract","Changes in intracellular Na+ and Ca2+ in inspiratory neurons of neonatal mice were examined by using ion-selective fluorescent indicator dyes SBF1 and fura-2, respectively. Both [Na+](i) and [Ca2+], signals showed rhythmic elevations, correlating with the inspiratory motor output. Brief (2-3 min) hypoxia, induced initial potentiation of rhythmic transients followed by their depression. During hypoxia, the basal [Na+](i) and [Ca2+](i) levels slowly increased, reflecting development of an inward current (I-m). By antagonizing specific mechanisms of Na+ and Ca2+ transport we found that increases in [Na+](i), [Ca2+](i) and I-m due to hypoxia are suppressed by CNQX, nifedipine, riluzole and flufenamic acid, indicating contribution of AMPA/kainate receptors, persistent Na+ channels, L-type Ca2+ channels and Ca2+ -sensitive non-selective cationic channels, respectively. The blockers decreased also the amplitude of the inspiratory bursts. Modification of mitochondrial properties with FCCP and cyclosporine A decreased [Ca2+](i) elevations due to hypoxia by about 25%. After depletion of internal Ca2+ stores with thapsigargin, the blockade of NMDA receptors, Na+/K+ pump, Na+/H+ and Na+/Ca2+ exchange, the hypoxic response was not changed. We conclude that slow [Na+](i) and [Ca2+](i) increases in inspiratory neurons during hypoxia are caused by Na+ and Ca2+ entry due to combined activation of persistent Na+ and L-type Ca2+ channels and AMPA/kainate receptors. © 2005 Elsevier Ltd. All rights reserved."],["dc.identifier.doi","10.1016/j.neuropharm.2005.01.021"],["dc.identifier.isi","000229160300014"],["dc.identifier.pmid","15857632"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/50427"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Pergamon-elsevier Science Ltd"],["dc.relation.issn","0028-3908"],["dc.title","Mechanisms of Na+ and Ca2+ influx into respiratory neurons during hypoxia"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","73"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Brain Research"],["dc.bibliographiccitation.lastpage","82"],["dc.bibliographiccitation.volume","1130"],["dc.contributor.author","Mironov, Sergej L."],["dc.contributor.author","Langohr, Kersten"],["dc.date.accessioned","2018-11-07T11:05:40Z"],["dc.date.available","2018-11-07T11:05:40Z"],["dc.date.issued","2007"],["dc.description.abstract","We examined signalling pathways which can involve No as a second messenger in the respiratory network. In the functional slice preparation, NO donors depressed the respiratory motor output and enhanced its depression after brief episodes of hypoxia. In the inspiratory neurons, NO donors suppressed spontaneous excitatory and inhibitory synaptic currents, activated single K-ATP channels and inhibited L-type Ca2+ channels. NO scavengers, PTIO and hemoglobin, and the blocker of NO synthase, N-monomethyl-L-arginine, induced effects opposite to those of NO donors and indicated the role of endogenously generated NO in the modulation of the respiratory activity. Using fluorescent dyes DAF-2 and DCF, we imaged NO and reactive oxygen species (ROS). Concentrations of NO and ROS increased during brief episodes of hypoxia and they both contributed to the activation of KATP channels due to oxygen withdrawal. The oxidizing agent t-butyl-hydroperoxide acted similarly to NO donors but it did not interfere with the effects of NO. Increase in cGMP levels with 8-Br-cGMP reproduced the actions of NO donors and occluded the effects of their subsequent applications. We propose that in the respiratory neurons, a constitutive production of NO is responsible for a tonic activation of cGMP-coupled signalling pathways and changes in No levels modulate the respiratory motor output by altering the activity of K-ATP and L-type Ca2+ channels. (c) 2006 Published by Elsevier B.V."],["dc.identifier.doi","10.1016/j.brainres.2006.09.114"],["dc.identifier.isi","000244072200008"],["dc.identifier.pmid","17169346"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/52121"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.relation.issn","0006-8993"],["dc.title","Modulation of synaptic and channel activities in the respiratory network of the mice by NO/cGMP signalling pathways"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]