Keller, Bernhard U.

[["dc.bibliographiccitation.firstpage","322"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Pflügers Archiv - European Journal of Physiology"],["dc.bibliographiccitation.lastpage","332"],["dc.bibliographiccitation.volume","440"],["dc.contributor.author","Ladewig, T."],["dc.contributor.author","Keller, B. U."],["dc.date.accessioned","2018-11-07T10:49:31Z"],["dc.date.available","2018-11-07T10:49:31Z"],["dc.date.issued","2000"],["dc.description.abstract","Intracellular calcium signals are critical for modulation of neuronal function, and also for pathophysiological states during human neurodegenerative disease, such as Morbus Alzheimer and amyotrophic lateral sclerosis (ALS). We investigated intracellular calcium signals in motoneurones of the nucleus hypoglossus from the mouse, which were maintained in a functionally intact state of rhythmic, respiratory-related activity. Simultaneous patch-clamp recordings and calcium imaging demonstrated that rhythmic inspiratory-related clusters of action potential (AP) discharges are paralleled by calcium oscillations both in somatic and dendritic compartments. Calcium oscillations resulted primarily from the AP-induced opening of voltage-dependent calcium channels in the soma and dendrites. Dendritic calcium transients differed from somatic responses in their kinetics, amplitude, voltage dependence and regulation of basal calcium levels. Based on a combination of infrared differential interference contrast optics, microfluorimetric calcium imaging and electrophysiological patch-clamp recordings, our results demonstrate that the brainstem slice preparation is an attractive model system to study the integration and superposition of calcium signals in a functionally intact neuronal net."],["dc.identifier.doi","10.1007/s004240000277"],["dc.identifier.isi","000087884600017"],["dc.identifier.pmid","10898534"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/48451"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","0031-6768"],["dc.title","Simultaneous patch-clamp recording and calcium imaging in a rhythmically active neuronal network in the brainstem slice preparation from mouse"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","64"],["dc.bibliographiccitation.journal","BMC Neuroscience"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Jaiswal, Manoj Kumar"],["dc.contributor.author","Zech, Wolf-Dieter"],["dc.contributor.author","Goos, Miriam"],["dc.contributor.author","Leutbecher, Christine"],["dc.contributor.author","Ferri, Alberto"],["dc.contributor.author","Zippelius, Annette"],["dc.contributor.author","Carri, Maria Teresa"],["dc.contributor.author","Nau, Roland"],["dc.contributor.author","Keller, Bernhard U."],["dc.date.accessioned","2018-11-07T08:28:40Z"],["dc.date.available","2018-11-07T08:28:40Z"],["dc.date.issued","2009"],["dc.description.abstract","Background: Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disorder characterized by the selective loss of motor neurons (MN) in the brain stem and spinal cord. Intracellular disruptions of cytosolic and mitochondrial calcium have been associated with selective MN degeneration, but the underlying mechanisms are not well understood. The present evidence supports a hypothesis that mitochondria are a target of mutant SOD1-mediated toxicity in familial amyotrophic lateral sclerosis (fALS) and intracellular alterations of cytosolic and mitochondrial calcium might aggravate the course of this neurodegenerative disease. In this study, we used a fluorescence charged cool device (CCD) imaging system to separate and simultaneously monitor cytosolic and mitochondrial calcium concentrations in individual cells in an established cellular model of ALS. Results: To gain insights into the molecular mechanisms of SOD1(G93A) associated motor neuron disease, we simultaneously monitored cytosolic and mitochondrial calcium concentrations in individual cells. Voltage - dependent cytosolic Ca(2+) elevations and mitochondria - controlled calcium release mechanisms were monitored after loading cells with fluorescent dyes fura-2 and rhod-2. Interestingly, comparable voltage-dependent cytosolic Ca(2+) elevations in WT (SH-SY5Y(WT)) and G93A (SH-SY5Y(G93A)) expressing cells were observed. In contrast, mitochondrial intracellular Ca(2+) release responses evoked by bath application of the mitochondrial toxin FCCP were significantly smaller in G93A expressing cells, suggesting impaired calcium stores. Pharmacological experiments further supported the concept that the presence of G93A severely disrupts mitochondrial Ca(2+) regulation. Conclusion: In this study, by fluorescence measurement of cytosolic calcium and using simultaneous [Ca(2+)]i and [Ca(2+)](mito) measurements, we are able to separate and simultaneously monitor cytosolic and mitochondrial calcium concentrations in individual cells an established cellular model of ALS. The primary goals of this paper are (1) method development, and (2) screening for deficits in mutant cells on the single cell level. On the technological level, our method promises to serve as a valuable tool to identify mitochondrial and Ca(2+)-related defects during G93A-mediated MN degeneration. In addition, our experiments support a model where a specialized interplay between cytosolic calcium profiles and mitochondrial mechanisms contribute to the selective degeneration of neurons in ALS."],["dc.identifier.doi","10.1186/1471-2202-10-64"],["dc.identifier.isi","000268695200001"],["dc.identifier.pmid","19545440"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/5754"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/16476"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.notes.submitter","Najko"],["dc.relation.issn","1471-2202"],["dc.rights","CC BY 2.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/2.0"],["dc.title","Impairment of mitochondrial calcium handling in a mtSOD1 cell culture model of motoneuron disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","European Journal of Neuroscience"],["dc.bibliographiccitation.volume","12"],["dc.contributor.author","Wachtmann, D."],["dc.contributor.author","Korner, M. R."],["dc.contributor.author","Stoffel, W."],["dc.contributor.author","Keller, B. U."],["dc.date.accessioned","2018-11-07T11:04:07Z"],["dc.date.available","2018-11-07T11:04:07Z"],["dc.date.issued","2000"],["dc.format.extent","14"],["dc.identifier.isi","000088236600081"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/51763"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Blackwell Science Ltd"],["dc.publisher.place","Oxford"],["dc.relation.issn","0953-816X"],["dc.title","Excitatory synaptic transmission in purkinje cells of glutamate transporter EAAC-1 and GLAST-1 knock-out mice"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","494"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","Trends in Neurosciences"],["dc.bibliographiccitation.lastpage","500"],["dc.bibliographiccitation.volume","28"],["dc.contributor.author","von Lewinski, Friederike"],["dc.contributor.author","Keller, B. U."],["dc.date.accessioned","2018-11-07T10:56:43Z"],["dc.date.available","2018-11-07T10:56:43Z"],["dc.date.issued","2005"],["dc.description.abstract","Motoneurons are selectively damaged in amyotrophic lateral sclerosis (ALS), a fatal neurodegenerative disorder. Although the underlying mechanisms are not completely understood, increasing evidence indicates that motoneurons are particularly sensitive to disruption of mitochondria and Ca2+ -dependent signalling cascades. Comparison of ALS-vulnerable and ALS-resistant neurons identified low Ca2+ -buffering capacity and a strong impact of mitochondrial signal cascades as important risk factors. Under physiological conditions, weak Ca2+ buffers are valuable because they facilitate rapid relaxation times of Ca (2+) transients in motoneurons during high-frequency rhythmic activity. However, under pathological conditions, weak Ca2+ buffers are potentially dangerous because they accelerate a vicious circle of mitochondrial disruption, Ca2+ disregulation and excitotoxic cell damage."],["dc.identifier.doi","10.1016/j.tins.2005.07.001"],["dc.identifier.isi","000232022300007"],["dc.identifier.pmid","16026864"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/50079"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science London"],["dc.relation.issn","0166-2236"],["dc.title","Ca2+, mitochondria and selective motoneuron vulnerability: implications for ALS"],["dc.type","review"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2723"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","The Journal of Physiology"],["dc.bibliographiccitation.lastpage","2745"],["dc.bibliographiccitation.volume","591"],["dc.contributor.author","Fuchs, Andrea"],["dc.contributor.author","Kutterer, Sylvie"],["dc.contributor.author","Mühling, Tobias"],["dc.contributor.author","Duda, Johanna"],["dc.contributor.author","Schütz, Burkhard"],["dc.contributor.author","Liss, Birgit"],["dc.contributor.author","Keller, Bernhard U."],["dc.contributor.author","Roeper, Jochen"],["dc.date.accessioned","2018-11-07T09:25:08Z"],["dc.date.available","2018-11-07T09:25:08Z"],["dc.date.issued","2013"],["dc.description.abstract","Key points center dot So far, increased excitability and calcium handling problems have been discussed as causes for motoneuron death in amyotrophic lateral sclerosis (ALS) mainly on the basis of studies in juvenile presymptomatic mice. center dot We developed a brainstem preparation to analyse excitability and calcium handling during disease progression up to disease endstage of motoneurons in an ALS mouse model. center dot Increased excitability of motoneurons is not seen at disease endstage, challenging this factor as a direct cause for motoneuron death in ALS. center dot We show that calcium handling is remodelled during disease progression from mitochondrial uptake to mitochondrial uptake failure and increased plasma membrane extrusion, providing a compensatory mechanism that fails at disease endstage and might lead to a toxic calcium overload of the cells. center dot Supporting this newly described compensatory endeavour of the motoneurons might be a promising therapeutic strategy. Abstract Amyotrophic lateral sclerosis is a progressive neurodegenerative disease that targets some somatic motoneuron populations, while others, e.g. those of the oculomotor system, are spared. The pathophysiological basis of this pattern of differential vulnerability, which is preserved in a transgenic mouse model of amyotrophic lateral sclerosis (SOD1G93A), and the mechanism of neurodegeneration in general are unknown. Hyperexcitability and calcium dysregulation have been proposed by others on the basis of data from juvenile mice that are, however, asymptomatic. No studies have been done with symptomatic mice following disease progression to the disease endstage. Here, we developed a new brainstem slice preparation for whole-cell patch-clamp recordings and single cell fura-2 calcium imaging to study motoneurons in adult wild-type and SOD1G93A mice up to disease endstage. We analysed disease-stage-dependent electrophysiological properties and intracellular Ca2+ handling of vulnerable hypoglossal motoneurons in comparison to resistant oculomotor neurons. Thereby, we identified a transient hyperexcitability in presymptomatic but not in endstage vulnerable motoneurons. Additionally, we revealed a remodelling of intracellular Ca2+ clearance within vulnerable but not resistant motoneurons at disease endstage characterised by a reduction of uniporter-dependent mitochondrial Ca2+ uptake and enhanced Ca2+ extrusion across the plasma membrane. Our study challenged the notion that hyperexcitability is a direct cause of neurodegeneration in SOD1G93A mice, but molecularly identified a Ca2+ clearance deficit in motoneurons and an adaptive Ca2+ handling strategy that might be targeted by future therapeutic strategies."],["dc.description.sponsorship","Ulm University; BMBF/EU ProgramEranet Goettingen [01EW0912]; [SFB 815]"],["dc.identifier.doi","10.1113/jphysiol.2012.247981"],["dc.identifier.isi","000319016200026"],["dc.identifier.pmid","23401612"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/29993"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.notes.submitter","Najko"],["dc.relation.issn","0022-3751"],["dc.title","Selective mitochondrial Ca2+ uptake deficit in disease endstage vulnerable motoneurons of the SOD1G93A mouse model of amyotrophic lateral sclerosis"],["dc.type","journal_article"],["dc.type.internalPublication","no"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Biophysical Journal"],["dc.bibliographiccitation.volume","86"],["dc.contributor.author","Bergmann, F."],["dc.contributor.author","Kasischke, K. A."],["dc.contributor.author","Zipfel, W. R."],["dc.contributor.author","Webb, W. W."],["dc.contributor.author","Keller, B. U."],["dc.date.accessioned","2018-11-07T10:52:09Z"],["dc.date.available","2018-11-07T10:52:09Z"],["dc.date.issued","2004"],["dc.format.extent","151A"],["dc.identifier.isi","000187971200782"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/49053"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Biophysical Society"],["dc.publisher.place","Bethesda"],["dc.relation.conference","48th Annual Meeting of the Biophysical Society"],["dc.relation.eventlocation","Baltimore, MD"],["dc.relation.issn","0006-3495"],["dc.title","Two-photon NADH imaging in the hypoglossal nucleus - implications for differential neuronal and astrocytic metabolism"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","230"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Muscle & Nerve"],["dc.bibliographiccitation.lastpage","236"],["dc.bibliographiccitation.volume","43"],["dc.contributor.author","Schomburg, Eike D."],["dc.contributor.author","Steffens, Heinz"],["dc.contributor.author","Zschuentzsch, Jana"],["dc.contributor.author","Dibaj, Payam"],["dc.contributor.author","Keller, Bernhard U."],["dc.date.accessioned","2018-11-07T08:59:54Z"],["dc.date.available","2018-11-07T08:59:54Z"],["dc.date.issued","2011"],["dc.description.abstract","Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease characterized by progressive loss of motor neurons. To analyze the progressive motor deficits during the course of this disease, we investigated fatigability and ability of recovery of spinal motor neurons by testing monosynaptic reflex transmission with increasing stimulus frequencies in the lumbar spinal cord of the SOD1(G93A) mouse model for ALS in a comparison with wild-type (WT) mice. Monosynaptic reflexes in WT and SOD1(G93A) mice without behavioral deficits showed no difference with respect to their resistance to increasing stimulus frequencies. During the progression of motor deficits in SOD1(G93A) mice, the vulnerability of monosynaptic reflexes to higher frequencies-increased, the required time for reflex recovery was extended, and recovery was often incomplete. Fatigability and demand for recovery of spinal motor neurons in SOD1(G93A) mice rose with increasing motor deficits. This supports the assumption that impairment of the energy supply may contribute to the pathogenesis of ALS. Muscle Nerve 43: 230-236, 2011"],["dc.identifier.doi","10.1002/mus.21835"],["dc.identifier.isi","000286558300013"],["dc.identifier.pmid","21254088"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/24015"],["dc.language.iso","en"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.relation.issn","0148-639X"],["dc.title","FATIGABILITY OF SPINAL REFLEX TRANSMISSION IN A MOUSE MODEL (SOD1(G93A)) OF AMYOTROPHIC LATERAL SCLEROSIS"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","812"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Journal of Neurochemistry"],["dc.bibliographiccitation.lastpage","824"],["dc.bibliographiccitation.volume","93"],["dc.contributor.author","Paarmann, I."],["dc.contributor.author","Frermann, D."],["dc.contributor.author","Keller, B. U."],["dc.contributor.author","Villmann, C."],["dc.contributor.author","Breitinger, H. G."],["dc.contributor.author","Hollmann, Manfred"],["dc.date.accessioned","2018-11-07T11:04:24Z"],["dc.date.available","2018-11-07T11:04:24Z"],["dc.date.issued","2005"],["dc.description.abstract","NMDA receptors are involved in a variety of brainstem functions. The excitatory postsynaptic NMDA currents of pre-Botzinger complex interneurons and hypoglossal motoneurons, which are located in the medulla oblongata, show remarkably fast deactivation kinetics of approximately 30 ms compared with NMDA receptors in other types of neurons. Because structural heterogeneity might be the basis for physiological properties, we examined the expression of six NMDA receptor subunits (NMDAR1, NR2A-2D, and NR3A) plus eight NMDR1 splice variants in pre-Botzinger complex, hypoglossal and, for comparison, neurons from the nucleus of the solitary tract in young rats using single cell multiplex RT-PCR. Expression of NR2A, NR2B, and NR2D was observed in all three cell types while NR3A was much more abundant in pre-Botzinger complex interneurons, which belong to the rhythm generator of respiratory activity. In hypoglossal neurons, the NMDAR1 splice variants NMDAR1-4a and NMDAR1-4b were found. In neurons of the nucleus of the solitary tract, instead of NMDAR1-4b, the NMDAR1-2a splice variant was detected. This differential expression of modulatory splice variants might be the molecular basis for the characteristic functional properties of NMDA receptors, as neurons expressing a special NMDAR1 splice variant at the mRNA level show fast kinetics compared with neurons lacking this splice variant."],["dc.identifier.doi","10.1111/j.1471-4159.2005.03027.x"],["dc.identifier.isi","000228721200004"],["dc.identifier.pmid","15857385"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/51837"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","0022-3042"],["dc.title","Kinetics and subunit composition of NMDA receptors in respiratory-related neurons"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1"],["dc.bibliographiccitation.issue","1-2"],["dc.bibliographiccitation.journal","Brain Research"],["dc.bibliographiccitation.lastpage","12"],["dc.bibliographiccitation.volume","1001"],["dc.contributor.author","Ladewig, T."],["dc.contributor.author","Lalley, Peter M."],["dc.contributor.author","Keller, B. U."],["dc.date.accessioned","2018-11-07T10:50:16Z"],["dc.date.available","2018-11-07T10:50:16Z"],["dc.date.issued","2004"],["dc.description.abstract","(1) Serotonin (5HT)-mediated calcium signaling was investigated in hypoglossal motoneurons (HGMs) in brain stein slices of neonatal mice. Electrical activity and associated calcium signaling were Studied by simultaneous patch clamp recordings and high resolution calcium imaging. (2) Bath application of 5HT (5-50 muM) depolarized membrane potential of HGMs and generated action potential discharges that were accompanied by elevations in intracellular calcium concentrations ([Ca2+](i)) in the soma and dendrites. Current-evoked bursts of action potentials were more intense in the presence of 5HT; however, the corresponding calcium signals were reduced. (3) The 5HT(2) receptor agonist alpha-Methyl-5HT (25, 50 muM) had effects on membrane potential, discharge properties and [Ca](i) that were identical to those observed for 5HT, whereas the 5HT(3) receptor agonist 1-(m-chlorophenyl) biguanide (50 muM) had no effect on membrane properties or intracellular calcium levels. (4) 8-OHDPAT (25, 50 muM), a 5HT(1A) receptor agonist, was without effect on steady-state membrane potential or basal [Ca](i). Similar to 5HT and alpha-Methyl-5HT, 8-OHDPAT depressed stimulus-evoked calcium transients in current and voltage clamp mode. (5) Our results suggest that calcium profiles in hypoglossal motoneurons are differentially regulated by 5HT(1A) and 5HT(2) receptors. Activation of 5HT(1A) receptors primarily reduced voltage-activated Ca2+ signals without a significant impact on basal [Ca]i. In contrast, activation of 5HT(2) receptors initiated a net inward current followed by membrane depolarization, where the resulting pattern of action potential discharges represents the essential determinant of global elevations in [Ca2+](i). Taken together, our results therefore identify 5HT-dependent signal pathways as a versatile tool to modulate hypoglossal motoneuron excitability under various physiological and pathophysiological conditions. (C) 2004 Elsevier B.V. All rights reserved."],["dc.identifier.doi","10.1016/j.brainres.2003.10.033"],["dc.identifier.isi","000220812400001"],["dc.identifier.pmid","14972649"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/48616"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.relation.issn","0006-8993"],["dc.title","Serotonergic modulation of intracellular calcium dynamics in neonatal hypoglossal motoneurons from mouse"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","775"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","The Journal of Physiology"],["dc.bibliographiccitation.lastpage","787"],["dc.bibliographiccitation.volume","547"],["dc.contributor.author","Ladewig, T."],["dc.contributor.author","Kloppenburg, P."],["dc.contributor.author","Lalley, Peter M."],["dc.contributor.author","Zipfel, W. R."],["dc.contributor.author","Webb, W. W."],["dc.contributor.author","Keller, B. U."],["dc.date.accessioned","2018-11-07T10:40:01Z"],["dc.date.available","2018-11-07T10:40:01Z"],["dc.date.issued","2003"],["dc.description.abstract","Hypoglossal motoneurones (HMN) are selectively damaged in both human amyotrophic lateral sclerosis (ALS) and corresponding mouse models of this neurodegenerative disease, a process which has been linked to their low endogenous Ca2+ buffering capacity and an exceptional vulnerability to Ca2+-mediated excitotoxic events. In this report, we investigated local Ca2+ profiles in low buffered HMNs by utilizing multiphoton microscopy, CCD imaging and patch clamp recordings in slice preparations. Bath application of caffeine induced highly localized Ca2+ release events, which displayed an initial peak followed by a slow 'shoulder' lasting several seconds. Peak amplitudes were paralleled by Ca2+-activated, apamin-sensitive K+ currents (I-KCa), demonstrating a functional link between Ca2+ stores and HMN excitability. The potential involvement of mitochondria was investigated by bath application of CCCP, which collapses the electrochemical potential across the inner mitochondrial membrane. CCCP reduced peak amplitudes of caffeine responses and consequently I-KCa, indicating that functionally intact mitochondria were critical for store-dependent modulation of HMN excitability. Taken together, our results indicate localized Ca2+ release profiles in HMNs, where low buffering capacities enhance the role of Ca2+-regulating organelles as local determinants of [Ca2+](i). This might expose HMN to exceptional risks during pathophysiological organelle disruptions and other ALS-related, cellular disturbances."],["dc.description.sponsorship","NCRR NIH HHS [P41-RR0422]"],["dc.identifier.doi","10.1113/jphysiol.2002.033605"],["dc.identifier.isi","000183985500006"],["dc.identifier.pmid","12562905"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/46199"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Cambridge Univ Press"],["dc.relation.issn","0022-3751"],["dc.title","Spatial profiles of store-dependent calcium release in motoneurones of the nucleus hypoglossus from newborn mouse"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]