Mironov, Sergej L.

[["dc.bibliographiccitation.firstpage","2944"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","Biophysical Journal"],["dc.bibliographiccitation.lastpage","2952"],["dc.bibliographiccitation.volume","92"],["dc.contributor.author","Mironov, Sergej L."],["dc.date.accessioned","2018-11-07T11:03:23Z"],["dc.date.available","2018-11-07T11:03:23Z"],["dc.date.issued","2007"],["dc.description.abstract","Mitochondria often reside in subcellular regions with high metabolic demands. We examined the mechanisms that can govern the relocation of mitochondria to these sites in respiratory neurons. Mitochondria were visualized using tetra-methylrhodamineethylester, and their movements were analyzed by applying single-particle tracking. Intracellular ATP ([ATP](i)) was assessed by imaging the luminescence of luciferase, the fluorescence of the ATP analog TNP-ATP, and by monitoring the activity of K( ATP) channels. Directed movements of mitochondria were accompanied by transient increases in TNP-ATP fluorescence. Application of glutamate and hypoxia reversibly decreased [ATP](i) levels and inhibited the directed transport. Injections of ATP did not rescue the motility of mitochondria after its inhibition by hypoxia. Introduction of ADP suppressed mitochondrial movements and occluded the effects of subsequent hypoxia. Mitochondria decreased their velocity in the proximity of synapses that correlated with local [ATP](i) depletions. Using a model of motor-assisted transport and Monte Carlo simulations, we showed that mitochondrial traffic is more sensitive to increases in [ADP](i) than to [ATP](i) depletions. We propose that consumption of synaptic ATP can produce local increases in [ADP](i) and facilitate the targeting of mitochondria to synapses."],["dc.identifier.doi","10.1529/biophysj.106.092981"],["dc.identifier.isi","000245164000031"],["dc.identifier.pmid","17277190"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/51606"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Biophysical Society"],["dc.relation.issn","0006-3495"],["dc.title","ADP regulates movements of mitochondria in neurons"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","60"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Brain Research"],["dc.bibliographiccitation.lastpage","67"],["dc.bibliographiccitation.volume","853"],["dc.contributor.author","Mironov, Sergej L."],["dc.contributor.author","Richter, Diethelm W."],["dc.date.accessioned","2018-11-07T10:57:54Z"],["dc.date.available","2018-11-07T10:57:54Z"],["dc.date.issued","2000"],["dc.description.abstract","K-ATP channels regulate the neuronal excitability and their activation during hypoxia/ischemia protect neurons. The activation of K-ATP channels during hypoxia is assumed to occur mainly due to the fall in intracellular ATP levels, but other intracellular signalling pathways can be also involved. We measured single K-ATP channel currents in inspiratory brainstem neurones of neonatal mice. The activity of K-ATP channels was enhanced in hypoosmotic bath solutions, or after applying negative pressure to the recording pipette. Cytochalasin B activated K-ATP, channels and prevented the effects of osmo-mechanical stress, indicating that cytoskeleton rearrangements, which occur during hypoxia, contribute to the activation of K-ATP channels. During hypoxia, extracellular levels of many neurotransmitters increase, leading to activation of corresponding metabotropic receptors that can modulate KA-rp channels. K-ATP channels were activated by GABA, agonist, baclofen, by mGLUR2/3 agonists and were inhibited by mCLUR1/5 agonists. K-ATP channels were activated by phorbol esters and were inhibited by staurosporine. These treatments did not occlude the modulating actions of mGLUR agonists, indicating that they are not mediated by protein kinase C. Activator of alpha-subunits of G-proteins Mas 7 increased and their inhibitor GPant-2 decreased the activity of K-ATP channels. In the presence of either agent, the modulatory actions of baclofen and mGLUR agonists were not observed. We conclude that K-ATP channels are modulated by G-proteins that are activated by metabotropic receptors for GABA and glutamate and their release during hypoxia complements activation of channels by osmo-mechanical stress and [ATP], depletion. (C) 2000 Elsevier Science B.V. All rights reserved."],["dc.identifier.doi","10.1016/S0006-8993(99)02234-9"],["dc.identifier.isi","000084900200008"],["dc.identifier.pmid","10627308"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/50361"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.relation.issn","0006-8993"],["dc.title","Intracellular signalling pathways modulate K-ATP channels in inspiratory brainstem neurones and their hypoxic activation: involvement of metabotropic receptors, G-proteins and cytoskeleton"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","114"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Experimental Cell Research"],["dc.bibliographiccitation.lastpage","127"],["dc.bibliographiccitation.volume","303"],["dc.contributor.author","Mueller, M."],["dc.contributor.author","Mironov, Sergej L."],["dc.contributor.author","Ivannikov, M. V."],["dc.contributor.author","Schmidt, J."],["dc.contributor.author","Richter, Diethelm W."],["dc.date.accessioned","2018-11-07T08:27:46Z"],["dc.date.available","2018-11-07T08:27:46Z"],["dc.date.issued","2005"],["dc.description.abstract","Two-photon microscopy of rhodamine 123-labeled mitochondria revealed that mitochondria of neurons cultured from mouse respiratory center form functionally coupled, dynamically organized aggregates such as chains and clusters, while single mitochondria were rarely seen. Mitochondrial chain structures predominate in dendrites, while irregularly shaped mitochondrial clusters are mostly found in the soma. Both types of mitochondrial structures showed chaotic Brownian motions and the mitochondrial chains also revealed well-directed movements. The latter dislocations were arrested upon mitochondrial depolarization or blockade of mitochondrial ATP synthesis. Depolymerization of microtubules by colchicine or nocodazole or inhibition of protein phosphatases by calyculin A disrupted mitochondrial chains and the mitochondria accumulated in the soma. Forskolin and IBMX reversibly blocked directed movements of mitochondria, but did not affect their overall spatial distribution. Thus, protein phosphorylation seems to control both mitochondrial transport and organization. Protein phosphorylation downstream of enhanced cytosolic CAMP levels apparently regulates the transition from motile to non-motile mitochondria, while phosphorylation resulting from inhibition of types 1 and 2A protein phosphatases massively disturbs mitochondrial organization. The complex phosphorylation processes seem to control the close interaction of mitochondria and cytoskeleton which may guarantee that mitochondria are immobilized at energetic hot spots and rearranged in response to changes in local energy demands. (C) 2004 Elsevier Inc. All rights reserved."],["dc.identifier.doi","10.1016/j.yexcr.2004.09.025"],["dc.identifier.isi","000226111600011"],["dc.identifier.pmid","15572032"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/16270"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Inc"],["dc.relation.issn","0014-4827"],["dc.title","Mitochondrial organization and motility probed by two-photon microscopy in cultured mouse brainstem neurons"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","20"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Brain Research"],["dc.bibliographiccitation.lastpage","27"],["dc.bibliographiccitation.volume","1033"],["dc.contributor.author","Mironov, Sergej L."],["dc.contributor.author","Hartelt, N."],["dc.contributor.author","Ivannikov, M. V."],["dc.date.accessioned","2018-11-07T11:25:04Z"],["dc.date.available","2018-11-07T11:25:04Z"],["dc.date.issued","2005"],["dc.description.abstract","Hypoxia is damaging in neurons, but it can also produce beneficial effects by consolidating the activity of neural networks such as facilitation of respiratory activity [T.L. Baker-Herman, D.D. Fuller, R.W. Bavis, A.G. Zabka, F.J. Golder, N.J. Doperalski, R.A. Johnson, J.J. Watters, G.S. Mitchell, Nature Neuroscience 7 (2004) 48-55; J.L. Feldman, G.S. Mitchell, E.E. Nattie, Ann. Rev. Neurosci. 26 (2003) 239-266; D.M. Blitz, J.M. Ramirez, J. Neurophysiol. 87 (2002) 2964-2971]. The underlying mechanisms are unknown, and we hypothesized they may be similar to ischemic preconditioning in the heart, involving mitochondrial K-ATP (mK(ATP)) channels. By measuring the mitochondrial potential (Psi(m)) and Ca2+ ([Ca2+](m)) in neurons of pre-Botzinger complex (pBC), we examined the functional expression of mK(ATP) channels in the respiratory network. The opener of mK(ATP) channels diazoxide decreased Psi(m) and [Ca2+](m) both in pBC neurons and in isolated immobilized mitochondria. 5-Hydroxydecanoate (5-HD), the blocker of mK(ATP) channels, increased both Psi(m) and [Ca2+](m). Phorbol 12-myristate-13-acetate (PMA) mimicked the effects of diazoxide. Protein kinase C (PKC) was stimulated during hypoxia that occurred mostly at the mitochondria. Brief hypoxia induced facilitation of the respiratory activity, which was prevented after blockade of mK(ATP) channels with 5-HD and PKC with staurosporine. Diazoxide potentiated the motor output and subsequent application of hypoxia was ineffective. We propose that a PKC-induced stimulation of K-ATP channels in the mitochondria of respiratory neurons is responsible for the hypoxic facilitation of rhythmic activity. (C) 2004 Elsevier B.V. All rights reserved."],["dc.identifier.doi","10.1016/j.brainres.2004.11.011"],["dc.identifier.isi","000227134200003"],["dc.identifier.pmid","15680335"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/56548"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.relation.issn","0006-8993"],["dc.title","Mitochondrial K-ATP channels in respiratory neurons and their role in the hypoxic facilitation of rhythmic activity"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","166"],["dc.bibliographiccitation.issue","1-2"],["dc.bibliographiccitation.journal","Brain Research"],["dc.bibliographiccitation.lastpage","177"],["dc.bibliographiccitation.volume","869"],["dc.contributor.author","Mironov, Sergej L."],["dc.contributor.author","Richter, Diethelm W."],["dc.date.accessioned","2021-06-01T10:50:03Z"],["dc.date.available","2021-06-01T10:50:03Z"],["dc.date.issued","2000"],["dc.description.abstract","Brief hypoxia (2 min) enhances the activity of L-type Ca2+ (Ca-L) channels. The effect is dye to glutamate release and concomitant stimulation of metabotropic glutamate receptors of the mGLUR1/5 type [22] [S.L. Mironov, D.W. Richter, L-type Ca2+ channels in inspiratory neurones and their modulation by hypoxia, J. Physiol. 512 (1998) 75-87.]. Besides increasing single channel activity, hypoxia induces a negative shift of the activation curve and slows down the inactivation of the Ca-L current. In the present study we investigated these effects further, aiming to reveal intracellular signalling pathways that mediate the coupling between mGLURs and Ca-L channels. Channel activity was recorded in cell-attached patches from inspiratory brainstem neurones of neonatal mice (PG-ll). Ca-L channels were inhibited by the mGluR2/3 agonists. mGluR1/5 agonists accelerated and mGluR2/3 agonists suppressed the respiratory output, and correspondingly modified the hypoxic response of the respiratory center. Ca-L channels were also modulated by protein kinase C-L but this did not prevent the hypoxic modification of channel activity. G-protein activators enhanced and G-protein inhibitors suppressed the Ca-L channel activity, and in the presence of these agents the effects of hypoxia were abolished. Ryanodine but not thapsigargin inhibited the channel activity and occluded the hypoxic potentiation. Only G-protein-specific agents and ryanodine prevented the slowing down of inactivation induced by hypoxia. Our data indicate that coupling between mGluR1/5 and Ca-L channels is mediated by pathways that utilize G-proteins and ryanodine receptors. Glutamate release and concomitant activation of Ca-L channels are responsible for accelerating of respiratory rhythm during early hypoxia. (C) 2000 Elsevier Science B.V. All rights reserved."],["dc.identifier.doi","10.1016/S0006-8993(00)02396-9"],["dc.identifier.isi","000087990300020"],["dc.identifier.pmid","10865071"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/86507"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.relation.issn","0006-8993"],["dc.title","Hypoxic modulation of L-type Ca2+ channels in inspiratory brainstem neurones: Intracellular signalling pathways and metabotropic glutamate receptors"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","349"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Biophysical Journal"],["dc.bibliographiccitation.lastpage","358"],["dc.bibliographiccitation.volume","94"],["dc.contributor.author","Mironova, Lidia A."],["dc.contributor.author","Mironov, Sergej L."],["dc.date.accessioned","2018-11-07T11:19:05Z"],["dc.date.available","2018-11-07T11:19:05Z"],["dc.date.issued","2008"],["dc.description.abstract","Local Ca2+ signaling controls many neuronal functions, which is often achieved through spatial localization of Ca2+ signals. These nanodomains are formed due to combined effects of Ca2+ diffusion and binding to the cytoplasmic buffers. In this article we derived simple analytical expressions to describe Ca2+ diffusion in the presence of mobile and immobile buffers. A nonlinear character of the reaction-diffusion problem was circumvented by introducing a logarithmic approximation of the concentration term. The obtained formulas reproduce free Ca2+ levels up to 50 mu M and their changes in the millisecond range. Derived equations can be useful to predict spatiotemporal profiles of large-amplitude [Ca2+] transients, which participate in various physiological processes."],["dc.identifier.doi","10.1529/biophysj.107.113340"],["dc.identifier.isi","000251924200007"],["dc.identifier.pmid","17872951"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/55189"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Biophysical Soc"],["dc.relation.issn","0006-3495"],["dc.title","Approximate analytical time-dependent solutions to describe large-amplitude local calcium transients in the presence of buffers"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2473"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","The Journal of Physiology"],["dc.bibliographiccitation.lastpage","2485"],["dc.bibliographiccitation.volume","587"],["dc.contributor.author","Mironov, Sergej L."],["dc.contributor.author","Skorova, Ekaterina Y."],["dc.contributor.author","Hartelt, N."],["dc.contributor.author","Mironova, Lidia A."],["dc.contributor.author","Hasan, Mazahir T."],["dc.contributor.author","Kuegler, Sebastian"],["dc.date.accessioned","2018-11-07T08:29:29Z"],["dc.date.available","2018-11-07T08:29:29Z"],["dc.date.issued","2009"],["dc.description.abstract","Rett syndrome caused by MeCP2 mutations is a devastating neurodevelopmental disorder accompanied by severe breathing irregularities. Using transduction of organotypic slices from model MeCP2-/y mice with neuron-specific calcium sensor protein D3cpv, we examined the slow calcium buffering in neurons in pre-Botzinger complex (preBotC), a component of the complex respiratory network. Examination of wild-type (WT) and MeCP2 null mice showed clear differences in the spatial organisations of neurons in preBotC and also in the disturbances in calcium homeostasis in mutant mice during early postnatal development. Deregulated calcium buffering in MeCP2-/y neurons was indicated by increased amplitude and kinetics of depolarisation-induced calcium transients. Both effects were related to an insufficient calcium uptake into the endoplasmic reticulum that was restored after pretreatment with brain-derived neurotrophic factor (BNDF). Conversely, the inhibition of BDNF signalling in WT neurons produced disturbances similar to those observed in MeCP2-/y mice. Brief hypoxia and calcium release from internal stores induced global calcium increases, after which the processes of many MeCP2-/y neurons were retracted, an effect that was also corrected by pretreatment with BDNF. The data obtained point to a tight connection between calcium homeostasis and long-term changes in neuronal connectivity. We therefore propose that calcium-dependent retraction of neurites in preBotC neurons can cause remodelling of the neuronal network during development and set up the conditions for appearance of breathing irregularities in Rett model mice."],["dc.identifier.doi","10.1113/jphysiol.2009.169805"],["dc.identifier.isi","000266492200010"],["dc.identifier.pmid","19359374"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/16662"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell Publishing, Inc"],["dc.relation.issn","0022-3751"],["dc.title","Remodelling of the respiratory network in a mouse model of Rett syndrome depends on brain-derived neurotrophic factor regulated slow calcium buffering"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","The FASEB Journal"],["dc.bibliographiccitation.volume","16"],["dc.contributor.author","Mueller, M."],["dc.contributor.author","Mironov, Sergej L."],["dc.contributor.author","Schmidt, J."],["dc.contributor.author","Richter, Diethelm W."],["dc.date.accessioned","2018-11-07T10:31:06Z"],["dc.date.available","2018-11-07T10:31:06Z"],["dc.date.issued","2002"],["dc.format.extent","A464"],["dc.identifier.isi","000174533602569"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/44025"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Federation Amer Soc Exp Biol"],["dc.publisher.place","Bethesda"],["dc.relation.issn","0892-6638"],["dc.title","Mitochondrial organization and motility probed by twin-photon microscopy in cultured murine brainstem neurons."],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","69"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","The Journal of Physiology"],["dc.bibliographiccitation.lastpage","81"],["dc.bibliographiccitation.volume","537"],["dc.contributor.author","Haller, M."],["dc.contributor.author","Mironov, Sergej L."],["dc.contributor.author","Karschin, A."],["dc.contributor.author","Richter, Diethelm W."],["dc.date.accessioned","2018-11-07T11:24:18Z"],["dc.date.available","2018-11-07T11:24:18Z"],["dc.date.issued","2001"],["dc.description.abstract","1.The respiratory centre within the brainstem is one of the most active neuronal networks that generates ongoing rhythmic activity. Stabilization of such vital activity requires efficient processes for activity-correlated adjustment of neuronal excitability. Recent, investigations have shown that a regulatory factor coupling electrical activity with cell metabolism comprises ATP-dependent K+ channels (K-ATP channels), which continuously adjust the excitability of respiratory neurons during normoxia and increasingly during hypoxia. 2. We used the single-cell antisense RNA amplification-polymerase chain reaction (PCR) technique to demonstrate that respiratory neurons co-express the sulphonylurea receptor SUR1 with the Kir6.2 potassium channel protein. 3. Single channel measurements on rhythmically active inspiratory neurons of the brainstem slice preparation of newborn mice revealed that K-ATP channels are periodically activated in synchrony with each respiratory cycle. 4. The Na+-K+-ATPase was inhibited with ouabain to demonstrate that oscillations of the channel open probability disappear, although respiratory activity persists for a longer time. Such findings indicate that K-ATP channel open probability reflects activity-dependent fluctuations in the ATP concentration within submembrane domains. 5. We also examined the effects of extracellular [K+] and hypoxia. All changes in the respiratory rhythm (i.e. changes in cycle length and burst durations) affected the periodic fluctuations of K-ATP. channel activity. 6. The data indicate that K-ATP channels continuously modulate central respiratory neurons and contribute to periodic adjustment of neuronal excitability. Such dynamic adjustment of channel activity operates over a high range of metabolic demands, starting below physiological conditions and extending into pathological situations of energy depletion."],["dc.identifier.doi","10.1111/j.1469-7793.2001.0069k.x"],["dc.identifier.isi","000172356100009"],["dc.identifier.pmid","11711562"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/56373"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Cambridge Univ Press"],["dc.relation.issn","0022-3751"],["dc.title","Dynamic activation of K-ATP channels in rhythmically active neurons"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e0202802"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","PLOS ONE"],["dc.bibliographiccitation.volume","13"],["dc.contributor.author","Balakrishnan, Saju"],["dc.contributor.author","Mironov, Sergej L."],["dc.date.accessioned","2019-07-09T11:46:07Z"],["dc.date.available","2019-07-09T11:46:07Z"],["dc.date.issued","2018"],["dc.description.abstract","Excess glutamate during intense neuronal activity is not instantly cleared and may accumulate in the extracellular space. This has various long-term consequences such as ectopic signaling, modulation of synaptic efficacy and excitotoxicity; the latter implicated in various neurodevelopmental and neurodegenerative diseases. In this study, the quantitative imaging of glutamate homeostasis of hippocampal slices from methyl-CpG binding protein 2 knock-out (Mecp2-/y) mice, a model of Rett syndrome (RTT), revealed unusual repetitive glutamate transients. They appeared in phase with bursts of action potentials in the CA1 neurons. Both glutamate transients and bursting activity were suppressed by the blockade of sodium, AMPA and voltage-gated calcium channels (T- and R-type), and enhanced after the inhibition of HCN channels. HCN and calcium channels in RTT and wild-type (WT) CA1 neurons displayed different voltage-dependencies and kinetics. Both channels modulated postsynaptic integration and modified the pattern of glutamate spikes in the RTT hippocampus. Spontaneous glutamate transients were much less abundant in the WT preparations, and, when observed, had smaller amplitude and frequency. The basal ambient glutamate levels in RTT were higher and transient glutamate increases (spontaneous and evoked by stimulation of Schaffer collaterals) decayed slower. Both features indicate less efficient glutamate uptake in RTT. To explain the generation of repetitive glutamate spikes, we designed a novel model of glutamate-induced glutamate release. The simulations correctly predicted the patterns of spontaneous glutamate spikes observed under different experimental conditions. We propose that pervasive spontaneous glutamate release is a hallmark of Mecp2-/y hippocampus, stemming from and modulating the hyperexcitability of neurons."],["dc.identifier.doi","10.1371/journal.pone.0202802"],["dc.identifier.pmid","30256804"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15395"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59378"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.intern","In goescholar not merged with http://resolver.sub.uni-goettingen.de/purl?gs-1/15697 but duplicate"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.subject.ddc","610"],["dc.title","Regenerative glutamate release in the hippocampus of Rett syndrome model mice"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]