@article{10396, abstract = {Stimfit is a free cross-platform software package for viewing and analyzing electrophysiological data. It supports most standard file types for cellular neurophysiology and other biomedical formats. Its analysis algorithms have been used and validated in several experimental laboratories. Its embedded Python scripting interface makes Stimfit highly extensible and customizable.}, author = {Schlögl, Alois and Jonas, Peter M and Schmidt-Hieber, C. and Guzman, S. J.}, issn = {1862-278X}, journal = {Biomedical Engineering / Biomedizinische Technik}, keywords = {biomedical engineering, data analysis, free software}, location = {Graz, Austria}, number = {SI-1-Track-G}, publisher = {De Gruyter}, title = {{Stimfit: A fast visualization and analysis environment for cellular neurophysiology}}, doi = {10.1515/bmt-2013-4181}, volume = {58}, year = {2013}, } @article{2954, abstract = {Spontaneous postsynaptic currents (PSCs) provide key information about the mechanisms of synaptic transmission and the activity modes of neuronal networks. However, detecting spontaneous PSCs in vitro and in vivo has been challenging, because of the small amplitude, the variable kinetics, and the undefined time of generation of these events. Here, we describe a, to our knowledge, new method for detecting spontaneous synaptic events by deconvolution, using a template that approximates the average time course of spontaneous PSCs. A recorded PSC trace is deconvolved from the template, resulting in a series of delta-like functions. The maxima of these delta-like events are reliably detected, revealing the precise onset times of the spontaneous PSCs. Among all detection methods, the deconvolution-based method has a unique temporal resolution, allowing the detection of individual events in high-frequency bursts. Furthermore, the deconvolution-based method has a high amplitude resolution, because deconvolution can substantially increase the signal/noise ratio. When tested against previously published methods using experimental data, the deconvolution-based method was superior for spontaneous PSCs recorded in vivo. Using the high-resolution deconvolution-based detection algorithm, we show that the frequency of spontaneous excitatory postsynaptic currents in dentate gyrus granule cells is 4.5 times higher in vivo than in vitro.}, author = {Pernia-Andrade, Alejandro and Goswami, Sarit and Stickler, Yvonne and Fröbe, Ulrich and Schlögl, Alois and Jonas, Peter M}, journal = {Biophysical Journal}, number = {7}, pages = {1429 -- 1439}, publisher = {Biophysical}, title = {{A deconvolution based method with high sensitivity and temporal resolution for detection of spontaneous synaptic currents in vitro and in vivo}}, doi = {10.1016/j.bpj.2012.08.039}, volume = {103}, year = {2012}, } @article{2969, abstract = {The coupling between presynaptic Ca^(2+) channels and Ca^(2+) sensors of exocytosis is a key determinant of synaptic transmission. Evoked release from parvalbumin (PV)-expressing interneurons is triggered by nanodomain coupling of P/Q-type Ca^(2+) channels, whereas release from cholecystokinin (CCK)-containing interneurons is generated by microdomain coupling of N-type channels. Nanodomain coupling has several functional advantages, including speed and efficacy of transmission. One potential disadvantage is that stochastic opening of presynaptic Ca^(2+) channels may trigger spontaneous transmitter release. We addressed this possibility in rat hippocampal granule cells, which receive converging inputs from different inhibitory sources. Both reduction of extracellular Ca^(2+) concentration and the unselective Ca^(2+) channel blocker Cd^(2+) reduced the frequency of miniature IPSCs (mIPSCs) in granule cells by ~50%, suggesting that the opening of presynaptic Ca^(2+) channels contributes to spontaneous release. Application of the selective P/Q-type Ca^(2+) channel blocker ω-agatoxin IVa had no detectable effects, whereas both the N-type blocker ω-conotoxin GVIa and the L-type blocker nimodipine reduced mIPSC frequency. Furthermore, both the fast Ca^(2+) chelator BAPTA-AM and the slow chelator EGTA-AM reduced the mIPSC frequency, suggesting that Ca^(2+)-dependent spontaneous release is triggered by microdomain rather than nanodomain coupling. The CB_(1) receptor agonist WIN 55212-2 also decreased spontaneous release; this effect was occluded by prior application of ω-conotoxin GVIa, suggesting that a major fraction of Ca^(2+)-dependent spontaneous release was generated at the terminals of CCK-expressing interneurons. Tonic inhibition generated by spontaneous opening of presynaptic N- and L-type Ca^(2+) channels may be important for hippocampal information processing. }, author = {Goswami, Sarit and Bucurenciu, Iancu and Jonas, Peter M}, journal = {Journal of Neuroscience}, number = {41}, pages = {14294 -- 14304}, publisher = {Society for Neuroscience}, title = {{Miniature IPSCs in hippocampal granule cells are triggered by voltage-gated Ca^(2+) channels via microdomain coupling}}, doi = {10.1523/JNEUROSCI.6104-11.2012}, volume = {32}, year = {2012}, } @article{3121, abstract = {Voltage-activated Ca(2+) channels (VACCs) mediate Ca(2+) influx to trigger action potential-evoked neurotransmitter release, but the mechanism by which Ca(2+) regulates spontaneous transmission is unclear. We found that VACCs are the major physiological triggers for spontaneous release at mouse neocortical inhibitory synapses. Moreover, despite the absence of a synchronizing action potential, we found that spontaneous fusion of a GABA-containing vesicle required the activation of multiple tightly coupled VACCs of variable type.}, author = {Williams, Courtney and Chen, Wenyan and Lee, Chia and Yaeger, Daniel and Vyleta, Nicholas and Smith, Stephen}, journal = {Nature Neuroscience}, number = {9}, pages = {1195 -- 1197}, publisher = {Nature Publishing Group}, title = {{Coactivation of multiple tightly coupled calcium channels triggers spontaneous release of GABA}}, doi = {10.1038/nn.3162}, volume = {15}, year = {2012}, } @article{3317, abstract = {The physical distance between presynaptic Ca2+ channels and the Ca2+ sensors that trigger exocytosis of neurotransmitter-containing vesicles is a key determinant of the signalling properties of synapses in the nervous system. Recent functional analysis indicates that in some fast central synapses, transmitter release is triggered by a small number of Ca2+ channels that are coupled to Ca2+ sensors at the nanometre scale. Molecular analysis suggests that this tight coupling is generated by protein–protein interactions involving Ca2+ channels, Ca2+ sensors and various other synaptic proteins. Nanodomain coupling has several functional advantages, as it increases the efficacy, speed and energy efficiency of synaptic transmission.}, author = {Eggermann, Emmanuel and Bucurenciu, Iancu and Goswami, Sarit and Jonas, Peter M}, journal = {Nature Reviews Neuroscience}, number = {1}, pages = {7 -- 21}, publisher = {Nature Publishing Group}, title = {{Nanodomain coupling between Ca(2+) channels and sensors of exocytosis at fast mammalian synapses}}, doi = {10.1038/nrn3125}, volume = {13}, year = {2012}, } @article{493, abstract = {The BCI competition IV stands in the tradition of prior BCI competitions that aim to provide high quality neuroscientific data for open access to the scientific community. As experienced already in prior competitions not only scientists from the narrow field of BCI compete, but scholars with a broad variety of backgrounds and nationalities. They include high specialists as well as students.The goals of all BCI competitions have always been to challenge with respect to novel paradigms and complex data. We report on the following challenges: (1) asynchronous data, (2) synthetic, (3) multi-class continuous data, (4) sessionto-session transfer, (5) directionally modulated MEG, (6) finger movements recorded by ECoG. As after past competitions, our hope is that winning entries may enhance the analysis methods of future BCIs.}, author = {Tangermann, Michael and Müller, Klaus and Aertsen, Ad and Birbaumer, Niels and Braun, Christoph and Brunner, Clemens and Leeb, Robert and Mehring, Carsten and Miller, Kai and Müller Putz, Gernot and Nolte, Guido and Pfurtscheller, Gert and Preissl, Hubert and Schalk, Gerwin and Schlögl, Alois and Vidaurre, Carmen and Waldert, Stephan and Blankertz, Benjamin}, journal = {Frontiers in Neuroscience}, publisher = {Frontiers Research Foundation}, title = {{Review of the BCI competition IV}}, doi = {10.3389/fnins.2012.00055}, volume = {6}, year = {2012}, } @article{3258, abstract = {CA3 pyramidal neurons are important for memory formation and pattern completion in the hippocampal network. It is generally thought that proximal synapses from the mossy fibers activate these neurons most efficiently, whereas distal inputs from the perforant path have a weaker modulatory influence. We used confocally targeted patch-clamp recording from dendrites and axons to map the activation of rat CA3 pyramidal neurons at the subcellular level. Our results reveal two distinct dendritic domains. In the proximal domain, action potentials initiated in the axon backpropagate actively with large amplitude and fast time course. In the distal domain, Na+ channel–mediated dendritic spikes are efficiently initiated by waveforms mimicking synaptic events. CA3 pyramidal neuron dendrites showed a high Na+-to-K+ conductance density ratio, providing ideal conditions for active backpropagation and dendritic spike initiation. Dendritic spikes may enhance the computational power of CA3 pyramidal neurons in the hippocampal network.}, author = {Kim, Sooyun and Guzmán, José and Hu, Hua and Jonas, Peter M}, issn = {1546-1726}, journal = {Nature Neuroscience}, number = {4}, pages = {600 -- 606}, publisher = {Nature Publishing Group}, title = {{Active dendrites support efficient initiation of dendritic spikes in hippocampal CA3 pyramidal neurons}}, doi = {10.1038/nn.3060}, volume = {15}, year = {2012}, } @phdthesis{2964, abstract = {CA3 pyramidal neurons are important for memory formation and pattern completion in the hippocampal network. These neurons receive multiple excitatory inputs from numerous sources. Therefore, the rules of spatiotemporal integration of multiple synaptic inputs and propagation of action potentials are important to understand how CA3 neurons contribute to higher brain functions at cellular level. By using confocally targeted patch-clamp recording techniques, we investigated the biophysical properties of rat CA3 pyramidal neuron dendrites. We found two distinct dendritic domains critical for action potential initiation and propagation: In the proximal domain, action potentials initiated in the axon backpropagate actively with large amplitude and fast time course. In the distal domain, Na+-channel mediated dendritic spikes are efficiently evoked by local dendritic depolarization or waveforms mimicking synaptic events. These findings can be explained by a high Na+-to-K+ conductance density ratio of CA3 pyramidal neuron dendrites. The results challenge the prevailing view that proximal mossy fiber inputs activate CA3 pyramidal neurons more efficiently than distal perforant inputs by showing that the distal synapses trigger a different form of activity represented by dendritic spikes. The high probability of dendritic spike initiation in the distal area may enhance the computational power of CA3 pyramidal neurons in the hippocampal network. }, author = {Kim, Sooyun}, issn = {2663-337X}, pages = {65}, publisher = {Institute of Science and Technology Austria}, title = {{Active properties of hippocampal CA3 pyramidal neuron dendrites}}, year = {2012}, } @article{3318, abstract = {Parvalbumin is thought to act in a manner similar to EGTA, but how a slow Ca2+ buffer affects nanodomain-coupling regimes at GABAergic synapses is unclear. Direct measurements of parvalbumin concentration and paired recordings in rodent hippocampus and cerebellum revealed that parvalbumin affects synaptic dynamics only when expressed at high levels. Modeling suggests that, in high concentrations, parvalbumin may exert BAPTA-like effects, modulating nanodomain coupling via competition with local saturation of endogenous fixed buffers.}, author = {Eggermann, Emmanuel and Jonas, Peter M}, journal = {Nature Neuroscience}, pages = {20 -- 22}, publisher = {Nature Publishing Group}, title = {{How the “slow” Ca(2+) buffer parvalbumin affects transmitter release in nanodomain coupling regimes at GABAergic synapses}}, doi = {10.1038/nn.3002}, volume = {15}, year = {2011}, } @article{3369, abstract = {Rab3 interacting molecules (RIMs) are highly enriched in the active zones of presynaptic terminals. It is generally thought that they operate as effectors of the small G protein Rab3. Three recent papers, by Han et al. (this issue of Neuron), Deng et al. (this issue of Neuron), and Kaeser et al. (a recent issue of Cell), shed new light on the functional role of RIM in presynaptic terminals. First, RIM tethers Ca2+ channels to active zones. Second, RIM contributes to priming of synaptic vesicles by interacting with another presynaptic protein, Munc13.}, author = {Pernia-Andrade, Alejandro and Jonas, Peter M}, journal = {Neuron}, number = {2}, pages = {185 -- 187}, publisher = {Elsevier}, title = {{The multiple faces of RIM}}, doi = {10.1016/j.neuron.2011.01.010}, volume = {69}, year = {2011}, } @article{469, abstract = {Spontaneous release of glutamate is important for maintaining synaptic strength and controlling spike timing in the brain. Mechanisms regulating spontaneous exocytosis remain poorly understood. Extracellular calcium concentration ([Ca2+]o) regulates Ca2+ entry through voltage-activated calcium channels (VACCs) and consequently is a pivotal determinant of action potential-evoked vesicle fusion. Extracellular Ca 2+ also enhances spontaneous release, but via unknown mechanisms. Here we report that external Ca2+ triggers spontaneous glutamate release more weakly than evoked release in mouse neocortical neurons. Blockade of VACCs has no effect on the spontaneous release rate or its dependence on [Ca2+]o. Intracellular [Ca2+] slowly increases in a minority of neurons following increases in [Ca2+]o. Furthermore, the enhancement of spontaneous release by extracellular calcium is insensitive to chelation of intracellular calcium by BAPTA. Activation of the calcium-sensing receptor (CaSR), a G-protein-coupled receptor present in nerve terminals, by several specific agonists increased spontaneous glutamate release. The frequency of spontaneous synaptic transmission was decreased in CaSR mutant neurons. The concentration-effect relationship for extracellular calcium regulation of spontaneous release was well described by a combination of CaSR-dependent and CaSR-independent mechanisms. Overall these results indicate that extracellular Ca2+ does not trigger spontaneous glutamate release by simply increasing calcium influx but stimulates CaSR and thereby promotes resting spontaneous glutamate release. }, author = {Vyleta, Nicholas and Smith, Stephen}, journal = {European Journal of Neuroscience}, number = {12}, pages = {4593 -- 4606}, publisher = {Wiley-Blackwell}, title = {{Spontaneous glutamate release is independent of calcium influx and tonically activated by the calcium-sensing receptor}}, doi = {10.1523/JNEUROSCI.6398-10.2011}, volume = {31}, year = {2011}, } @article{490, abstract = {BioSig is an open source software library for biomedical signal processing. The aim of the BioSig project is to foster research in biomedical signal processing by providing free and open source software tools for many different application areas. Some of the areas where BioSig can be employed are neuroinformatics, brain-computer interfaces, neurophysiology, psychology, cardiovascular systems, and sleep research. Moreover, the analysis of biosignals such as the electroencephalogram (EEG), electrocorticogram (ECoG), electrocardiogram (ECG), electrooculogram (EOG), electromyogram (EMG), or respiration signals is a very relevant element of the BioSig project. Specifically, BioSig provides solutions for data acquisition, artifact processing, quality control, feature extraction, classification, modeling, and data visualization, to name a few. In this paper, we highlight several methods to help students and researchers to work more efficiently with biomedical signals. }, author = {Schlögl, Alois and Vidaurre, Carmen and Sander, Tilmann}, journal = {Computational Intelligence and Neuroscience}, publisher = {Hindawi Publishing Corporation}, title = {{BioSig: The free and open source software library for biomedical signal processing}}, doi = {10.1155/2011/935364}, volume = {2011}, year = {2011}, } @article{3718, abstract = {Long-term depression (LTD) is a form of synaptic plasticity that may contribute to information storage in the central nervous system. Here we report that LTD can be elicited in layer 5 pyramidal neurons of the rat prefrontal cortex by pairing low frequency stimulation with a modest postsynaptic depolarization. The induction of LTD required the activation of both metabotropic glutamate receptors of the mGlu1 subtype and voltage-sensitive Ca(2+) channels (VSCCs) of the T/R, P/Q and N types, leading to the stimulation of intracellular inositol trisphosphate (IP3) receptors by IP3 and Ca(2+). The subsequent release of Ca(2+) from intracellular stores activated the protein phosphatase cascade involving calcineurin and protein phosphatase 1. The activation of purinergic P2Y(1) receptors blocked LTD. This effect was prevented by P2Y(1) receptor antagonists and was absent in mice lacking P2Y(1) but not P2Y(2) receptors. We also found that activation of P2Y(1) receptors inhibits Ca(2+) transients via VSCCs in the apical dendrites and spines of pyramidal neurons. In addition, we show that the release of ATP under hypoxia is able to inhibit LTD by acting on postsynaptic P2Y(1) receptors. In conclusion, these data suggest that the reduction of Ca(2+) influx via VSCCs caused by the activation of P2Y(1) receptors by ATP is the possible mechanism for the inhibition of LTD in prefrontal cortex.}, author = {Guzmán, José and Schmidt, Hartmut and Franke, Heike and Krügel, Ute and Eilers, Jens and Illes, Peter and Gerevich, Zoltan}, journal = {Neuropharmacology}, number = {6}, pages = {406 -- 415}, publisher = {Elsevier}, title = {{P2Y1 receptors inhibit long-term depression in the prefrontal cortex.}}, doi = {10.1016/j.neuropharm.2010.05.013}, volume = {59}, year = {2010}, } @article{3832, abstract = {A recent paper by von Engelhardt et al. identifies a novel auxiliary subunit of native AMPARs, termedCKAMP44. Unlike other auxiliary subunits, CKAMP44 accelerates desensitization and prolongs recovery from desensitization. CKAMP44 is highly expressed in hippocampal dentate gyrus granule cells and decreases the paired-pulse ratio at perforant path input synapses. Thus, both principal and auxiliary AMPAR subunits control the time course of signaling at glutamatergic synapses.}, author = {Guzmán, José and Jonas, Peter M}, journal = {Neuron}, number = {1}, pages = {8 -- 10}, publisher = {Elsevier}, title = {{Beyond TARPs: The growing list of auxiliary AMPAR subunits}}, doi = {10.1016/j.neuron.2010.04.003}, volume = {66}, year = {2010}, } @article{3833, author = {Jonas, Peter M and Hefft, Stefan}, journal = {The European Journal of Neuroscience}, number = {7}, pages = {1194 -- 1195}, publisher = {Wiley-Blackwell}, title = {{GABA release at terminals of CCK-interneurons: synchrony, asynchrony and modulation by cannabinoid receptors (commentary on Ali & Todorova)}}, doi = {10.1111/j.1460-9568.2010.07189.x}, volume = {31}, year = {2010}, }