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Walz H.,Bernstein Center for Computational Neuroscience Munich | Hupe G.J.,University of Ottawa | Benda J.,University of Tubingen | Lewis J.E.,University of Ottawa
Journal of Physiology Paris | Year: 2013

Weakly-electric fish are a well-established model system for neuroethological studies on communication and aggression. Sensory encoding of their electric communication signals, as well as behavioural responses to these signals, have been investigated in great detail under laboratory conditions. In the wave-type brown ghost knifefish, Apteronotus leptorhynchus, transient increases in the frequency of the generated electric field, called chirps, are particularly well-studied, since they can be readily evoked by stimulating a fish with artificial signals mimicking conspecifics. When two fish interact, both their quasi-sinusoidal electric fields (called electric organ discharge, EOD) superimpose, resulting in a beat, an amplitude modulation at the frequency difference between the two EODs. Although chirps themselves are highly stereotyped signals, the shape of the amplitude modulation resulting from a chirp superimposed on a beat background depends on a number of parameters, such as the beat frequency, modulation depth, and beat phase at which the chirp is emitted. Here we review the influence of these beat parameters on chirp encoding in the three primary stages of the electrosensory pathway: electroreceptor afferents, the hindbrain electrosensory lateral line lobe, and midbrain torus semicircularis. We then examine the role of these parameters, which represent specific features of various social contexts, on the behavioural responses of A. leptorhynchus. Some aspects of the behaviour may be explained by the coding properties of early sensory neurons to chirp stimuli. However, the complexity and diversity of behavioural responses to chirps in the context of different background parameters cannot be explained solely on the basis of the sensory responses and thus suggest that critical roles are played by higher processing stages. © 2012 Elsevier Ltd.

Huber M.,Ludwig Maximilians University of Munich | Su Y.-H.,TU Munich | Kruger M.,TU Munich | Kruger M.,Ludwig Maximilians University of Munich | And 4 more authors.
PLoS ONE | Year: 2014

When walking in open space, collision avoidance with other pedestrians is a process that successfully takes place many times. To pass another pedestrian (an interferer) walking direction, walking speed or both can be adjusted. Currently, the literature is not yet conclusive of how humans adjust these two parameters in the presence of an interferer. This impedes the development of models predicting general obstacle avoidance strategies in humans' walking behavior. The aim of this study was to investigate the adjustments of path and speed when a pedestrian is crossing a non-reactive human interferer at different angles and speeds, and to compare the results to general model predictions. To do so, we designed an experiment where a pedestrian walked a 12 m distance to reach a goal position. The task was designed in such a way that collision with an interferer would always occur if the pedestrian would not apply a correction of movement path or speed. Results revealed a strong dependence of path and speed adjustments on crossing angle and walking speed, suggesting local planning of the collision avoidance strategy. Crossing at acute angles (i.e. 45° and 90°) seems to require more complex collision avoidance strategies involving both path and speed adjustments than crossing at obtuse angles, where only path adjustments were observed. Overall, the results were incompatible with predictions from existing models of locomotor collision avoidance. The observed initiations of both adjustments suggest a collision avoidance strategy that is temporally controlled. The present study provides a comprehensive picture of human collision avoidance strategies in walking, which can be used to evaluate and adjust existing pedestrian dynamics models, or serve as an empirical basis to develop new models. © 2014 Huber et al.

Porres C.P.,Ludwig Maximilians University of Munich | Meyer E.M.M.,Ludwig Maximilians University of Munich | Meyer E.M.M.,Friedrich Miescher Institute for Biomedical Research | Grothe B.,Ludwig Maximilians University of Munich | And 2 more authors.
Journal of Neuroscience | Year: 2011

Neurons in the dorsal nucleus of the lateral lemniscus (DNLL) receive excitatory and inhibitory inputs from the superior olivary complex (SOC) and convey GABAergic inhibition to the contralateral DNLL and the inferior colliculi. Unlike the fast glycinergic inhibition in the SOC, this GABAergic inhibition outlasts auditory stimulation by tens of milliseconds. Two mechanisms have been postulated to explain this persistent inhibition. One, an "integration-based" mechanism, suggests that postsynaptic excitatory integration in DNLL neurons generates prolonged activity, and the other favors the synaptic time course of the DNLL output itself. The feasibility of the integration-based mechanism was tested in vitro in DNLL neurons of Mongolian gerbils by quantifying the cellular excitability and synaptic input-output functions (IO-Fs). All neurons were sustained firing and generated a near monotonic IO-F on current injections. From synaptic stimulations, we estimate that activation of approximately five fibers, each on average liberating ∼18 vesicles, is sufficient to trigger a single postsynaptic action potential. A strong single pulse of afferent fiber stimulation triggered multiple postsynaptic action potentials. The steepness of the synaptic IO-F was dependent on the synaptic NMDA component. The synaptic NMDA receptor current defines the slope of the synaptic IO-F by enhancing the temporal and spatial EPSP summation. Blocking this NMDA-dependent amplification during postsynaptic integration of train stimulations resulted into a ∼20%reduction of the decay time course of the GABAergic inhibition. Thus, our data show that the NMDA-dependent amplification of the postsynaptic activity contributes to the GABAergic persistent inhibition generated by DNLL neurons. Copyright © 2011 the authors.

Schnaitmann C.,Max Planck Institute For Neurobiologie | Schnaitmann C.,Albert Ludwigs University of Freiburg | Garbers C.,Ludwig Maximilians University of Munich | Wachtler T.,Ludwig Maximilians University of Munich | And 3 more authors.
Current Biology | Year: 2013

Background Color vision is commonly assumed to rely on photoreceptors tuned to narrow spectral ranges. In the ommatidium of Drosophila, the four types of so-called inner photoreceptors express different narrow-band opsins. In contrast, the outer photoreceptors have a broadband spectral sensitivity and were thought to exclusively mediate achromatic vision. Results Using computational models and behavioral experiments, we demonstrate that the broadband outer photoreceptors contribute to color vision in Drosophila. The model of opponent processing that includes the opsin of the outer photoreceptors scored the best fit to wavelength discrimination data. To experimentally uncover the contribution of individual photoreceptor types, we restored phototransduction of targeted photoreceptor combinations in a blind mutant. Dichromatic flies with only broadband photoreceptors and one additional receptor type can discriminate different colors, indicating the existence of a specific output comparison of the outer and inner photoreceptors. Furthermore, blocking interneurons postsynaptic to the outer photoreceptors specifically impaired color but not intensity discrimination. Conclusions Our findings show that receptors with a complex and broad spectral sensitivity can contribute to color vision and reveal that chromatic and achromatic circuits in the fly share common photoreceptors. © 2013 Elsevier Ltd.

Greene G.,Ludwig Maximilians University of Munich | Greene G.,Bernstein Center for Computational Neuroscience Munich | Gollisch T.,Bernstein Center for Computational Neuroscience Munich | Gollisch T.,University of Gottingen | And 3 more authors.
Vision Research | Year: 2016

Fixational eye movements can rapidly shift the retinal image, but typically remain unnoticed. We identify and simulate a model mechanism for the suppression of erroneous motion signals under fixational eye movements. This mechanism exploits the non-linearities common to many classes of large retinal ganglion cells in the mammalian retina, and negates the need for extra-retinal signals or explicit gaze information. When tested using natural images undergoing simulated fixational eye movements, our model successfully distinguishes "real world" motion from retinal motion induced by eye movements. In addition, this model suggests a possible explanation for several fixational eye movement related visual illusions such as the Ouchi-Spillmann and "Out-of-focus" illusions. © 2015 Elsevier Ltd.

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