83 research outputs found

    Determination of the Michel Parameters rho, xi, and delta in tau-Lepton Decays with tau --> rho nu Tags

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    Using the ARGUS detector at the e+ee^+ e^- storage ring DORIS II, we have measured the Michel parameters ρ\rho, ξ\xi, and ξδ\xi\delta for τ±l±ννˉ\tau^{\pm}\to l^{\pm} \nu\bar\nu decays in τ\tau-pair events produced at center of mass energies in the region of the Υ\Upsilon resonances. Using τρν\tau^\mp \to \rho^\mp \nu as spin analyzing tags, we find ρe=0.68±0.04±0.08\rho_{e}=0.68\pm 0.04 \pm 0.08, ξe=1.12±0.20±0.09\xi_{e}= 1.12 \pm 0.20 \pm 0.09, ξδe=0.57±0.14±0.07\xi\delta_{e}= 0.57 \pm 0.14 \pm 0.07, ρμ=0.69±0.06±0.08\rho_{\mu}= 0.69 \pm 0.06 \pm 0.08, ξμ=1.25±0.27±0.14\xi_{\mu}= 1.25 \pm 0.27 \pm 0.14 and ξδμ=0.72±0.18±0.10\xi\delta_{\mu}= 0.72 \pm 0.18 \pm 0.10. In addition, we report the combined ARGUS results on ρ\rho, ξ\xi, and ξδ\xi\delta using this work und previous measurements.Comment: 10 pages, well formatted postscript can be found at http://pktw06.phy.tu-dresden.de/iktp/pub/desy97-194.p

    A Search for the Electric Dipole Moment of the Tau-Lepton

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    Using the ARGUS detector at the e+e- storage ring DORIS II, we have searched for the real and imaginary part of the electric dipole formfactor d_tau of the tau lepton in the production of tau pairs at q^2=100 GeV^2. This is the first direct measurement of this CP violating formfactor. We applied the method of optimised observables which takes into account all available information on the observed tau decay products. No evidence for CP violation was found, and we derive the following results: Re(d_tau)=(1.6+-.9)*10^(-16) ecm and Im(d_tau)=(-0.2+-0.8)*10^(-16) ecm, where statistical and systematic errors have been combined.Comment: 8 pages, 5 figures (10 subfigures

    Unstable neurons underlie a stable learned behavior

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    Motor skills can be maintained for decades, but the biological basis of this memory persistence remains largely unknown. The zebra finch, for example, sings a highly stereotyped song that is stable for years, but it is not known whether the precise neural patterns underlying song are stable or shift from day to day. Here we demonstrate that the population of projection neurons coding for song in the premotor nucleus, HVC, change from day to day. The most dramatic shifts occur over intervals of sleep. In contrast to the transient participation of excitatory neurons, ensemble measurements dominated by inhibition persist unchanged even after damage to downstream motor nerves. These observations offer a principle of motor stability: spatiotemporal patterns of inhibition can maintain a stable scaffold for motor dynamics while the population of principal neurons that directly drive behavior shift from one day to the next

    Interplay of inhibition and excitation shapes a premotor neural sequence

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    In the zebra finch, singing behavior is driven by a sequence of bursts within premotor neurons located in the forebrain nucleus HVC (proper name). In addition to these excitatory projection neurons, HVC also contains inhibitory interneurons with a role in premotor patterning that is unclear. Here, we used a range of electrophysiological and behavioral observations to test previously described models suggesting discrete functional roles for inhibitory interneurons in song production. We show that single HVC premotor neuron bursts are sufficient to drive structured activity within the interneuron network because of pervasive and facilitating synaptic connections. We characterize interneuron activity during singing and describe reliable pauses in the firing of those neurons. We then demonstrate that these gaps in inhibition are likely to be necessary for driving normal bursting behavior in HVC premotor neurons and suggest that structured inhibition and excitation may be a general mechanism enabling sequence generation in other circuits

    Inhibition protects acquired song segments during vocal learning in zebra finches

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    Vocal imitation involves incorporating instructive auditory information into relevant motor circuits through processes that are poorly understood. In zebra finches, we find that exposure to a tutor’s song drives spiking activity within premotor neurons in the juvenile but that inhibition suppresses such responses upon learning in adulthood. We measure inhibitory currents evoked by the tutor song throughout development while simultaneously quantifying each bird’s learning trajectory. Surprisingly, we find that the maturation of synaptic inhibition onto premotor neurons is correlated with learning but not age. We used synthetic tutoring to demonstrate that inhibition is selective for specific song elements that have already been learned and not those still in refinement. Our results suggest that structured inhibition is playing a crucial role during song acquisition, enabling a piece-by-piece mastery of complex tasks

    General anesthesia globally synchronizes activity selectively in layer 5 cortical pyramidal neurons

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    General anesthetics induce loss of consciousness, a global change in behavior. However, a corresponding global change in activity in the context of defined cortical cell types has not been identified. Here, we show that spontaneous activity of mouse layer 5 pyramidal neurons, but of no other cortical cell type, becomes consistently synchronized invivo by different general anesthetics. This heightened neuronal synchrony is aperiodic, present across large distances, and absent in cortical neurons presynaptic to layer 5 pyramidal neurons. During the transition to and from anesthesia, changes in synchrony in layer 5 coincide with the loss and recovery of consciousness. Activity within both apical and basal dendrites is synchronous, but only basal dendrites' activity is temporally locked to somatic activity. Given that layer 5 is a major cortical output, our results suggest that brain-wide synchrony in layer 5 pyramidal neurons may contribute to the loss of consciousness during general anesthesia. Copyright © 2022 The Authors. Published by Elsevier Inc. All rights reserved

    Nature Neuroscience

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    A fundamental impediment to understanding the brain is the availability of inexpensive and robust methods for targeting and manipulating specific neuronal populations. The need to overcome this barrier is pressing because there are considerable anatomical, physiological, cognitive and behavioral differences between mice and higher mammalian species in which it is difficult to specifically target and manipulate genetically defined functional cell types. In particular, it is unclear the degree to which insights from mouse models can shed light on the neural mechanisms that mediate cognitive functions in higher species, including humans. Here we describe a novel recombinant adeno-associated virus that restricts gene expression to GABAergic interneurons within the telencephalon. We demonstrate that the viral expression is specific and robust, allowing for morphological visualization, activity monitoring and functional manipulation of interneurons in both mice and non-genetically tractable species, thus opening the possibility to study GABAergic function in virtually any vertebrate species
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