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  • 1
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    Frontiers Media SA
    Publication Date: 2024-04-05
    Description: During the last decades, investigations on the olivo-cerebellar system have attained a high level of sophistication, which led to redefinitions of several structural and functional properties of neurons, synapses, connections and circuits. Research has expanded and deepened in so many directions and so many theories and models have been proposed that an ensemble review of the matter is now needed. Yet, hot topics remain open and scientific discussion is very lively at several fronts. One major question, here as well as in other major brain circuits, is how single neurons and synaptic properties emerge at the network level and contribute to behavioural regulation via neuronal plasticity. Other major aspects that this Research Topic covers and discusses include the development and circuit organization of the olivo-cerebellar network, the established and recent theories of learning and motor control, and the emerging role of the cerebellum in cognitive processing. By touching on such varied and encompassing subjects, this Frontiers Special Topic aims to highlight the state of the art and stimulate future research. We hope that this unique collection of high-quality articles from experts in the field will provide scientists with a powerful basis of knowledge and inspiration to enucleate the major issues deserving further attention.
    Keywords: RC321-571 ; Q1-390 ; Climbing fibres ; network synchrony ; compartmental organization ; Sensorimotor control ; Cerebellar Nuclei ; plasticity ; Purkinje cell ; thema EDItEUR::P Mathematics and Science::PS Biology, life sciences::PSA Life sciences: general issues::PSAN Neurosciences
    Language: English
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  • 2
    Publication Date: 2024-04-05
    Description: The cytoplasmic free Ca2+ concentration ([Ca2+]i) is a key determinant of neuronal information transfer and processing. It controls a plethora of fundamental processes, including transmitter release and the induction of synaptic plasticity. This enigmatic second messenger conveys its wide variety of actions by binding to a subgroup of Ca2+ binding proteins (CaBPs) known as “Ca2+ sensors”. Well known examples of Ca2+ sensors are Troponin-C in skeletal muscle, Synaptotagmin in presynaptic terminals, and Calmodulin (CaM) in all eukaryotic cells. Since the levels of [Ca2+]i directly influence the potency of Ca2+ sensors, the Ca2+ concentration is tightly controlled by several mechanisms including another type of Ca2+ binding proteins, the Ca2+ buffers. Prominent examples of Ca2+ buffers include Parvalbumin (PV), Calbindin-D28k (CB) and Calretinin (CR), although for the latter two Ca2+ sensor functions were recently also suggested. Ca2+ buffers are distinct from sensors by their purely buffering action, i.e. they influence the spatio-temporal extent of Ca2+ signals, without directly binding downstream target proteins. Details of their action depend on their binding kinetics, mobility, and concentration. Thus, neurons can control the range of action of Ca2+ by the type and concentration of CaBPs expressed. Since buffering strongly limits the range of action of free Ca2+, the structure of the Ca2+ signaling domain and the topographical relationships between the sites of Ca2+ influx and the location of the Ca2+ sensors are central determinants in neuronal information processing. For example, postsynaptic dendritic spines act to compartmentalize Ca2+ depending on their geometry and expression of CaBPs, thereby influencing dendritic integration. At presynaptic sites it has been shown that tight, so called nanodomain coupling between Ca2+ channels and the sensor for vesicular transmitter release increases speed and reliability of synaptic transmission. Vice versa, the influence of an individual CaBP on information processing depends on the topographical relationships within the signaling domain. If e.g. source and sensor are very close, only buffers with rapid binding kinetics can interfere with signaling. This Research Topic contains a collection of work dealing with the relationships between different [Ca2+]i controlling mechanisms in the structural context of synaptic sites and their functional implications for synaptic information processing as detailed in the Editorial.
    Keywords: RC321-571 ; Q1-390 ; localization ; dendritic integration ; calcium buffer ; storm ; Calcium ; transmitter release ; calcium sensor ; STED ; plasticity ; thema EDItEUR::P Mathematics and Science::PS Biology, life sciences::PSA Life sciences: general issues::PSAN Neurosciences
    Language: English
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  • 3
    Publication Date: 2024-04-05
    Description: There seems little doubt that from the earliest evolutionary beginnings, inhibition has been a fundamental feature of neuronal circuits - even the simplest life forms sense and interact with their environment, orienting or approaching positive stimuli while avoiding aversive stimuli. This requires internal signals that both drive and suppress behavior. Traditional descriptions of inhibition sometimes limit its role to the suppression of action potential generation. This view fails to capture the vast breadth of inhibitory function now known to exist in neural circuits. A modern perspective on inhibitory signaling comprises a multitude of mechanisms. For example, inhibition can act via a shunting mechanism to speed the membrane time constant and reduce synaptic integration time. It can act via G-protein coupled receptors to initiate second messenger cascades that influence synaptic strength. Inhibition contributes to rhythm generation and can even activate ion channels that mediate inward currents to drive action potential generation. Inhibition also appears to play a role in shaping the properties of neural circuitry over longer time scales. Experience-dependent synaptic plasticity in developing and mature neural circuits underlies behavioral memory and has been intensively studied over the past decade. At excitatory synapses, adjustments of synaptic efficacy are regulated predominantly by changes in the number and function of postsynaptic glutamate receptors. There is, however, increasing evidence for inhibitory modulation of target neuron excitability playing key roles in experience-dependent plasticity. One reason for our limited knowledge about plasticity at inhibitory synapses is that in most circuits, neurons receive convergent inputs from disparate sources. This problem can be overcome by investigating inhibitory circuits in a system with well-defined inhibitory nuclei and projections, each with a known computational function. Compared to other sensory systems, the auditory system has evolved a large number of subthalamic nuclei each devoted to processing distinct features of sound stimuli. This information once extracted is then re-assembled to form the percept the acoustic world around us. The well-understood function of many of these auditory nuclei has enhanced our understanding of inhibition's role in shaping their responses from easily distinguished inhibitory inputs. In particular, neurons devoted to processing the location of sound sources receive a complement of discrete inputs for which in vivo activity and function are well understood. Investigation of these areas has led to significant advances in understanding the development, physiology, and mechanistic underpinnings of inhibition that apply broadly to neuroscience. In this series of papers, we provide an authoritative resource for those interested in exploring the variety of inhibitory circuits and their function in auditory processing. We present original research and focused reviews touching on development, plasticity, anatomy, and evolution of inhibitory circuitry. We hope our readers will find these papers valuable and inspirational to their own research endeavors.
    Keywords: RC321-571 ; Q1-390 ; Gap Junctions ; Sound Localization ; GABA ; inhibition ; plasticity ; Nitric Oxide ; MNTB ; Glycine ; co-release ; thema EDItEUR::P Mathematics and Science::PS Biology, life sciences::PSA Life sciences: general issues::PSAN Neurosciences
    Language: English
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  • 4
    Publication Date: 2024-04-05
    Description: The plasticity of the living matter of our nervous system, in short, is the reason why we do a thing with difficulty the first time, but soon do it more and more easily, and finally, with sufficient practice, do it semi-mechanically, or with hardly any consciousness at all. William James, 1899. It is over 100 years since James described the acquisition of skill. How much, or how little, have recent advances in science changed the way we think about skill learning? What theories and ideas do we still hold dear and which have we discarded? Advances in neuroimaging over the past 20 years have provided insight into the dynamic neural processes underlying human motor skill acquisition, focusing primarily on brain networks that are engaged during early versus late stages of learning. What has been challenging for the field is to tightly link these shifting neural processes with what is known about measureable behavioral changes and strategic processes that occur during learning. The complex nature of behavior and strategy in motor learning often result in a trade-off between experimental control and external validity. The articles assembled for this special issue cut across a number of related disciplines and investigate skill learning across multiple domains. The broad range of theoretical, analytical and methodological approaches offer complementary approaches that can be exploited to develop integrated models of skilled learning. It is our hope that this collection inspires innovation and collaboration amongst researchers, and thereby, accelerates development of societally relevant translational paradigms.
    Keywords: RC321-571 ; Q1-390 ; motor learning ; neural ; sensorimotor ; adaptation ; Skilled Learning ; plasticity ; sequence learning ; neuroimaging ; thema EDItEUR::P Mathematics and Science::PS Biology, life sciences::PSA Life sciences: general issues::PSAN Neurosciences
    Language: English
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