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Tuesday, October 13, 2020 | History

5 edition of Calcium, Neuronal Function and Transmitter Release (Topics in the Neurosciences) found in the catalog.

Calcium, Neuronal Function and Transmitter Release (Topics in the Neurosciences)

  • 318 Want to read
  • 38 Currently reading

Published by Springer .
Written in English

    Subjects:
  • Neuroscience,
  • Science,
  • Neurochemistry,
  • Molecular Biology,
  • Medical,
  • Physiological effect,
  • Neurotransmitters,
  • Neurons,
  • Life Sciences - Zoology - General,
  • Medical / Neuroscience,
  • Neurosciences,
  • Congresses,
  • Calcium

  • Edition Notes

    ContributionsRami Rahamimoff (Editor), Bernard Katz (Editor)
    The Physical Object
    FormatHardcover
    Number of Pages640
    ID Numbers
    Open LibraryOL8269681M
    ISBN 100898387914
    ISBN 109780898387919

      Inhibition of quantal trans- mitter release in the absence of calcium influx by a G protein- linked adenosine receptor at hippocampal synapses. Neuron 8, Simon, S. M., and Llin~is, R. R. (). Compartmentalization of the submembrane calcium activity during calcium influx and its significance in transmitter release. Biophys. J.   A novel function of roscovitine, i.e. an effect on Ca 2+ channels and transmitter release in central neurons, was studied by whole-cell voltage-clamp recordings and time-lapse fluorescence imaging techniques. Extracellular application of roscovitine markedly enhanced the tail calcium current following repolarization from depolarized voltages.

    Intracellular calcium ions are involved in many forms of cellular function. To accommodate so many control functions, a complex spatiotemporal organization of calcium signaling has developed. In both excitable and nonexcitable cells, calcium signaling was found to fluctuate. Sudden localized increases in the intracellular calcium concentration—or calcium sparks—were found in heart. Sudden localized increases in the intracellular calcium concentration-or calcium sparks-were found in heart, striated and smooth muscle, Xenopus Laevis oocytes, and HeLa and P12 cells. In the nervous system, intracellular calcium ions were found important in key processes such as transmitter release, repetitive firing, and gene expression.

    Calcium-induced calcium release gene expression, metabolic function and transmitter release in rods and cones. Ca 2+ release from intracellular stores was suggested to regulate the level of tonic neuronal activity at some central synapses by contributing to spontaneous neurotransmitter release that sets the frequency of mEPSCs. A neuromuscular junction (or myoneural junction) is a chemical synapse between a motor neuron and a muscle fiber. It allows the motor neuron to transmit a signal to the muscle fiber, causing muscle contraction.. Muscles require innervation to function—and even just to maintain muscle tone, avoiding the neuromuscular system nerves from the central nervous system and the peripheral.


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Calcium, Neuronal Function and Transmitter Release (Topics in the Neurosciences) Download PDF EPUB FB2

Calcium, Neuronal Function and Transmitter Release: Proceedings of the Symposium on Calcium, Neuronal Function and Transmitter Release held at the 28–31, (Topics in the Neurosciences (1)): Medicine & Health Science Books @ Calcium, Neuronal Function and Transmitter Release Proceedings of the Symposium on Calcium, Neuronal Function and Transmitter Release held at the International Congress of Physiology Jerusalem, Israel—August 28–31, Editors: Rahamimoff, Rami, Katz, Bernard (Eds.) Free Preview.

Calcium, Neuronal Function and Transmitter Release This Calcium entitled Calcium, Neuronal Function and Transmitter Re­ lease, was in the framework of the regional meeting of the International Union of Physiological Sciences, that took place in Jerusalem between Augustretyping large portions of the Neuronal Function and Transmitter Release book, and getting the.

Calcium, Neuronal Function and Transmitter Release: Proceedings of the Symposium on Calcium, Neuronal Function and Transmitter Release held at the International Congress of Physiology Jerusalem, Israel-AugustHardback; Topics in the Neurosciences; English.

Calcium, Neuronal Function and Transmitter Release: Proceedings of the Symposium on Calcium, Neuronal Function and Transmitter Release held at the International Congress of Physiology Jerusalem, Israel-August- Topics in the Neurosciences 1 (Paperback) Rami Rahamimoff (editor), Bernard Katz (editor)Book Edition: Softcover Reprint of The Original 1st Ed.

Full text Full text is available as a scanned copy of the original print version. Get a printable copy (PDF file) of the complete article (K), or click on a page image below to browse page by : BS Meldrum. This symposium entitled Calcium, Neuronal Function and Transmitter Re- lease, was in the framework of the regional meeting of the International Union of Physiological Sciences, that took place in Jerusalem between AugustThe symposium dealt with the role of calcium ions in regulation of a large number of important processes in modern neurobiology, from molecular and cellular.

Ca2+ is an essential co-factor for transmitter release. In the absence of external Ca2+, a presynaptic impulse reaches the nerve terminal but does not release the transmitter.

Intracellular injections of Ca2+ into a presynaptic terminal enhances the release of individual transmitter quanta. It is thus the entry of Ca2+ into the nerve terminal that is required for transmitter release. Thesleff S., Lupa M.T. () Calcium Independent Quantal Transmitter Release at the Neuromuscular Junction.

In: Rahamimoff R., Katz B. (eds) Calcium, Neuronal Function and Transmitter Release. Topics in the Neurosciences, vol 1. Calcium (Ca2+) is a vital element in the process of neurotransmitter release; when Ca2+ channels are blocked, neurotransmitter release is inhibited.

When the action potential reaches the nerve terminal, voltage-dependent Ca 2+ channels open and Ca 2+ rushes into the neuron terminal due to a greater extracellular concentration. Terminal Calcium Influx by Casey Henley is licensed under a Creative Commons Attribution Non-Commercial Share-Alike (CC BY-NC-SA) International License.

Active Zones. The voltage-gated calcium channels are concentrated in the presynaptic terminal at active zones, the regions of small molecule neurotransmitter release. Pincus J. () Phenytoin, Transmitter Release and Calcium Flux.

In: Rahamimoff R., Katz B. (eds) Calcium, Neuronal Function and Transmitter Release. Topics in the Neurosciences, vol 1. Abstract. In Dodge and Rahamimoff (1) proposed a model for the relation between [Ca 2+] out and transmitter release at the neuromuscular junction that has dominated subsequent work on this problem.

We have modified their model by adding one additional. Function. The word “glia” illustrates the original belief among scientists that these cells play a passive role in neural signaling, being responsible only for neuronal structure and support within the brain.

Glial cells cannot produce action potentials and therefore were not suspected as playing an important and active communicative role in the central nervous system, because synaptic. Get this from a library. Calcium, Neuronal Function and Transmitter Release: Proceedings of the Symposium on Calcium, Neuronal Function and Transmitter Release held at the International Congress of Physiology Jerusalem, Israel--August[Rami Rahamimoff; Bernard Katz] -- This symposium entitled Calcium, Neuronal Function and Transmitter ReƯ lease, was in the framework.

Moore J.W., Hines M. () Some Consequences of Intracellular Calcium Binding on Phasic Synaptic Transmitter Release. In: Rahamimoff R., Katz B. (eds) Calcium, Neuronal Function and Transmitter Release. INTRODUCTION. Neurotransmitter release from a single vesicle activates a small postsynaptic voltage change and comprises the elementary unit of synaptic communication (Fatt and Katz, ; Del Castillo and Katz, ).Vesicle fusion is triggered by calcium entry through presynaptic voltage-activated calcium channels (VACC) or may occur spontaneously in the absence of an action.

Calcium ions serve as a signal for numerous neuronal functions. This requires a very low, modulated, resting cytosolic free Ca 2+ concentration, and diverse mechanisms to regulate the time course and spatial distribution of transient Ca 2+ increases, so that Ca 2+ can separately activate multiple processes within the same neuron.

The interplay of several systems that release Ca 2+ into the. Other articles where Neurotransmitter release is discussed: nervous system: Neurotransmitter release: Two factors are essential for the release of the neurotransmitter from the presynaptic terminal: (1) depolarization of the terminal and (2) the presence of calcium ions (Ca2+) in the extracellular fluid.

The membrane of the presynaptic terminal contains voltage-dependent calcium channels that. BAPTA--> Significantly reduced neurotransmitter release -Since the faster calcium buffer was able to compete with the vesicles for calcium, this showed that calcium channels that provide the source for calcium-triggered neurotransmitter release must be very close to the calcium.

important in key processes such as transmitter release, repetitive firing, and gene expression. Hence, we examined whether calcium sparks also exist in neurons. Using confocal laser-scanning micros-copy and fluorescent probes, we found that calcium sparks exist in two types of neuronal preparations: the presynaptic boutons of.

Neuron 5, Robitaille R, Chariton MP () Presynaptic calcium signals and transmitter release are modulated by calcium-activated potassium channels.

J Neurosci Sano K, Enomoto Ki, Maeno T () Effects of synthetic w-conotoxin, a new type Ca 2+ antagonist, on frog and mouse neuromuscular transmission.

1. Introduction. An elevation of intracellular free Ca 2+ concentration ([Ca 2+] i) is the trigger for neurotransmitter release from synaptic vesicles at neuronal synapses.Alterations in [Ca 2+] i also bring about many different changes in neuronal function including modulation of ion channels, gene expression and effects on neuronal survival and apoptosis.