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      Voltage-Gated Calcium Channels: Key Players in Sensory Coding in the Retina and the Inner Ear

      Author(s): 1 , 1 , 1
      Publication date Created:
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      Journal: Physiological Reviews
      Publisher: American Physiological Society

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          Abstract

          <p class="first" id="d520065e161">Calcium influx through voltage-gated Ca (Ca <sub>V</sub>) channels is the first step in synaptic transmission. This review concerns Ca <sub>V</sub> channels at ribbon synapses in primary sense organs and their specialization for efficient coding of stimuli in the physical environment. Specifically, we describe molecular, biochemical, and biophysical properties of the Ca <sub>V</sub> channels in sensory receptor cells of the retina, cochlea, and vestibular apparatus, and we consider how such properties might change over the course of development and contribute to synaptic plasticity. We pay particular attention to factors affecting the spatial arrangement of Ca <sub>V</sub> channels at presynaptic, ribbon-type active zones, because the spatial relationship between Ca <sub>V</sub> channels and release sites has been shown to affect synapse function critically in a number of systems. Finally, we review identified synaptopathies affecting sensory systems and arising from dysfunction of L-type, Ca <sub>V</sub>1.3, and Ca <sub>V</sub>1.4 channels or their protein modulatory elements. </p>

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          Voltage-gated calcium channels.

          William Catterall (2011)
          Voltage-gated calcium (Ca(2+)) channels are key transducers of membrane potential changes into intracellular Ca(2+) transients that initiate many physiological events. There are ten members of the voltage-gated Ca(2+) channel family in mammals, and they serve distinct roles in cellular signal transduction. The Ca(V)1 subfamily initiates contraction, secretion, regulation of gene expression, integration of synaptic input in neurons, and synaptic transmission at ribbon synapses in specialized sensory cells. The Ca(V)2 subfamily is primarily responsible for initiation of synaptic transmission at fast synapses. The Ca(V)3 subfamily is important for repetitive firing of action potentials in rhythmically firing cells such as cardiac myocytes and thalamic neurons. This article presents the molecular relationships and physiological functions of these Ca(2+) channel proteins and provides information on their molecular, genetic, physiological, and pharmacological properties.
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            Mechanisms underlying spontaneous patterned activity in developing neural circuits.

            Aaron Blankenship, Marla B Feller (2010)
            Patterned, spontaneous activity occurs in many developing neural circuits, including the retina, the cochlea, the spinal cord, the cerebellum and the hippocampus, where it provides signals that are important for the development of neurons and their connections. Despite there being differences in adult architecture and output across these various circuits, the patterns of spontaneous network activity and the mechanisms that generate it are remarkably similar. The mechanisms can include a depolarizing action of GABA (gamma-aminobutyric acid), transient synaptic connections, extrasynaptic transmission, gap junction coupling and the presence of pacemaker-like neurons. Interestingly, spontaneous activity is robust; if one element of a circuit is disrupted another will generate similar activity. This research suggests that developing neural circuits exhibit transient and tunable features that maintain a source of correlated activity during crucial stages of development.
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              RIM proteins tether Ca2+ channels to presynaptic active zones via a direct PDZ-domain interaction.

              Pascal S Kaeser, Lunbin Deng, Yun Wang … (2011)
              At a synapse, fast synchronous neurotransmitter release requires localization of Ca(2+) channels to presynaptic active zones. How Ca(2+) channels are recruited to active zones, however, remains unknown. Using unbiased yeast two-hybrid screens, we here identify a direct interaction of the central PDZ domain of the active-zone protein RIM with the C termini of presynaptic N- and P/Q-type Ca(2+) channels but not L-type Ca(2+) channels. To test the physiological significance of this interaction, we generated conditional knockout mice lacking all multidomain RIM isoforms. Deletion of RIM proteins ablated most neurotransmitter release by simultaneously impairing the priming of synaptic vesicles and by decreasing the presynaptic localization of Ca(2+) channels. Strikingly, rescue of the decreased Ca(2+)-channel localization required the RIM PDZ domain, whereas rescue of vesicle priming required the RIM N terminus. We propose that RIMs tether N- and P/Q-type Ca(2+) channels to presynaptic active zones via a direct PDZ-domain-mediated interaction, thereby enabling fast, synchronous triggering of neurotransmitter release at a synapse. Copyright © 2011 Elsevier Inc. All rights reserved.
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                Author and article information

                Journal
                Title: Physiological Reviews
                Abbreviated Title: Physiological Reviews
                Publisher: American Physiological Society
                ISSN (Print): 0031-9333
                ISSN (Electronic): 1522-1210
                Publication date Created: October 2018
                Publication date (Print): October 2018
                Volume: 98
                Issue: 4
                Pages: 2063-2096
                Affiliations
                [1 ]Synaptic Physiology of Mammalian Vestibular Hair Cells Group, Institute for Auditory Neuroscience and InnerEarLab, University Medical Center Göttingen and Auditory Neuroscience Group, Max Planck Institute of Experimental Medicine, Göttingen, Germany; Department of Biology, University of Maryland, College Park, Maryland; and Pharmacology and Toxicology, Institute of Pharmacy, University of Innsbruck, Innsbruck, Austria
                Article
                DOI: 10.1152/physrev.00030.2017
                PMC ID: 6170976
                PubMed ID: 30067155
                SO-VID: 28d86621-16d0-408b-b3c7-48045f281a9b
                Copyright © © 2018
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