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L-type calcium channels in the photoreceptor ribbon synapse: Localization and role in plasticity
Calcium (Ca2+) influx through voltage‐gated Ca2+channels stimulates a variety of neural activities, including process outgrowth, neurotransmission, and synaptic plasticity. In general, L‐type channels control Ca2+ influx into the soma and dendrites, whereas other Ca2+ channel types control presynapt...
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Published in: | Journal of comparative neurology (1911) 1999-12, Vol.415 (1), p.1-16 |
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Main Authors: | , , |
Format: | Article |
Language: | English |
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Citations: | Items that this one cites |
Online Access: | Get full text |
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Summary: | Calcium (Ca2+) influx through voltage‐gated Ca2+channels stimulates a variety of neural activities, including process outgrowth, neurotransmission, and synaptic plasticity. In general, L‐type channels control Ca2+ influx into the soma and dendrites, whereas other Ca2+ channel types control presynaptic activities. Neurons that make ribbon synapses, however, are among a select group of nerve cells whose presynaptic Ca2+‐dependent secretion is linked to L‐type channels. Recently, photoreceptor ribbon synapses have been shown to be capable of dramatic structural remodeling and neuritic outgrowth. Here, we have examined 1) the distribution of dihydropyridine (DHP)‐sensitive (L‐type) Ca2+ channels in photoreceptor presynaptic structures and 2) the role of these channels in axonal plasticity and process outgrowth in culture. Using anti‐alpha1C and the fluorescent dihydropyridine, (–)‐DM‐BODIPY DHP, L‐type channels were localized in the outer plexiform layer of retinal sections and in presynaptic terminals of freshly isolated photoreceptors. In the rod terminal, dense patches of label were present; their distribution and number matched that of synaptic ribbons. After 1–7 days in vitro, punctate alpha1C staining occurred along newly formed neurites and presynaptic varicosities. Functional channels were present throughout the culture period, as determined by fura‐2 imaging. Channel blockage by nicardipine, a DHP antagonist, inhibited axonal remodeling. Specifically, it prevented axon retraction and lamellipodium formation, reduced neurite growth, and produced long, thin processes on some, primarily cone, photoreceptors. L‐type Ca2+ channel activity, therefore, not only stimulates neurotransmission but contributes to presynaptic structural plasticity at the ribbon synapse. J. Comp. Neurol. 415:1–16, 1999. © 1999 Wiley‐Liss, Inc. |
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ISSN: | 0021-9967 1096-9861 |
DOI: | 10.1002/(SICI)1096-9861(19991206)415:1<1::AID-CNE1>3.0.CO;2-G |