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Expression of voltage‐gated calcium channel α 2 δ 4 subunits in the mouse and rat retina

High‐voltage activated Ca channels participate in multiple cellular functions, including transmitter release, excitation, and gene transcription. Ca channels are heteromeric proteins consisting of a pore‐forming α 1 subunit and auxiliary α 2 δ and β subunits. Although there are reports of α 2 δ 4 su...

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Bibliographic Details
Published in:Journal of comparative neurology (1911) 2013-08, Vol.521 (11), p.2486-2501
Main Authors: De Sevilla Müller, Luis Pérez, Liu, Janelle, Solomon, Alexander, Rodriguez, Allen, Brecha, Nicholas C.
Format: Article
Language:English
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Summary:High‐voltage activated Ca channels participate in multiple cellular functions, including transmitter release, excitation, and gene transcription. Ca channels are heteromeric proteins consisting of a pore‐forming α 1 subunit and auxiliary α 2 δ and β subunits. Although there are reports of α 2 δ 4 subunit mRNA in the mouse retina and localization of the α 2 δ 4 subunit immunoreactivity to salamander photoreceptor terminals, there is a limited overall understanding of its expression and localization in the retina. α 2 δ 4 subunit expression and distribution in the mouse and rat retina were evaluated by using reverse transcriptase polymerase chain reaction, western blot, and immunohistochemistry with specific primers and a well‐characterized antibody to the α 2 δ 4 subunit. α 2 δ 4 subunit mRNA and protein are present in mouse and rat retina, brain, and liver homogenates. Immunostaining for the α 2 δ 4 subunit is mainly localized to Müller cell processes and endfeet, photoreceptor terminals, and photoreceptor outer segments. This subunit is also expressed in a few displaced ganglion cells and bipolar cell dendrites. These findings suggest that the α 2 δ 4 subunit participates in the modulation of L‐type Ca 2+ current regulating neurotransmitter release from photoreceptor terminals and Ca 2+ ‐dependent signaling pathways in bipolar and Müller cells. J. Comp. Neurol. 521:2486–2501, 2013. © 2013 Wiley Periodicals, Inc.
ISSN:0021-9967
1096-9861
DOI:10.1002/cne.23294