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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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Published in: | Journal of comparative neurology (1911) 2013-08, Vol.521 (11), p.2486-2501 |
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Main Authors: | , , , , |
Format: | Article |
Language: | English |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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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. |
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ISSN: | 0021-9967 1096-9861 |
DOI: | 10.1002/cne.23294 |