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Article ; Online: Identification of calcium channel alpha1 subunit mRNA expressed in retinal bipolar neurons.

Logiudice, Lisamarie / Henry, Diane / Matthews, Gary

Molecular vision

2006  Volume 12, Page(s) 184–189

Abstract: Purpose: Glutamate release from goldfish bipolar cell terminals is driven by Ca2+ influx through L-type calcium channels that exhibit several uncommon features, including rapid kinetics of activation and deactivation, slow inactivation, and activation ... ...

Abstract Purpose: Glutamate release from goldfish bipolar cell terminals is driven by Ca2+ influx through L-type calcium channels that exhibit several uncommon features, including rapid kinetics of activation and deactivation, slow inactivation, and activation at an unusually negative voltage range for L-type channels. The purpose of this study was to establish the molecular identities of the alpha1 subunits responsible for these distinctive properties.
Methods: Transcripts for calcium channel alpha1 subunits expressed in individual goldfish ON-type bipolar cells were identified using single-cell reverse transcriptase polymerase chain reaction (RT-PCR). After cloning the goldfish homologs of the zebrafish and mammalian subunits, we designed sets of nested primers that are specific for Cav1.3a, and Cav1.3b L-type calcium channels.
Results: Large-terminal, ON-type bipolar cells express transcripts of Cav1.3a and/or Cav1.3b.
Conclusions: The endogenous expression of only one or both subunits in a single cell raises the possibility of functionally distinct classes of bipolar cells that differ in calcium current properties.
MeSH term(s) Amino Acid Sequence ; Animals ; Calcium Channels/genetics ; Cloning, Molecular ; Goldfish ; RNA, Messenger/metabolism ; Retina/cytology ; Retina/metabolism ; Retinal Bipolar Cells/metabolism ; Reverse Transcriptase Polymerase Chain Reaction
Chemical Substances Calcium Channels ; RNA, Messenger
Language English
Publishing date 2006-03-17
Publishing country United States
Document type Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID 2017540-1
ISSN 1090-0535 ; 1090-0535
ISSN (online) 1090-0535
ISSN 1090-0535
Database MEDical Literature Analysis and Retrieval System OnLINE

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