Purpose. The molecular identity of the calcium channels that mediate glutamate release from photoreceptors is unknown. Mutations in the recently identified, retina-specific α1F calcium channel subunit cause incomplete X-linked congenital stationary night blindness (CSNB2), the phenotype of which is consistent with a defect in neurotransmission within the retina. The purpose of this study was to determine the cellular distribution of the α1F subunit in the retina. Methods. Antibodies were raised against a unique peptide from the human a α1F sequence. Rat retina sections were labeled with affinity-purified α1F antibodies and the immunofluorescence analyzed by confocal microscopy. The α1F staining was compared with that obtained with a pan-α1 antibody, used to reveal the distribution of known voltage-gated calcium channels in the retina. Some sections were double labeled for α1F and the photoreceptor synaptic ribbon marker, bassoon. Results. Staining of retina sections with anti-α1F resulted in strong punctate labeling in the outer plexiform layer (OPL) and weak punctate labeling in the inner plexiform layer (IPL), consistent with a synaptic localization. Staining was also observed in the outer nuclear layer. Within the OPL, α1F immunoreactivity was clustered in discrete, horseshoe-shaped patches, the shape and dimensions of which are characteristic of rod active zones. Similar structures were labeled with the pan-α1 antibody. Localization of α1F immunoreactivity to rod active zones was confirmed by double labeling for bassoon, a component of photoreceptor synaptic ribbons. Conclusions. The distribution of α1F immunoreactivity in the OPL suggests that calcium influx through α1F or α1F-like channels mediates glutamate release from rod photoreceptors.
|Original language||English (US)|
|Number of pages||5|
|Journal||Investigative Ophthalmology and Visual Science|
|State||Published - Sep 26 2001|
ASJC Scopus subject areas
- Sensory Systems
- Cellular and Molecular Neuroscience