A subset of cone bipolar cells expresses the Na+ channel SCN2A in the human retina

Some bipolar cells in the human retina are known to express voltage-gated Na+ channels. However, it is unclear which types of channels are expressed, and whether Na+ channel expression is limited to specific types of bipolar cells. In the present study, we examined the types of voltage-gated Na+ channels expressed in human bipolar cells and the morphology of bipolar cells with voltage-gated Na+ currents. To investigate the expression of voltage-gated Na+ channels in human bipolar cells, we examined whether Na+ channel transcripts could be detected in single bipolar cells using the reverse transcription polymerase chain reaction (RT-PCR) technique. The voltage-gated Na+ current was recorded from isolated bipolar cells using the patch-clamp recording technique. Types of bipolar cells that have the Na+ currents were investigated by analyzing their morphology after staining with Lucifer yellow. Using RT-PCR, the SCN2A Na+ channel was detected in 5 of 6 isolated bipolar cells. This suggests that a subset of human bipolar cells expresses the SCN2A Na+ channel. Under voltage-clamp conditions, depolarizing voltage steps induced a fast transient inward current in cone bipolar cells with axon terminal boutons that stratified at the ON layer, which includes the stratum 3, 4, and 5 of the inner plexiform layer (IPL, n = 2/11 cells). The fast transient inward current of isolated bipolar cells was blocked by 1 mu M of tetrodotoxin (TTX), a voltage-gated Na+ channel blocker. No fast transient inward current was recorded with axon terminals that stratify at the OFF layer, which includes stratum 1 and 2 of the IPL (n = 4). Thus, a subset of ON cone bipolar cells at least expresses the putative voltage-gated Na+ channel SCN2A in the human retina. The Na+ channels in the bipolar cells may serve to amplify the release of neurotransmitter, glutamate, when membrane potential is rapidly depolarized and thereby selectively accelerating light responses.

Automated summary

Some human bipolar cells express SCN2A Na+ channel, which may amplify the release of neurotransmitter glutamate when the membrane potential is rapidly depolarized, selectively accelerating light responses.