In axon-bearing neurons, action potentials conventionally initiate at the axon initial segment (AIS) and are important for neuron excitability and cell-to-cell communication. However in axonless neurons, spike origin has remained unclear. Here we report in the axonless, spiking AII amacrine cell of the mouse retina a dendritic process sharing organizational and functional similarities with the AIS. This process was revealed through viral-mediated expression of channelrhodopsin-2-GFP with the AIS-targeting motif of sodium channels (Na(v)II-III). The AII processes showed clustering of voltage-gated Na+ channel 1.1 (Na(v)1.1) as well as AIS markers ankyrin-G and neurofascin. Furthermore, Na(v)II-III targeting disrupted Na(v)1.1 clustering in the AII process, which drastically decreased Na+ current and abolished the ability of the AII amacrine cell to generate spiking. Our findings indicate that, despite lacking an axon, spiking in the axonless neuron can originate at a specialized AIS-like process.
Pubmed ID: 21994381 RIS Download
Mesh terms: Action Potentials | Amacrine Cells | Animals | Ankyrins | Cytochrome P-450 Enzyme System | Dendrites | Electric Stimulation | Female | Green Fluorescent Proteins | In Vitro Techniques | Male | Mice | Mice, Inbred C57BL | Mice, Transgenic | NAV1.1 Voltage-Gated Sodium Channel | Nerve Tissue Proteins | Patch-Clamp Techniques | Photic Stimulation | Retina | Rhodopsin | Sodium Channel Blockers | Sodium Channels | Tetrodotoxin
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