| First Author | Meyer A | Year | 2014 |
| Journal | J Cell Sci | Volume | 127 |
| Issue | Pt 6 | Pages | 1190-202 |
| PubMed ID | 24463820 | Mgi Jnum | J:213007 |
| Mgi Id | MGI:5582682 | Doi | 10.1242/jcs.133066 |
| Citation | Meyer A, et al. (2014) AII amacrine cells discriminate between heterocellular and homocellular locations when assembling connexin36-containing gap junctions. J Cell Sci 127(Pt 6):1190-202 |
| abstractText | Electrical synapses (gap junctions) rapidly transmit signals between neurons and are composed of connexins. In neurons, connexin36 (Cx36) is the most abundant isoform; however, the mechanisms underlying formation of Cx36-containing electrical synapses are unknown. We focus on homocellular and heterocellular gap junctions formed by an AII amacrine cell, a key interneuron found in all mammalian retinas. In mice lacking native Cx36 but expressing a variant tagged with enhanced green fluorescent protein at the C-terminus (KO-Cx36-EGFP), heterocellular gap junctions formed between AII cells and ON cone bipolar cells are fully functional, whereas homocellular gap junctions between two AII cells are not formed. A tracer injected into an AII amacrine cell spreads into ON cone bipolar cells but is excluded from other AII cells. Reconstruction of Cx36-EGFP clusters on an AII cell in the KO-Cx36-EGFP genotype confirmed that the number, but not average size, of the clusters is reduced - as expected for AII cells lacking a subset of electrical synapses. Our studies indicate that some neurons exhibit at least two discriminatory mechanisms for assembling Cx36. We suggest that employing different gap-junction-forming mechanisms could provide the means for a cell to regulate its gap junctions in a target-cell-specific manner, even if these junctions contain the same connexin. |
