Abstract
Electrical synapses (gap junctions) rapidly transmit signals between neurons and are composed of connexins. In neurons, connexin36 (C×36) is the most abundant isoform; however, the mechanisms underlying formation of C×36-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 C×36 but expressing a variant tagged with enhanced green fluorescent protein at the C-terminus (KO-C×36-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 C×36-EGFP clusters on an AII cell in the KO-C×36-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 C×36. We suggest that employing different gapjunction- 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.
Original language | English |
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Pages (from-to) | 1190-1202 |
Number of pages | 13 |
Journal | Journal of Cell Science |
Volume | 127 |
Issue number | 6 |
DOIs | |
Publication status | Published - 15 Mar 2014 |
Externally published | Yes |
Keywords
- Amacrine cell
- Bipolar cell
- Connexin
- Electrical synapse
- Gap junction
- Retina