Figure 6.

In Cx30.2^lacZ/lacZ mice, the primary rod pathway is unaffected from lack of Cx30.2. (A,B) Electroretinograms under scotopic conditions did not differ between Cx30.2^lacZ/lacZ mice and their wild-type littermates. The amplitudes of a- and b-wave did not show any significant differences. (C–H) Representative results of AII cell tracer-coupling experiments (asterisks represent Alexa-Fluor-488-injected AII cells; the tracer neurobiotin is shown in magenta). Rotated projections show the injected AII amacrine cell (asterisk) and neurobiotin-containing coupled cells (C,F). Whole-mount views of an AII amacrine cell (asterisk) with its tracer-coupled partners in the proximal and distal INL, representing AII (D,G) and ON cone bipolar cells (E,H), respectively. (I) The amount of tracer coupling of AII amacrine cells did not differ between Cx30.2-deficient and wild-type mice. In contrast, coupling to both AII amacrine and ON cone bipolar cells was completely abolished when Cx36 was knocked out. (J–L) Lack of Cx30.2 was not compensated by upregulation of Cx36 in the OFF (K₁,L₁) or ON sublamina of the IPL (K₂,L₂). The number of Cx36-positive clusters did not differ between genotypes. Scale bars: (C–H) 20 μm; (K,L) 10 μm.