The All amacrine cell is a critical interneuron in the rod pathway of the m
ammalian retina. Rod signals pass into cone pathways by means of gap juncti
ons between All amacrine cells and ON cone bipolar cells. Filling All amacr
ine cells with Neurobiotin produces labeling of cone bipolar cells by means
of these gap junctions. However, tracer injections into bipolar cells do n
ot produce labeling of the All network (Vaney [1997] Invest Ophthalmol Vis
Sci. 38:267-273), which suggests that the AII/bipolar gap junctions allow t
he passage of tracer in only one direction. This mechanism stands in contra
st to physiological results, which indicate that light adapted signals can
pass from ON cone bipolar cells into the All network (Xin and Bloomfield [1
999] Vis Neurosci. 16:653-665). Here, we report that a variety of ON and OF
F bipolar cells are sometimes anomalously coupled to the A-type horizontal
cell network. These relatively rare examples do not result from dye injecti
on errors, but seem to represent minor developmental errors. However, this
provides a method to obtain Neurobiotin-filled cone bipolar cells without t
he necessity of impaling them with a microelectrode. Under these conditions
, Neurobiotin spreads from ON cone bipolar cells into neighboring All amacr
ine cells. The dye-coupled All amacrine cells, positively identified by dou
ble labeling with an antibody against calretinin, were centered around anom
alously coupled ON bipolar culls. These results indicate that AII/bipolar c
ell gap junctions allow tracer coupling in both directions, consistent with
previous physiological results. The previous failure to detect the passage
of neuronal tracer from injected bipolar cells to All amacrine cells may r
eflect electrode damage or perhaps the asymmetrical voltage sensitivity of
a heterotypic gap junction. J. Comp. Neurol. 437:408-422, 2001. (C) 2001 Wi
ley-Liss, Inc.