In the mammalian retina, gap junctions have been found to be permeable to glycine, which was first revealed in the junctions between cone depolarizing bipolar cells (DBC
Cs) and AII ACs.
9,10 Gap junctions between GCs and ACs are permeable to Neurobiotin (NB) and likely permeable to GABA, as well.
8,11 GCs and ACs in the mammalian retina are both classified into more than 20 morphological subtypes.
6,8,12–14 NB filling of individual GCs, facilitated by electric currents, has contributed much to the study of GC-AC coupling. However, for most GC subtypes, the identity and number of coupled ACs are unclear.
8 GCs and ACs may both reside in the GC layer (GCL) and inner nuclear layer (INL), and they are not obviously distinguishable by soma size,
15,16 axons,
17,18 or dendritic tree shape.
6,15,19 Amacrine cells are often identified immunologically by antibodies against GABA, glycine,
20,21 Choline acetyltransferase (ChAT),
20,22 tyrosine hydroxylase (TH),
23–25 and neuronal or brain-type nitric oxide synthase (nNOS or bNOS),
26–28 while antibodies against calcium-binding proteins, such as parvalbumin (PV)
29–31 and calretinin (CR),
32–34 may label GCs. A more reliable way to distinguish GCs from ACs, however, is retrograde labeling of GCs.
35–37 In the retrogradely labeled mouse retina, the specificity of GABA, glycine, ChAT, and nNOS antibodies in labeling retinal ACs has been recently confirmed,
28 but similar investigations have not been done for TH,
38 CR,
32–34 and PV.
29–31