Gamma-aminobutyric acid (GABA) modulates the pattern of correlated spontaneous bursting activity between amacrine cells and ganglion cells of the ferret retina during the first postnatal month. Here, we demonstrate the presence of an anatomical network which may underlie these interactions throughout the period when correlated bursting activity is observed, by immunolabelling the neonatal ferret retina for GABA, GABAA receptors, and synapse-associated proteins. GABA immunoreactivity was detected in cell somata in the ganglion cell layer (GCL), in amacrine cells, and in the inner plexiform layer (IPL) by embryonic day 38. This pattern remained largely unchanged throughout neonatal development and in the adult. By contrast to other mammals, the outer plexiform layer (OPL) was only very weakly labelled for GABA, at all ages studied. Strong, punctate, immunolabelling for the beta 2/3 subunit of the GABAA receptor was apparent in the IPL by birth, and appeared in the OPL by the second postnatal week. The possibility that synaptic interactions in the IPL occur during bursting activity was examined by immunolabelling for synapse-associated proteins. Strong immunoreactivity for synaptic vesicle proteins, Synapsin I and II, and synaptic vesicle-2 (SV2), a synaptic vesicle transporter protein, was observed in the IPL by birth. Immunoreactivity for SNAP-25, a protein associated with vesicle fusion, was also intense at the level of the IPL and in the nerve fiber layer of the retina at birth. Taken together, these patterns of immunoreactivity suggest the presence of a GABAergic network in the IPL of the ferret retina by birth, coinciding with the appearance of correlated bursting activity in the inner retina.