The goldfish retina grows throughout the animal’s life, primarily by a balloon-like expansion. With this expansion, dendritic arbors of ganglion cells show scaled growth; arbors increase in size from small to large with no change in their architecture (Hitchcock & Easter, 1986; Bloomfield & Hitchcock, 1991). The study reported here showed that ganglion cell arbors acquire new synapses with this growth. Arbors from a single type of ganglion cell in retinas of small, young and large, old fish were intracellularly filled with horseradish peroxidase, examined electron microscopically, and the synapses contacting them counted and compared (small arbors vs. large arbors). The small and large arbors had similar numbers and orders of dendritic branches (i.e. similar architectures), but the large arbors were significantly larger than the small ones. The increase in arbor size was correlated with a 2.7x and 1.9x increase in the number of ribbon and conventional synaptic contacts, respectively. The addition of new synapses is proposed as a mechanism by which the signaling properties of the enlarging ganglion cells can remain constant.

A labeled ON parasol ganglion cell from a macaque retina was analyzed in serial, ultrathin sections. It received 13% of its input from diffuse bipolar cells. These directed a large proportion of their output to amacrine cells but received a relatively small proportion of their amacrine cell input via feedback synapses. In these respects, they were similar to the DB3 bipolar cells that make synapses onto OFF parasol cells. Bipolar cell axons that contacted the ON parasol cell in stratum 4 of the inner plexiform layer always made synapses onto the dendrite, and therefore, the number of bipolar cell synapses onto these ganglion cells could be estimated reliably by light microscopy in the future. Amacrine cells provided the majority of inputs to the ON parasol cell. Only a few of the presynaptic amacrine cell processes received inputs from the same bipolar cells as the parasol cells, and most of the presynaptic amacrine cell processes did not receive any inputs at all within the series. These findings suggest that most of the inhibitory input to the ON parasol cell originates from other areas of the retina. Amacrine cells presynaptic to the parasol ganglion cell interacted very infrequently with other neurons in the circuit, and therefore, they would be expected to act independently, for the most part.

We have previously reported that a small number of retinal ganglion cells (RGCs) of adult cats survive 2 months after transection of the optic nerve (ON) and that α cells have the greatest ability to survive among different types of RGCs (Watanabe et al., 1995). Here we report the time course of RGC survival within 15 days after ON transection using retrograde labeling with DiI injected into the bilateral lateral geniculate nuclei of cats. The density of DiI-labeled RGCs in the central retina as well as in the periphery did not change until day 3 after ON transection, then decreased rapidly, to 43% of the original density on day 7, and falling to 19% by day 14. We then intracellularly injected Lucifer yellow into the DiI-labeled RGCs to examine the difference in the time course between surviving α and β cells. Similar to the density change in total surviving RGCs, the proportion of surviving β cells did not change until day 3, then decreased rapidly to 65% of the original density on day 4, falling to 12% by day 14. By contrast, 64% of α cells survived for 14 days after axotomy. Analysis of regression lines for survival time courses indicated that death of β cells was characterized with a rapid period phase from day 3 to day 7 after axotomy whereas that of α cells lacked it. Axon-like sprouting from surviving β cells was first recognized in the nerve fiber layer on day 3, and were later more conspicuous.