Ontogeny of catecholaminergic and cholinergic cell distributions in the cat's retina.

The development of catecholaminergic and cholinergic neurones in the cat's retina has been examined with antibodies against their respective rate-limiting enzymes, tyrosine hydroxylase (TH) and choline acetyl transferase (ChAT). ChAT-immunoreactive (IR) cells were first detected at E (embryonic day) 56 with somata in the ganglion cell layer (GCL) or in the inner cytoblast layer (CBL). At P (postnatal day) 1, two faint bands of ChAT-IR fibres were evident in an inner and outer strata of the inner plexiform layer (IPL) and by P26, the bands were similar to those in the adult. TH immunoreactivity was first detected at E59 in either darkly labelled somata in the inner CBL with processes extending toward the IPL or in lightly labelled somata also located in CBL but with no processes. At P1, most TH-IR cells had prominently labelled dendrites and, by P8, most of the features of the adult cells were evident. Soma size gradients among TH-IR cells were first detected at P8, with cells in temporal retina being larger than those in nasal retina or at the area centralis. The smaller sizes of cells at the area centralis emerged after P26. The smaller sizes of ChAT-IR somata at the area centralis, by contrast, emerged between P8 and P26. The number of both TH-IR and ChAT-IR cells declined from the time they first appeared till adulthood. The decline was smaller among ChAT-IR cells (24%) than among TH-IR cells (68%). In distribution, the differential expansion of the retina appeared to be largely responsible for generating the final adult distribution of ChAT-IR cells. However, during late postnatal development (P26 to adulthood), the density of ChAT-IR cells in the periphery declined more than that of the ganglion cells, suggesting that some ChAT-IR cells may die in the periphery during this time. Prior to P26, the changes in the distribution of TH-IR cells were inconsistent with the pattern of retinal expansion. It is suggested that during this period, regional cell loss and cell addition may account for the changes in distribution of TH-IR cells. Later in development (P26 to adulthood), the changes in the density of TH-IR cells closely conformed to the differential expansion of the retina.