Postnatal development of glycinergic neurons in the rabbit retina.

Certain neurons in the adult rabbit retina possess a high-affinity uptake mechanism for glycine and release it in response to elevated K+ concentrations in the medium. Although the evidence is not yet complete, these properties, together with pharmacological studies, suggest that the glycine-accumulating neurons may be a subpopulation of amacrine cells and may use glycine as a neurotransmitter. In the present study, we have used the uptake and K+-stimulated release of glycine as physiological probes to follow the emergence and maturation of putative glycinergic neurons during postnatal development of the rabbit retina. We show that certain neurons in the newborn retina already possess a specific high-affinity mechanism for glycine uptake. The positions and density of these cells in the developing retina suggest that they will become glycine-accumulating neurons of the adult retina. Thus, similar to our earlier study on the development of GABA-ergic neurons in this retina, the commitment by certain retinal neurons to be glycinergic, if indeed these cells use glycine as the transmitter, is made prenatally. These putative glycinergic neurons are, however, probably immature at birth, because they do not release the accumulated glycine in response to high K+ concentrations in the medium. In fact, there is practically no K+-stimulated release of preloaded glycine from the retina until about 7 days after birth, after which the release increases drastically to about 65% of the adult level on day 10 and 80% on day 12. Assuming that this release originates synaptically, our finding suggests that the putative glycinergic neurons may be functionally mature by 10-12 days after birth. Additionally, our results show that during development of the rabbit retina, the mechanism for high-affinity glycine uptake emerges and matures much earlier than the mechanism for K+-stimulated glycine release.