Y retinal terminals contact interneurons in the cat dorsal lateral geniculate nucleus.

One of the largest influences on dorsal lateral geniculate nucleus (dLGN) activity comes from interneurons, which use the neurotransmitter gamma-aminobutyric acid (GABA). It is well established that X retinogeniculate terminals contact interneurons and thalamocortical cells in complex synaptic arrangements known as glomeruli. However, there is little anatomical evidence for the involvement of dLGN interneurons in the Y pathway. To determine whether Y retinogeniculate axons contact interneurons, we injected the superior colliculus (SC) with biotinylated dextran amine (BDA) to backfill retinal axons, which also project to the SC. Within the A lamina of the dLGN, this BDA labeling allowed us to distinguish Y retinogeniculate axons from X retinogeniculate axons, which do not project to the SC. In BDA-labeled tissue prepared for electron microscopic analysis, we subsequently used postembedding immunocytochemical staining for GABA to distinguish interneurons from thalamocortical cells. We found that the majority of profiles postsynaptic to Y retinal axons were GABA-negative dendrites of thalamocortical cells (117/200 or 58.5%). The remainder (83/200 or 41.5%) were GABA-positive dendrites, many of which contained vesicles (59/200 or 29.5%). Thus, Y retinogeniculate axons do contact interneurons. However, these contacts differed from X retinogeniculate axons, in that triadic arrangements were rare. This indicates that the X and Y pathways participate in unique circuitries but that interneurons are involved in the modulation of both pathways.

A novel means of Y cell identification in the developing lateral geniculate nucleus of the cat.

We examined the postnatal development of putative Y cells in the dorsal lateral geniculate nucleus (dLGN) using the SMI-32 antibody, which has been demonstrated in the adult cat to stain cells with Y cell morphology. At birth, SMI-32 stained cells were concentrated in the interlaminar zones. During postnatal development, the SMI-32 staining gradually becomes more disperse and by P21 stained cells are found throughout the A and magnocellular C laminae. By the end of the first postnatal week, and in all later ages examined, the SMI-32 stained cells were significantly larger than the overall population of Nissl stained cells and interneurons (stained with an antibody against glutamic acid decarboxylase). Postnatal SMI-32 staining revealed a dramatic increase in soma sizes and the expansion of putative geniculate Y cell dendritic arbors that continued past the second postnatal month. In contrast, the growth of interneurons appeared to be complete by 3-4 postnatal weeks, at which time cell somas stained with SMI-32 have only reached a little over one half of their adult size. Similar to the adult cat, SMI-32 appears to selectively stain the Y cell population during development and may provide a useful morphological marker to examine the participation of Y cells in the developing postnatal circuitry of the dLGN. This further establishes the cat dLGN as a novel model system to study the normal function and pathological reorganization of neurofilaments.

Development of the cholinergic, nitrergic, and GABAergic innervation of the cat dorsal lateral geniculate nucleus.

Cholinergic projections from the brainstem have been shown to be important modulators of visual activity in the dorsal lateral geniculate nucleus (dLGN) of the adult, but little is known about the role of these modulatory inputs during development. We examined the postnatal development of the cholinergic innervation of the dLGN by using an monoclonal antibody against choline acetyl transferase (ChAT). We also investigated the development of GABAergic interneurons in the dLGN by using an antibody against glutamic acid decarboxylase (GAD), and the developmental expression of brain nitric oxide synthase (BNOS) by using an antibody against this enzyme. We found that brainstem cells surrounding the brachium conjunctivum express ChAT at birth, although axons in the dLGN do not express ChAT until the end of the first postnatal week. Cholinergic synaptic contacts were observed as early as the second postnatal week. The number of axons stained with the ChAT antibody increased slowly during the subsequent weeks in the dLGN and reached adult levels by the eighth postnatal week. GABAergic interneurons were present at birth and reached their adult soma size by the third postnatal week. GABAergic fibers are dense at birth but change during development from a diffuse pattern to clustered arrangements that can be recognized as distinct rings of GAD staining by P35. Cellular expression of BNOS was seen within all dLGN laminae during development. The BNOS-stained cells are tentatively identified as interneurons because their soma sizes were similar to those of GAD-stained cells. Although cellular BNOS staining remained robust in the C1-3 laminae through adulthood, cellular expression of BNOS in the A laminae declined during the first five postnatal weeks and remains sparse in the adult. As cellular BNOS staining declined, there was a steady increase in BNOS-stained fibers, which paralleled the increase of ChAT-stained fibers that are known to colocalize BNOS in the adult. Our results emphasize the continued transformations of intrinsic as well as extrinsic innervation patterns that occur during the development, of the dLGN.