In normal adult cats, a monoclonal antibody directed
toward the NR-1 subunit of the N-methyl-d-aspartate
(NMDA) receptor (Pharmingen, clone 54.1) produced dense
cellular and neuropil labeling throughout all layers of
the lateral geniculate nucleus (LGN) and adjacent thalamic
nuclei, including the thalamic reticular, perigeniculate,
medial intralaminar, and ventral lateral geniculate nuclei.
Cellular staining revealed well-defined somata, and in
some cases proximal dendrites. NMDAR-1 cell labeling was
also evident in the LGN of early postnatal kittens, suggesting
that developing LGN cells possess this receptor subunit
at or before eye opening. Within the A-layers of the adult
LGN, staining encompassed a wide range of soma sizes. Soma
size comparisons of NMDAR-1 stained cells with those stained
with an antibody directed toward a nonphosphorylated neurofilament
protein (SMI-32), which selectively stains Y-relay cells
(Bickford et al., 1998), or an antibody to glutamic acid
decarboxylase (GAD), which stains for GABAergic interneurons,
suggested that NMDA receptors are utilized by relay cells
and interneurons. NMDAR-1 staining was also observed in
the LGN of cats with early monocular lid suture. Although
labeling was apparent in both deprived and nondeprived
A-layers of LGN, the distribution of soma sizes was significantly
different. In the deprived A-layers of LGN, staining was
limited to small- and medium-sized cells. Cells with relatively
large soma were lacking. However, cell density measurements
as well as soma size comparisons with cells stained for
Nissl substance suggested these differences were due to
deprivation-induced cell shrinkage and not to a loss of
NMDAR-1 staining in Y-cells. Taken together, these results
suggest that NMDA receptors are utilized by both relay
cells and interneurons in LGN and that alterations in early
visual experience do not necessarily affect the expression
of NMDA receptors in the LGN.