We have studied the presence and distribution of α-amino-3–hydroxy-5–methyl-4–isoxazolepropionate (AMPA)-selective glutamate receptor subunits (GluR 1, 2, 3, and 4) in the adult cat visual cortical areas 17, 18, 19, and the lateral suprasylvian areas (LSA). Reverse transcription-polymerase chain reaction (RT-PCR) amplification indicated that the genes encoding GluR 1, 2, 3, and 4 are expressed in these areas and Western blot analysis revealed that the size of the corresponding peptides is similar to those described in the rat brain. In situ hybridization (ISH) using digoxigenin-labeled riboprobes showed that mRNAs coding for GluR1 and GluR3 were located in cells in all layers of the areas examined and also in the underlying white matter. GluR1 mRNA was relatively abundant throughout layers II–VI while GluR3 mRNA revealed a more laminated pattern of expression, preferentially labeling cells in layers II, III, V, and VI. The distribution of AMPA-selective receptor subunit peptides was studied by immunohistochemistry using subunit specific antibodies and found to be consistent with ISH results. In addition, we observed that most of the cells strongly labeled by the anti-GluR1 antibody were non-pyramidal neurons and that intense GluR2/3 immunoreactivity was seen preferentially in pyramidal neurons. Interestingly, double-labeling experiments indicated that neurons expressing γ-aminobutyric acid (GABA) as well as the GluR1 subunit were particularly abundant in deeper layers. The GluR4 peptide was predominantly found in a relatively low number of layer III and layer V neurons with either pyramidal or non-pyramidal morphology. Finally, the distribution of neurons expressing the various receptor subunits was similar in all the visual cortical areas studied. These findings indicate a high expression of GluR1–3 subunits in the cat visual cortex and that GluR1 and GluR2/3 subunits are particularly abundant in non-pyramidal and pyramidal neurons, respectively. In addition, the results described here provide a reference for future studies dealing with the effect of visual deprivation on the expression of this receptor type.

The role of excitatory amino acid (EAA) receptors in primate retinal ganglion cell function was analyzed in a superfused retina-eyecup preparation using single-unit, extracellular recording techniques. The effects of bath applied L-2–amino-4–phosphonobutyrate (APB), N-methyl-D-aspartate (NMDA), and non-NMDA EAA receptor agonists and antagonists were examined on the light-evoked responses and resting firing rates of ganglion cells. APB (30–100 μM) reduced or blocked the light-evoked responses and resting firing rates of all ON-center ganglion cells; higher doses of APB (100 μM) were required to block the light-evoked responses of ON-transient cells. In contrast, an increase in resting firing rates was observed when L-APB was applied to some OFF-center ganglion cells. The EAA agonists kainate (KA) (10–20 μM) and NMDA (200–350 μM) increased the firing rate of virtually all ganglion cells examined. Quisqualate (10–20 μM) increased firing in most cells, but occasionally (4/13 cases) produced inhibition. The NMDA antagonist D-amino-phosphono-heptanoic acid (D-AP7) (200–250 μM) reduced the light-evoked responses of ganglion cells by an average of 12% from control levels, while resting firing rates declined 37%. In the presence of D-AP7, the basic receptive-field characteristics of cells were not significantly altered. In contrast, two non-NMDA receptor antagonists, NBQX (2,3–Dihydroxy-6–nitro-7–sulfamoyl-benzo-(F)-quinoxalinedione) and DNQX (6,7–dinitro-quinoxaline-2,3–dione), produced substantial reductions in the light-evoked responses (82%) and resting firing rates (87%) of all ganglion cell classes. A striking observation in some neurons was the recovery of a persistent transient light-evoked response in the presence of NBQX. This NBQX-insensitive, light-evoked response was always blocked by adding D-AP7. Thus, neurotransmission from bipolar to ganglion cells in primates is mediated predominantly by non-NMDA EAA receptors, with NMDA receptors forming a minor component of the light-evoked response.

The role of N-methyl-D-aspartate (NMDA) receptors in the mediation of cortical inputs to visual neurones in the superficial layers of the superior colliculus (SSC) has been investigated. Extracellular recording with iontophoresis in the SSC of cortically intact cats has demonstrated that visual responses of most neurones were reduced by iontophoretic application of the NMDA receptor antagonist D-2-amino-5-phosphonopentanoate (APS). Following inactivation of areas 17 and 18 of the visual cortex with topical lignocaine, the visual responses of 11, previously AP5-sensitive, neurones were no longer reduced by APS ejection. The cortical input is generally assumed to influence the directional responses of visual neurones in SSC. However, detailed study of the directional bias showed that the degree of directional tuning in SSC neurones was similar to that of retinal ganglion cells, as previously described by others. Moreover, inactivation of the visual cortex with topical lignocaine did not alter the directional bias of SSC neurones. Likewise, the directional bias of SSC neurones was not reduced by iontophoretic ejection of APS in the SSC. These data imply that NMDA receptors have an important role in mediating the cortical input to the SSC. However, cortical input does not appear to be responsible for conferring directional bias upon SSC neurones' visual responsiveness.