Immunocytochemical localization of the NMDA-R2A receptor subunit in the cat retina

Distinct perisynaptic and synaptic localization of NMDA and AMPA receptors on ganglion cells in rat retina

“…Second, in previous studies of synaptic glutamate receptor localization in the IPL (Hartveit et al, 1994;Pourcho, 1996,1999;Fletcher et al, 2000;Pourcho et al, 2001;Hack et al, 2002), the specific cellular identity of the immunopositive postsynaptic processes was not positively determined. NMDAR-immunopositive processes, therefore, may have belonged to amacrine cells, a subset of which receive synaptic inputs mediated by NMDARs (Dixon and Copenhagen, 1992;Goebel et al, 1998;Fletcher et al, 2000;Gründer et al, 2000). Here, retrograde labeling of RGCs by CTB provided a reliable marker of RGC process in the IPL (Figure 2), enabling receptor localization to be examined on identified RGC processes.…”

“…AB1557P) was raised in rabbit against an affinity-purified C-terminal fusion protein (amino acids 984-1104). This antibody has been characterized previously in rat and cat retina by Western blotting (recognizing a band at ~ 180 kD) and immunocytochemistry (Goebel et al, 1998;Gründer et al, 2000;Pourcho et al, 2001). Polyclonal anti-GluR2/3 (Cat.…”

Neuronal nitric oxide synthase immunoreactive neurons in the mammalian retina

“…In the brain, NO has also been shown to modulate the activity of ␥-aminobutyric acid A (GABA A ) receptors (Zarri et al, 1994;Wexler et al, 1998) and NMDA receptors (Lei et al, 1992;Manzoni et al, 1992;Manzoni and Bockaert, 1993). In the mammalian retina, a subset of amacrine cells, displaced amacrine cells, and ganglion cells have been shown to express GABA A receptors (Hughes et al, 1989(Hughes et al, , 1991Brecha, 1991Brecha, , 1992Greferath et al, 1993;Grü nert and Hughes, 1993;Wä ssle et al, 1998) and NMDA receptors (Hartveit et al, 1994;Brandstä tter et al, 1998;Goebel et al, 1998). Thus, NO could influence both amacrine cells and ganglion cells.…”

Inhibition of N-Methyl-d-aspartate-induced Retinal Neuronal Death by Polyarginine Peptides Is Linked to the Attenuation of Stress-induced Hyperpolarization of the Inner Mitochondrial Membrane Potential

“…Implicated in these disorders, the N-methyl-D-aspartate subtype of glutamate receptor (NMDAR), 2 which contributes to ON and OFF light-evoked responses in retinal ganglion cells (RGC) (5), has also been linked to mitochondrial dysfunction and RGC death when hyperstimulated (6 -8). Both RGCs and a large population of NMDAR-expressing amacrine cells (9,10) are highly susceptible to cell death in the presence of elevated levels of glutamate (11,12), whereby excessive calcium perturbs the mitochondrial membrane potential (⌬⌿ m ) promoting both programmed and nonprogrammed cell death pathways (7,13). In particular, the C terminus of the NMDAR GluN2B subunit contains a motif with high affinity for the PSD-95/Discs-large/ ZO-1 homology (PDZ) scaffold protein PSD-95 (14) that is believed to couple PSD-95 to neuronal nitric oxide synthase (NOS), resulting in a pro-death decrease in CREB activity (15).…”