El. Fletcher et M. Kalloniatis, NEUROCHEMICAL ARCHITECTURE OF THE NORMAL AND DEGENERATING RAT RETINA, Journal of comparative neurology, 376(3), 1996, pp. 343-360
We used post-embedding immunocytochemistry to determine the cellular l
ocalization of glutamate, gamma-amino butyric acid (GABA), glycine, as
partate, glutamine, arginine, and taurine in the normal and degenerati
ng rat retina. Muller's cell function was also evaluated by determinin
g the uptake and degradation characteristics for glutamate. Immunocyto
chemical localization of amino acids in adult Royal College of Surgeon
s (RCS) and control rat retinas were similar with respect to cell clas
ses. Differences in the intensity of labelling for glutamate, aspartat
e, glutamine, and glycine were observed in several classes of neurons,
but the most prominent differences were shown by bipolar cells of the
adult RCS rat retina. In addition, glutamine labelling within Muller'
s cells was higher in the RCS rat than the control. These changes may
have occurred because of alterations in the glutamate production or de
gradation pathways. We tested this hypothesis by determining Muller's
cells glutamate uptake and degradation characteristics in adult and po
stnatal day 16 RCS retinas. High affinity uptake of (3)[H]-glutamate r
evealed an accumulation of grains over Muller's cell bodies in the adu
lt RCS retina implying glutamate degradation anomalies. We confirmed a
nomalies in glutamate metabolism in RCS Muller's cells by showing that
exogenously applied glutamate was degraded over a longer time course
in postnatal day 16 RCS retinas, compared to control retinas. Differen
ces in arginine immunoreactivity in adult and immature RCS retinas con
form to the presumed dysfunction of Muller's cells in these degenerati
ng retinas. The anomalies of amino acid localization, uptake and degra
dation lead us to conclude that Muller's cells in the RCS retina show
abnormal function by postnatal day 16; an earlier time to previously r
eported anatomical and functional changes in this animal model of reti
nal degeneration. (C) 1996 Wiley-Liss, Inc.