TY - JOUR
T1 - Glutamate receptors of ganglion cells in the rabbit retina
T2 - evidence for glutamate as a bipolar cell transmitter.
AU - Massey, S. C.
AU - Miller, R. F.
N1 - Copyright:
Copyright 2016 Elsevier B.V., All rights reserved.
PY - 1988/11/1
Y1 - 1988/11/1
N2 - 1. Intracellular and extracellular recordings were obtained from ganglion cells in the rabbit retina. The effects of glutamate analogues and antagonists were studied using a perfusion method for drug application. 2. Kainate (KA) excited all ganglion cells directly and caused a large increase in firing rate. N‐Methyl‐DL‐aspartate (NMDLA) also excited ganglion cells but it was less potent and caused burst firing. 3. Quisqualate (QQ) and (RS)‐2‐amino‐3‐hydroxy‐5‐methyl‐isoxazole‐4‐propionic acid (AMPA) excited many ganglion cells and were approximately as potent as KA. Less frequently, QQ and AMPA had inhibitory effects possibly due to polysynaptic action. 4. General glutamate antagonists such as cis‐2,3‐piperidine dicarboxylic acid (PDA) and kynurenic acid blocked the light input to all ganglion cells. PDA and kynurenic acid blocked the effects of KA and NMDLA, but not carbachol, indicating that they act as glutamate antagonists in the rabbit retina. Kynurenic acid did not block the excitatory action of QQ, even though light responses were abolished. 5. Amacrine cells were depolarized by KA or QQ and less potently by NMDLA. Their light‐evoked responses were blocked by PDA. 6. We conclude that the light input to ganglion cells in the rabbit retina is predominantly mediated by KA receptors. This is consistent with the idea that ‘on’ and ‘off’ bipolar cells are excitatory and release glutamate.
AB - 1. Intracellular and extracellular recordings were obtained from ganglion cells in the rabbit retina. The effects of glutamate analogues and antagonists were studied using a perfusion method for drug application. 2. Kainate (KA) excited all ganglion cells directly and caused a large increase in firing rate. N‐Methyl‐DL‐aspartate (NMDLA) also excited ganglion cells but it was less potent and caused burst firing. 3. Quisqualate (QQ) and (RS)‐2‐amino‐3‐hydroxy‐5‐methyl‐isoxazole‐4‐propionic acid (AMPA) excited many ganglion cells and were approximately as potent as KA. Less frequently, QQ and AMPA had inhibitory effects possibly due to polysynaptic action. 4. General glutamate antagonists such as cis‐2,3‐piperidine dicarboxylic acid (PDA) and kynurenic acid blocked the light input to all ganglion cells. PDA and kynurenic acid blocked the effects of KA and NMDLA, but not carbachol, indicating that they act as glutamate antagonists in the rabbit retina. Kynurenic acid did not block the excitatory action of QQ, even though light responses were abolished. 5. Amacrine cells were depolarized by KA or QQ and less potently by NMDLA. Their light‐evoked responses were blocked by PDA. 6. We conclude that the light input to ganglion cells in the rabbit retina is predominantly mediated by KA receptors. This is consistent with the idea that ‘on’ and ‘off’ bipolar cells are excitatory and release glutamate.
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U2 - 10.1113/jphysiol.1988.sp017353
DO - 10.1113/jphysiol.1988.sp017353
M3 - Article
C2 - 2908248
AN - SCOPUS:0023687073
VL - 405
SP - 635
EP - 655
JO - Journal of Physiology
JF - Journal of Physiology
SN - 0022-3751
IS - 1
ER -