scholarly journals Effect of excitatory amino acids and analogues on [3H]acetylcholine release from amacrine cells of the rabbit retina.

1985 ◽  
Vol 366 (1) ◽  
pp. 47-62 ◽  
Author(s):  
J R Cunningham ◽  
M J Neal
Keyword(s):  
Amino Acids ◽  
Excitatory Amino Acids ◽  
Acetylcholine Release ◽  
Amacrine Cells ◽  
Rabbit Retina

scholarly journals AMPA receptors mediate acetylcholine release from starburst amacrine cells in the rabbit retina

2003 ◽  
Vol 466 (1) ◽  
pp. 80-90 ◽  
Author(s):  
Sally I. Firth ◽  
Wei Li ◽  
Stephen C. Massey ◽  
David W. Marshak
Keyword(s):  
Ampa Receptors ◽  
Acetylcholine Release ◽  
Amacrine Cells ◽  
Rabbit Retina ◽  
Starburst Amacrine Cells

A comparison of the inhibitory actions of glycine and GABA on acetylcholine release from the rabbit retina

1998 ◽  
Vol 15 (6) ◽  
pp. 1057-1065 ◽  
Author(s):  
DAVID M. LINN
Keyword(s):  
Acetylcholine Release ◽  
Amacrine Cells ◽  
Rabbit Retina ◽  
Evoked Responses ◽  
Ach Release ◽  
Cholinergic Pathway ◽  
Basal Release ◽  
Temporal Inhibition ◽  
Sustained Inhibition

The inhibition of [3H]acetylcholine (ACh) release from cholinergic amacrine cells by glycine and GABA was studied using an in vivo eyecup preparation in anesthetized rabbits. Glycine (1 mM) had no effect on basal ACh release, but completely blocked the light-evoked release of ACh. Glycine also blocked the strong potentiating effects of picrotoxin (20 μM) normally observed on basal and light-evoked release. Strychnine (20 μM) increased basal release, albeit less than picrotoxin, but partially inhibited and altered the shape of light-evoked responses. Co-perfusion of picrotoxin and strychnine after strychnine application resulted in a larger additional basal increase. However, light-evoked responses were not restored to a control shape and magnitude, or to potentiated levels as with picrotoxin alone, but remained altered and partially inhibited. These results support the concept of a sustained GABA-mediated inhibition of the cholinergic pathway in the intact retina. In contrast, glycine-mediated inhibition of the cholinergic pathway differs, with the present results indicating a significantly smaller sustained inhibition of basal release and a temporal inhibition of light-evoked release. The lack of effect of any of these compounds on kainate-evoked responses indicates that these effects are predominately indirect, possibly on the presynaptic bipolar cell.

The resting release of acetylcholine by a retinal neuron

1987 ◽  
Vol 232 (1267) ◽  
pp. 227-238 ◽  
Keyword(s):  
Neuromuscular Junction ◽  
Acetylcholine Release ◽  
Biological Significance ◽  
Amacrine Cells ◽  
Rabbit Retina ◽  
Retinal Neuron ◽  
Independent Mechanism ◽  
Release Of Acetylcholine ◽  
Stimulation Of ◽  
Cholinergic Amacrine Cells

The cholinergic amacrine cells of the rabbit retina secrete acetylcholine by two mechanisms. One is activated by stimulation of the retina by light or depolarization of the amacrine cells by K + ions. It requires the presence of extracellular Ca 2+ . The second is independent of extracellular Ca 2+ and is unaffected by large depolarizations of the cells. It bears some similarity to the acetylcholine ‘leakage’ described at the neuromuscular junction. Although the Ca 2+ -independent mechanism accounts for about two thirds of the total acetylcholine release in the dark, the amount of acetylcholine released in this way is small compared with the release of acetylcholine triggered by stimulation of the retina with light. Its biological significance is unclear.

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