scholarly journals Baclofen enhancement of acetylcholine release from amacrine cells in the rabbit retina by reduction of glycinergic inhibition.

1995 ◽  
Vol 482 (2) ◽  
pp. 363-372 ◽  
Author(s):  
M J Neal ◽  
J R Cunningham
Keyword(s):  
Acetylcholine Release ◽  
Amacrine Cells ◽  
Rabbit Retina ◽  
Glycinergic Inhibition

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.

Comparison of the responses of AII amacrine cells in the dark- and light-adapted rabbit retina

1999 ◽  
Vol 16 (4) ◽  
pp. 653-665 ◽  
Author(s):  
DAIYAN XIN ◽  
STEWART A. BLOOMFIELD
Keyword(s):  
Receptive Field ◽  
Light Adaptation ◽  
Amacrine Cells ◽  
Bipolar Cells ◽  
Rabbit Retina ◽  
Response Component ◽  
Synaptic Inputs ◽  
Field Organization ◽  
Receptive Field Organization ◽  
Aii Amacrine Cells

We studied the light-evoked responses of AII amacrine cells in the rabbit retina under dark- and light-adapted conditions. In contrast to the results of previous studies, we found that AII cells display robust responses to light over a 6–7 log unit intensity range, well beyond the operating range of rod photoreceptors. Under dark adaptation, AII cells showed an ON-center/OFF-surround receptive-field organization. The intensity–response profile of the center-mediated response component followed a dual-limbed sigmoidal function indicating a transition from rod to cone mediation as stimulus intensities were increased. Following light adaptation, the receptive-field organization of AII cells changed dramatically. Light-adapted AII cells showed both ON- and OFF-responses to stimulation of the center receptive field, but we found no evidence for an antagonistic surround. Interestingly, the OFF-center response appeared first following rapid light adaptation and was then replaced gradually over a 1–4 min period by the emerging ON-center response component. Application of the metabotropic glutamate receptor agonist APB, the ionotropic glutamate blocker CNQX, 8-bromo-cGMP, and the nitric oxide donor SNAP all showed differential effects on the various center-mediated responses displayed by dark- and light-adapted AII cells. Taken together, these pharmacological results indicated that different synaptic circuits are responsible for the generation of the different AII cell responses. Specifically, the rod-driven ON-center responses are apparently derived from rod bipolar cell synaptic inputs, whereas the cone-driven ON-center responses arise from signals crossing the gap junctions between AII cells and ON-center cone bipolar cells. Additionally, the OFF-center response of light-adapted AII cells reflects direct synaptic inputs from OFF-center cone bipolar cells to AII dendritic processes in the distal inner plexiform layer.

Amacrine-to-amacrine cell inhibition: Spatiotemporal properties of GABA and glycine pathways

2011 ◽  
Vol 28 (3) ◽  
pp. 193-204 ◽  
Author(s):  
XIN CHEN ◽  
HAIN ANN HSUEH ◽  
FRANK S. WERBLIN
Keyword(s):  
Amacrine Cell ◽  
Ganglion Cells ◽  
Amacrine Cells ◽  
Peak Level ◽  
Wide Field ◽  
Gabaergic Inhibition ◽  
Onset Latency ◽  
Temporal Properties ◽  
Glycinergic Inhibition ◽  
Cell Inhibition

AbstractWe measured the spatial and temporal properties of GABAergic and glycinergic inhibition to amacrine cells in the whole-mount rabbit retina. The amacrine cells were parsed into two morphological classes: narrow-field cells with processes spreading less than 200 μm and wide-field cells with processes extending more than 300 μm. The inhibition was also parsed into two types: sustained glycine and transient GABA. Narrow-field amacrine cells receive 1) very transient GABAergic inhibition with a fast onset latency of 140 ± 16 ms decaying to 30% of the peak level within 208 ± 27 ms elicited broadly over a lateral distance of up to 1500 μm and 2) sustained glycinergic inhibition with a medium onset latency of 286 ± 23 ms that was elicited over a spatial area often broader than the processes of the narrow-field amacrine cells. Wide-field amacrine cells received sustained glycinergic inhibition but no broad transient GABAergic inhibition. Surprisingly, neither of these amacrine cell classes received sustained local GABAergic inhibition, commonly found in an earlier study of ganglion cells.

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