Dendritic maturation of displaced putative cholinergic amacrine cells in the rabbit retina

1989 ◽  
Vol 287 (2) ◽  
pp. 164-178 ◽  
Author(s):  
R. O. L. Wong ◽  
S. P. Collin
Keyword(s):  
Amacrine Cells ◽  
Rabbit Retina ◽  
Cholinergic Amacrine Cells

GABA inhibits ACh release from the rabbit retina: A direct effect or feedback to bipolar cells?

1992 ◽  
Vol 8 (2) ◽  
pp. 97-106 ◽  
Author(s):  
David M. Linn ◽  
Stephen C. Massey
Keyword(s):  
Direct Effect ◽  
Negative Feedback ◽  
Bipolar Cell ◽  
Amacrine Cells ◽  
Bipolar Cells ◽  
Rabbit Retina ◽  
Ach Release ◽  
Gaba Antagonists ◽  
Direct Input ◽  
Cholinergic Amacrine Cells

AbstractThe cholinergic amacrine cells of the rabbit retina may be labeled with [3H]-Ch and the activity of the cholinergic population monitored by following the release of [3H]-ACh. We have tested the effect of muscimol, a potent GABAA agonist, on (1) the light-evoked release of ACh, presumably mediated via bipolar cells, which are known to have a direct input to the cholinergic amacrine cells and (2) ACh release produced by exogenous glutamate analogs that probably have a direct effect on cholinergic amacrine cells. Muscimol blocked the light-evoked release of ACh with an IC50 of 1.0 μM. In contrast, ACh release produced by nonsaturating doses of kainate or NMDA was not reduced even by 100 μM muscimol. Thus, we have been unable to demonstrate a direct effect of GABA on the cholinergic amacrine cells.GABA antagonists, such as picrotoxin, caused a large increase in the base release and potentiated the light-evoked release of ACh. Both these effects were abolished by DNQX, a kainate antagonist that blocks the input to cholinergic amacine cells from bipolar cells. DNQX blocked the effects of picrotoxin even when controls showed that the mechanism of ACh release was still functional. Together, these results imply that the dominant site for the GABA-mediated inhibition of ACh release is on the bipolar cell input to the cholinergic amacrine cells. This is consistent with previous anatomical and physiological evidence that bipolar cells receive negative feedback from GABA amacrine cells.

GABA-like immunoreactivity in cholinergic amacrine cells of the rabbit retina

1988 ◽  
Vol 438 (1-2) ◽  
pp. 369-373 ◽  
Author(s):  
David I. Vaney ◽  
Heather M. Young
Keyword(s):  
Amacrine Cells ◽  
Rabbit Retina ◽  
Cholinergic Amacrine Cells

Cholinergic amacrine cells in the rabbit retina accumulate muscimol

1991 ◽  
Vol 6 (2) ◽  
pp. 113-117 ◽  
Author(s):  
Stephen C. Massey ◽  
Kevin Blankenship ◽  
Stephen L. Mills
Keyword(s):  
Ganglion Cell ◽  
Ganglion Cell Layer ◽  
Cell Layer ◽  
Plexiform Layer ◽  
Amacrine Cells ◽  
Inner Plexiform Layer ◽  
Rabbit Retina ◽  
Neuronal Marker ◽  
Dapi Fluorescence ◽  
Cholinergic Amacrine Cells

AbstractThe cholinergic amacrine cells of the rabbit retina form two mosaics placed symmetrically on either side of the inner plexiform layer. Recently, these cells have been reported to contain immunocytochemical markers for GABA. In this paper, we labeled the cholinergic cells with DAPI, then incubated the retina in [3H]-muscimol, a neuronal marker for GABA. Subsequently, we converted the DAPI fluorescence of the displaced cholinergic matrix to an opaque product by photooxidation in the presence of DAB. Autoradiography showed that all of the displaced cholinergic amacrine cells were labeled with ]3H]-muscimol, thus confirming the immunocytochemical results. The cholinergic cells account for approximately 80% of the cells in the ganglion cell layer which take up ]3H]-muscimol.

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