Ultrastructural evidence that horizontal cell axon terminals are presynaptic in the human retina

1988 ◽  
Vol 268 (2) ◽  
pp. 281-297 ◽  
Author(s):  
Kenneth A. Linberg ◽  
Steven K. Fisher
Nature ◽  
1979 ◽  
Vol 280 (5717) ◽  
pp. 60-62 ◽  
Author(s):  
RICHARD A. NORMANN ◽  
HELGA KOLB ◽  
MENACHEM HANANI ◽  
EFREM PASINO ◽  
RICHARD HOLUB

1999 ◽  
Vol 260 (3) ◽  
pp. 185-188 ◽  
Author(s):  
Chang-Sub Jung ◽  
Sung-Jong Lee ◽  
Sun-Sook Paik ◽  
Sun-Ho Bai

1985 ◽  
Vol 359 (1-2) ◽  
pp. 104-112 ◽  
Author(s):  
K. Negishi ◽  
T. Teranishi ◽  
S. Kato

1991 ◽  
Vol 6 (4) ◽  
pp. 357-370 ◽  
Author(s):  
You-Wel Peng ◽  
Dominic Man-Kit lam

AbstractWe have produced and characterized a monoclonal antibody, AT101, which selectively labels both viable and formaldehyde-fixed horizontal cell axon terminals, but not their somas or axons, of the goldfish (Carassius auratus) retina. The antigen recognized by AT101 appears to be a cell surface glycoprotein with a molecular weight of about 35,000 Daltons, and is present exclusively or predominantly in nervous tissues of all vertebrate species examined. We have used AT101 as a probe to analyze immunocytochemically the organization of horizontal cell axon terminals (HCATs) in the adult goldfish retina, and the emergence and maturation of these terminals during retinal development. Because of continued growth at the retinal margin in adult goldfish, there is a peripheral-to-central gradient in the age of cells, with the most mature in the center and the youngest in the periphery. In the center and near periphery of the adult retina, HCATs have a fusiform morphology and form a dense network in the middle and proximal part of the inner nuclear layer. In the far peripheral retina, the axon terminals appear round or ellipsoid. The retina closest to the retinal margin is devoid of AT101 staining, indicating that either HCATs are absent or the antigen recognized by AT101 is not present on HCATs at this stage. A similar sequence of changes in staining pattern is seen during development. Although AT101 staining can first be demonstrated in the larval retina at 1 month after hatching, it appears mostly as punctate structures. At a later stage, there are round or ellipsoid structures that resemble in morphology and location (in the inner nuclear layer) those found in the far peripheral adult retina. Double-labeling experiments with AT101 and antiserum against tubulin also indicate that AT101 labels the HCATs when they first appear during development. These data suggest that the emergence and maturation of HCAT is a late event in retinal development.


Neuron ◽  
2021 ◽  
Author(s):  
Akihiro Matsumoto ◽  
Weaam Agbariah ◽  
Stella Solveig Nolte ◽  
Rawan Andrawos ◽  
Hadara Levi ◽  
...  

1998 ◽  
Vol 80 (2) ◽  
pp. 1011-1015 ◽  
Author(s):  
Matt Wachowiak ◽  
Lawrence B. Cohen

Wachowiak, Matt and Lawrence B. Cohen. Presynaptic afferent inhibition of lobster olfactory receptor cells: reduced action-potential propagation into axon terminals. J. Neurophysiol. 80: 1011–1015, 1998. Action-potential propagation into the axon terminals of olfactory receptor cells was measured with the use of voltage-sensitive dye imaging in the isolated spiny lobster brain. Conditioning shocks to the olfactory nerve, known to cause long-lasting suppression of olfactory lobe neurons, allowed the selective imaging of activity in receptor cell axon terminals. In normal saline the optical signal from axon terminals evoked by a test stimulus was brief (40 ms) and small in amplitude. In the presence of low-Ca2+/high-Mg2+ saline designed to reduce synaptic transmission, the test response was unchanged in time course but increased significantly in amplitude (57 ± 16%, means ± SE). This increase suggests that propagation into receptor cell axon terminals is normally suppressed after a conditioning shock; this suppression is presumably synaptically mediated. Thus our results show that presynaptic inhibition occurs at the first synapse in the olfactory pathway and that the inhibition is mediated, at least in part, via suppression of action-potential propagation into the presynaptic terminal.


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