Immunocytochemical staining of AII-amacrine cells in the rat retina with antibodies against parvalbumin

1993 ◽  
Vol 332 (4) ◽  
pp. 407-420 ◽  
Author(s):  
Heinz Wäussle ◽  
Ulrike Grüunert ◽  
Jürgen Röhrenbeck
2004 ◽  
Vol 480 (3) ◽  
pp. 251-263 ◽  
Author(s):  
Gloria J. Partida ◽  
Sherwin C. Lee ◽  
Leah Haft-Candell ◽  
Grant S. Nichols ◽  
Andrew T. Ishida

1997 ◽  
Vol 77 (4) ◽  
pp. 1716-1730 ◽  
Author(s):  
Espen Hartveit

Hartveit, Espen. Functional organization of cone bipolar cells in the rat retina. J. Neurophysiol. 77: 1716–1730, 1997. The responses of cone bipolar cells in slices of rat retina to ionotropic glutamate receptor agonists were recorded with the whole cell voltage-clamp technique in the presence of 5 mM Co2+ and nominally 0 mM Ca2+ extracellularly. Application of the non- N-methyl-d-aspartate (non-NMDA) receptor agonists kainate and (S)-α-amino-3-hydroxy-5-methyl-4-isoxazolepropionate had a series of effects on cone bipolar cells (types 1–9), and the different cell types could be classified as on- or off-type cells according to which type(s) of responses they displayed. First, direct responses were observed in cell types 1–4 as short-latency inward currents at −70 mV with reversal potentials ( E revs) close to 0 mV, characteristic of nonselective cation channels. Second, some cells, among types 5–9, did not display short-latency inward currents to kainate at −70 mV. Other type 5–8 cells displayed short-latency kainate responses, but the currents could not be reversed ( E rev of +40 mV or greater). I suggest that these responses are conveyed to the cone bipolar cells through gap junctions, most likely with AII amacrine cells. The lack of reversal is likely due to a substantial voltage drop across the gap junctions resulting in an inadequate voltage control of AII amacrine cells when the recording pipette is on the cone bipolar cell. Kainate responses recorded directly from AII amacrine cells had E rev ∼ 0 mV. Third, long-latency indirect responses selective for chloride ions ( E rev ∼ chloride equilibrium potential) were observed in many cone bipolar cells during longer-lasting application of kainate. The long-latency response component was suppressed by coapplication of the γ-aminobutyric acid-A (GABAA) receptor antagonist picrotoxin and the GABAC receptor antagonist 3-aminopropyl(methyl)phosphinic acid. This long-latency component was absent in axotomized bipolar cells, suggesting that it was due to external Ca2+-independent release of GABA onto the axon terminals of the cone bipolar cells. All kainate-evoked response components were blocked by the non-NMDA receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione. Application of NMDA evoked no response in cone bipolar cells. These results suggest that cone bipolar cells types 1–4 are off cone bipolar cells, whereas cone bipolar cells types 5–9 are on cone bipolar cells.


2014 ◽  
Vol 127 (6) ◽  
pp. 1190-1202 ◽  
Author(s):  
A. Meyer ◽  
G. Hilgen ◽  
B. Dorgau ◽  
E. M. Sammler ◽  
R. Weiler ◽  
...  

2009 ◽  
Vol 101 (5) ◽  
pp. 2339-2347 ◽  
Author(s):  
Margaret Lin Veruki ◽  
Espen Hartveit

Gap junction channels constitute specialized intercellular contacts that can serve as electrical synapses. In the rod pathway of the retina, electrical synapses between AII amacrine cells express connexin 36 (Cx36) and electrical synapses between AII amacrines and on-cone bipolar cells express Cx36 on the amacrine side and Cx36 or Cx45 on the bipolar side. For physiological investigations of the properties and functions of these electrical synapses, it is highly desirable to have access to potent pharmacological blockers with selective and reversible action. Here we use dual whole cell voltage-clamp recordings of pairs of AII amacrine cells and pairs of AII amacrine and on-cone bipolar cells in rat retinal slices to directly measure the junctional conductance ( Gj) between electrically coupled cells and to study the effect of the drug meclofenamic acid (MFA) on Gj. Consistent with previous tracer coupling studies, we found that MFA reversibly blocked the electrical synapse currents in a concentration-dependent manner, with complete block at 100 μM. Whereas MFA evoked a detectable decrease in Gj within minutes of application, the time to complete block of Gj was considerably longer, typically 20–40 min. After washout, Gj recovered to 20–90% of the control level, but the time to maximum recovery was typically >1 h. These results suggest that MFA can be a useful drug to investigate the physiological functions of electrical synapses in the rod pathway, but that the slow kinetics of block and reversal might compromise interpretation of the results and that explicit monitoring of Gj is desirable.


2013 ◽  
Vol 14 (S1) ◽  
Author(s):  
Hermann Riecke ◽  
Hannah Choi ◽  
Mark S Cembrowski ◽  
William L Kath ◽  
Joshua H Singer

2018 ◽  
Vol 28 (17) ◽  
pp. 2739-2751.e3 ◽  
Author(s):  
Cole W. Graydon ◽  
Evan E. Lieberman ◽  
Nao Rho ◽  
Kevin L. Briggman ◽  
Joshua H. Singer ◽  
...  

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