Whole-cell currents activated at nicotinic acetylcholine receptors on ganglion cells isolated from goldfish retina

1993 ◽  
Vol 10 (2) ◽  
pp. 353-361 ◽  
Author(s):  
Bruce Yazejian ◽  
Gordon L. Fain
Keyword(s):  
Retinal Ganglion Cells ◽  
Nicotinic Acetylcholine Receptors ◽  
Acetylcholine Receptors ◽  
Ganglion Cells ◽  
Hill Coefficient ◽  
Retinal Ganglion ◽  
Whole Cell ◽  
Induced Currents ◽  
Inwardly Rectifying ◽  
Goldfish Retina

AbstractWe have recorded whole-cell membrane currents in response to exogenously applied acetylcholine (ACh), nicotine, and 1,1 dimethyl-4-phenyl piperazinium iodide on retinal ganglion cells enzymatically dissociated from goldfish retina. Agonist applications induced nicotinic-type responses in a majority of cells when cells were isolated under optimal conditions. Currents were reminiscent of nicotinic-type ganglionic responses. Dose-response measurements of ACh-induced currents indicated an EC50 of 52 μM and a Hill coefficient of 0.6. Currents were selective for Na+ over Cl− and were highly inwardly rectifying. Responses were blocked reversibly by d-tubocurarine, hexamethonium chloride, and N-methyl-D-glucamine. In 50% of the cases, α-bungarotoxin reversibly blocked the current induced by ACh application. The blocking action of mecamylamine was irreversible and independent of the presence of agonist but was more effective in the presence of ACh. We conclude that functional nicotinic ACh receptors exist on most goldfish retinal ganglion cells.

Strychnine, but not PMBA, inhibits neuronal nicotinic acetylcholine receptors expressed by rabbit retinal ganglion cells

2007 ◽  
Vol 24 (4) ◽  
pp. 503-511 ◽  
Author(s):  
J.M. RENNA ◽  
C.E. STRANG ◽  
F.R. AMTHOR ◽  
K.T. KEYSER
Keyword(s):  
Ganglion Cell ◽  
Retinal Ganglion Cells ◽  
Nicotinic Acetylcholine Receptors ◽  
Acetylcholine Receptors ◽  
Ganglion Cells ◽  
Glycine Receptor ◽  
Retinal Ganglion ◽  
Competitive Antagonist ◽  
Cell Responses ◽  
Α7 Nachrs

Strychnine is considered a selective competitive antagonist of glycine gated Cl− channels (Saitoh et al., 1994) and studies have used strychnine at low micromolar concentrations to study the role of glycine in rabbit retina (Linn, 1998; Protti et al., 2005). However, other studies have shown that strychnine, in the concentrations commonly used, is also a potent competitive antagonist of α7 nicotinic acetylcholine receptors (nAChRs; Matsubayashi et al., 1998). We tested the effects of low micromolar concentrations of strychnine and 3-[2′-phosphonomethyl[1,1′-biphenyl]-3-yl] alanine (PMBA), a specific glycine receptor blocker (Saitoh et al., 1994; Hosie et al., 1999) on the activation of both α7 nAChRs on retinal ganglion cells and on ganglion cell responses to a light flash. Extracellular recordings were obtained from ganglion cells in an isolated retina/choroid preparation and 500 μM choline was used as an α7 agonist (Alkondon et al., 1997). We recorded from brisk sustained and brisk transient OFF cells, many of which have been previously shown to have α7 receptors (Strang et al., 2005). Further, we tested the effect of strychnine, PMBA and α-bungarotoxin on the binding of tetramethylrhodamine α-bungarotoxin in the inner plexiform layer. Our data indicates that strychnine, at doses as low as 1.0 μM, can inhibit the α7 nAChR-mediated response to choline, but PMBA at concentrations as high as 0.4 μM does not. Binding studies show strychnine and α-bungarotoxin inhibit binding of labeled α-bungarotoxin in the IPL. Thus, the effects of strychnine application may be to inhibit glycine receptors expressed by ganglion cell or to inhibit amacrine cell α7 nAChRs, both of which would result in an increase in the ganglion cell responses. Further research will be required to disentangle the effects of strychnine previously believed to be caused by a single mechanism of glycine receptor inhibition.

Action Potentials in the Dendrites of Retinal Ganglion Cells

1999 ◽  
Vol 81 (3) ◽  
pp. 1412-1417 ◽  
Author(s):  
Toby J. Velte ◽  
Richard H. Masland
Keyword(s):  
Retinal Ganglion Cells ◽  
Action Potentials ◽  
Ganglion Cells ◽  
Retinal Ganglion ◽  
Muller Glia ◽  
Müller Glia ◽  
Whole Cell ◽  
The Absolute ◽  
Somatic Action Potentials ◽  
Site Of Stimulation

Action potentials in the dendrites of retinal ganglion cells. The somas and dendrites of intact retinal ganglion cells were exposed by enzymatic removal of the overlying endfeet of the Müller glia. Simultaneous whole cell patch recordings were made from a ganglion cell’s dendrite and the cell’s soma. When a dendrite was stimulated with depolarizing current, impulses often propagated to the soma, where they appeared as a mixture of small depolarizations and action potentials. When the soma was stimulated, action potentials always propagated back through the dendrite. The site of initiation of action potentials, as judged by their timing, could be shifted between soma and dendrite by changing the site of stimulation. Applying QX-314 to the soma could eliminate somatic action potentials while leaving dendritic impulses intact. The absolute amplitudes of the dendritic action potentials varied somewhat at different distances from the soma, and it is not clear whether these variations are real or technical. Nonetheless, the qualitative experiments clearly suggest that the dendrites of retinal ganglion cells generate regenerative Na+ action potentials, at least in response to large direct depolarizations.

scholarly journals Ih Without Kir in Adult Rat Retinal Ganglion Cells

2007 ◽  
Vol 97 (5) ◽  
pp. 3790-3799 ◽  
Author(s):  
Sherwin C. Lee ◽  
Andrew T. Ishida
Keyword(s):  
Ganglion Cell ◽  
Retinal Ganglion Cells ◽  
Ganglion Cells ◽  
Reversal Potential ◽  
Inward Rectification ◽  
Retinal Ganglion ◽  
Membrane Hyperpolarization ◽  
Adult Rat ◽  
Inwardly Rectifying ◽  
Cell Somata

Antisera directed against hyperpolarization-activated mixed-cation (“ Ih”) and K+ (“Kir”) channels bind to some somata in the ganglion cell layer of rat and rabbit retina. Additionally, the termination of hyperpolarizing current injections can trigger spikes in some cat retinal ganglion cells, suggesting a rebound depolarization arising from activation of Ih. However, patch-clamp studies showed that rat ganglion cells lack inward rectification or present an inwardly rectifying K+ current. We therefore tested whether hyperpolarization activates Ih in dissociated, adult rat retinal ganglion cell somata. We report here that, although we found no inward rectification in some cells, and a Kir-like current in a few cells, hyperpolarization activated Ih in roughly 75% of the cells we recorded from in voltage clamp. We show that this current is blocked by Cs+ or ZD7288 and only slightly reduced by Ba2+, that the current amplitude and reversal potential are sensitive to extracellular Na+ and K+, and that we found no evidence of Kir in cells presenting Ih. In current clamp, injecting hyperpolarizing current induced a slowly relaxing membrane hyperpolarization that rebounded to a few action potentials when the hyperpolarizing current was stopped; both the membrane potential relaxation and rebound spikes were blocked by ZD7288. These results provide the first measurement of Ih in mammalian retinal ganglion cells and indicate that the ion channels of rat retinal ganglion cells may vary in ways not expected from previous voltage and current recordings.

Rabbit retinal ganglion cell responses mediated by α-bungarotoxin-sensitive nicotinic acetylcholine receptors

2002 ◽  
Vol 19 (4) ◽  
pp. 427-438 ◽  
Author(s):  
B.T. REED ◽  
F.R. AMTHOR ◽  
K.T. KEYSER
Keyword(s):  
Ganglion Cell ◽  
Nicotinic Acetylcholine Receptors ◽  
Acetylcholine Receptors ◽  
Ganglion Cells ◽  
Cell Types ◽  
Evoked Responses ◽  
Retinal Ganglion ◽  
Nicotinic Acetylcholine ◽  
Low Concentrations ◽  
Cholinergic Agents

The responses of many ganglion cells in the rabbit retina are mediated, at least in part, by acetylcholine (ACh) acting on neuronal nicotinic acetylcholine receptors (nAChRs). nAChRs are comprised of α and β subunits; three β subunits and nine α subunits of nAChRs have been identified and these subunits can combine to form a large number of functionally distinct nAChR subtypes. We examined the effects of cholinergic agents on the light-evoked responses of ganglion cells to determine which nAChR subtypes mediate the effects of ACh. Extracellular recordings of retinal ganglion cells were made in intact everted eyecup preparations and nicotinic agonists and antagonists were added to the superfusate. While several ganglion cell classes exhibited methyllycaconitine (MLA) sensitivity, the directionally selective (DS) ganglion cells were most sensitive; exposure to 30 nanomolar MLA, a concentration reportedly too low to affect αBgt-insensitive nAChRs, suppressed the stimulus-evoked responses of DS cells without eliminating directional selectivity. Epibatidine, which at low concentrations is an agonist selective for αBgt-insensitive nAChRs, stimulated firing of various cell types including DS ganglion cells at low nanomolar concentrations. The effects of the various agents tested persisted under cobalt-induced synaptic blockade. The low nanomolar MLA and epibatidine sensitivity of DS cells suggests that DS ganglion cells express both αBgt-sensitive and αBgt-insensitive nAChRs. Other ganglion cell types appear to express only αBgt-sensitive nAChRs but not αBgt-insensitive nAChRs.

GABA-activated single channel currents in outside-out membrane patches from rat retinal ganglion cells

1989 ◽  
Vol 3 (3) ◽  
pp. 275-279 ◽  
Author(s):  
Stuart A. Lipton
Keyword(s):  
Retinal Ganglion Cells ◽  
Cortical Neurons ◽  
Single Channel ◽  
Ganglion Cells ◽  
Retinal Ganglion ◽  
Whole Cell ◽  
Cell Recording ◽  
Excised Patches ◽  
Patch Configuration ◽  
Single Channel Currents

Abstractγ-aminobutyric acid (GABA) evokes large whole-cell currents in solitary mammalian retinal ganglion cells studied by the patch-clamp method. This evidence suggests that GABA acts directly on the retinal ganglion cells as an inhibitory transmitter as it does elsewhere in the mammalian central nervous system. Here, single-channel recordings of the currents underlying the GABA-induced responses were studied in outside-out patches of cell membrane. In some other preparations, single GABAA channels recorded in the excised patch configuration have been shown to have altered properties in comparison to responses elicited during whole-cell recording. For example, in cortical neurons single GABA-activated channels in excised patches display accelerated desensitization kinetics as well as rapid rundown of the response. Therefore, in retinal ganglion cells, responses generated by GABA in cell-free patches were compared to whole-cell responses. After determining that the responses to GABA in acutely isolated outside-out patches were indeed similar to those of the whole-cell currents in retinal ganglion cells, the unitary conductances were studied. It was determined that these single-channel events resemble those reported in other nervous tissues with 4 elementary conductances of ~10 pS, 19–22 pS, 30–33 pS, and 45–50 pS at 33–35°C.

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