Interactions between PI and Slow PIII in the Generation of the Electroretinogram c-Wave1

2015 ◽  
pp. 53-58 ◽  
Author(s):  
Sven Erik G. Nilsson
Keyword(s):  
Slow Piii

scholarly journals Extracellular K+ activity changes related to electroretinogram components. I. Amphibian (I-type) retinas.

1985 ◽  
Vol 85 (6) ◽  
pp. 885-909 ◽  
Author(s):  
E Dick ◽  
R F Miller
Keyword(s):  
Profile Analysis ◽  
Müller Cell ◽  
Extracellular Potassium ◽  
Pharmacological Properties ◽  
Pharmacological Agents ◽  
Activity Measurements ◽  
Slow Piii ◽  
Muller Cell ◽  
Depolarizing Bipolar Cell ◽  
K Activity

Electroretinographic (ERG) and extracellular potassium activity measurements were carried out in superfused eyecup preparations of several amphibians. Light-evoked changes in extracellular K+ activity were characterized on the bases of depth profile analysis and latency measurements and through the application of pharmacological agents that have selective actions on the retinal network. Three different extracellular potassium modulations evoked at light onset were identified and characterized according to their phenomenological and pharmacological properties. These modulations include two separable sources of light-evoked increases in extracellular K+: (a) a proximal source that is largely post-bipolar in origin, and (b) a distal source that is primarily or exclusively of depolarizing bipolar cell origin. The pharmacological properties of the distal extracellular potassium increase closely parallel those of the b-wave. A distal light-evoked decrease in extracellular potassium appears to be associated with the slow PIII potential, based on a combination of simultaneous intracellular Müller cell recordings and extracellular ERG and potassium activity measurements before and during pharmacological isolation of the photoreceptor responses. The extracellular potassium activity increases are discussed with respect to the Müller cell theory of b-wave generation.

Characteristics of receptor potential and slow piii-component to light and dark flashes in the isolated superfused rabbit retina

1981 ◽  
Vol 21 (11) ◽  
pp. 1709-1712 ◽  
Author(s):  
Renate Hanitzsch ◽  
K. Bykow
Keyword(s):  
Receptor Potential ◽  
Rabbit Retina ◽  
Slow Piii ◽  
Piii Component

Barium suppresses slow PIII in perfused bullfrog retina

1979 ◽  
Vol 19 (10) ◽  
pp. 1117-1119 ◽  
Author(s):  
David A. Bolnick ◽  
Alfred E. Walter ◽  
Arnold J. Sillman
Keyword(s):  
Slow Piii

scholarly journals Light-Evoked Responses of the Retinal Pigment Epithelium: Changes Accompanying Photoreceptor Loss in the Mouse

2010 ◽  
Vol 104 (1) ◽  
pp. 391-402 ◽  
Author(s):  
Ivy S. Samuels ◽  
Gwen M. Sturgill ◽  
Gregory H. Grossman ◽  
Mary E. Rayborn ◽  
Joe G. Hollyfield ◽  
...  
Keyword(s):  
Retinal Pigment Epithelium ◽  
Structural Changes ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Retinal Disease ◽  
Rod Photoreceptor ◽  
Evoked Responses ◽  
Photoreceptor Degeneration ◽  
Rod Photoreceptors ◽  
Slow Piii

Mutations in genes expressed in the retinal pigment epithelium (RPE) underlie a number of human inherited retinal disorders that manifest with photoreceptor degeneration. Because light-evoked responses of the RPE are generated secondary to rod photoreceptor activity, RPE response reductions observed in human patients or animal models may simply reflect decreased photoreceptor input. The purpose of this study was to define how the electrophysiological characteristics of the RPE change when the complement of rod photoreceptors is decreased. To measure RPE function, we used an electroretinogram (dc-ERG)-based technique. We studied a slowly progressive mouse model of photoreceptor degeneration ( Prph Rd2/+), which was crossed onto a Nyxnob background to eliminate the b-wave and most other postreceptoral ERG components. On this background, Prph Rd2/+ mice display characteristic reductions in a-wave amplitude, which parallel those in slow PIII amplitude and the loss of rod photoreceptors. At 2 and 4 mo of age, the amplitude of each dc-ERG component (c-wave, fast oscillation, light peak, and off response) was larger in Prph Rd2/+ mice than predicted by rod photoreceptor activity (RmP3) or anatomical analysis. At 4 mo of age, the RPE in Prph Rd2/+ mice showed several structural abnormalities including vacuoles and swollen, hypertrophic cells. These data demonstrate that insights into RPE function can be gained despite a loss of photoreceptors and structural changes in RPE cells and, moreover, that RPE function can be evaluated in a broader range of mouse models of human retinal disease.

A mathematical model of slow PIII of the ERG: Variation of stimulus duration

1981 ◽  
Vol 21 (11) ◽  
pp. 1721-1724
Author(s):  
Robert Trappl ◽  
Astrid v. Lützow
Keyword(s):  
Mathematical Model ◽  
Stimulus Duration ◽  
Slow Piii

Blockade of amiloride-sensitive sodium channels alters multiple components of the mammalian electroretinogram

2005 ◽  
Vol 22 (2) ◽  
pp. 143-151 ◽  
Author(s):  
LAURA M. BROCKWAY ◽  
DALE J. BENOS ◽  
KENT T. KEYSER ◽  
TIMOTHY W. KRAFT
Keyword(s):  
Physiological Role ◽  
Müller Cells ◽  
Müller Cell ◽  
Cell Physiology ◽  
Muller Cells ◽  
Retinal Neurons ◽  
Multiple Components ◽  
Cell Components ◽  
Slow Piii ◽  
Muller Cell

Retinal neurons and Müller cells express amiloride-sensitive Na+ channels (ASSCs). Although all major subunits of these channels are expressed, their physiological role is relatively unknown in this system. In the present study, we used the electroretinogram (ERG) recorded from anesthetized rabbits and isolated rat and rabbit retina preparations to investigate the physiological significance of ASSCs in the retina. Based upon our previous study showing expression of α-ENaC and functional amiloride-sensitive currents in rabbit Müller cells, we expected changes in Müller cell components of the ERG. However, we observed changes in other components of the ERG as well. The presence of amiloride elicited changes in all major components of the ERG; the a-wave, b-wave, and d-wave (off response) were enhanced, while there was a reduction in the amplitude of the Müller cell response (slow PIII). These results suggest that ASSCs play an important role in retinal function including neuronal and Müller cell physiology.

scholarly journals Extracellular K+ activity changes related to electroretinogram components. II. Rabbit (E-type) retinas.

1985 ◽  
Vol 85 (6) ◽  
pp. 911-931 ◽  
Author(s):  
E Dick ◽  
R F Miller ◽  
S Bloomfield
Keyword(s):  
Retinal Pigment Epithelium ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Müller Cells ◽  
Extracellular Potassium ◽  
Muller Cells ◽  
Positive Component ◽  
Pharmacological Agents ◽  
Slow Piii ◽  
K Activity

Electroretinogram (ERG) and extracellular potassium activity (K+o) measurements were carried out in isolated superfused rabbit eyecup preparations under control conditions and during the application of pharmacological agents that selectively modify the light-responsive retinal network. Light-evoked K+o changes in the rabbit (E-type) retina resemble those previously described in amphibian (I-type) retinas. Different components of the light-evoked K+o changes can be distinguished on the bases of retinal depth, V vs. log I properties, and their responses to pharmacological agents. We find two separable sources of light-evoked increases in extracellular K+: a proximal source and a distal source. The properties of the distal light-evoked K+o increase are consistent with the hypothesis that it initiates a K+-mediated current through Müller cells that is detected as the primary voltage of the electroretinographic b-wave. These experiments also support previous studies indicating that both the corneal-positive component of c-wave and the corneal-negative slow PIII potential result from K+-mediated influences on, respectively, the retinal pigment epithelium and Müller cells.

Intraretinal analysis of the threshold dark-adapted ERG of cat retina

1989 ◽  
Vol 61 (6) ◽  
pp. 1221-1232 ◽  
Author(s):  
L. J. Frishman ◽  
R. H. Steinberg
Keyword(s):  
Time Course ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Receptor Potential ◽  
Neural Retina ◽  
Negative Response ◽  
Subretinal Space ◽  
Cat Retina ◽  
Slow Piii ◽  
Near Threshold

1. The dark-adapted electroretinogram (ERG) obtained with 4-s flashes near threshold and at low intensities has three clear negative components: 1) a fast negative response at stimulus onset, 2) a slow negative response that increases in amplitude for about 2 s, and 3) a negative-going OFF response. The fast negative response was previously shown to originate from the scotopic threshold response (STR) arising in the proximal portion of neural retina. We investigated the intraretinal origins of the other two negative components and found that they also have origins in neural retina proximal to the photoreceptors. 2. In this study the ERG evoked in response to diffuse illumination of the dark-adapted cat retina was recorded between a chlorided silver wire in the vitreous and a plate behind the eye. Extracellular field potentials were recorded simultaneously with a microelectrode placed intraretinally at different retinal depths. In some cases light-dependent changes in extracellular K+ concentration ([K+]o) were recorded with the K+-selective barrel of a double-barreled microelectrode. 3. The three negative-going ERG potentials increased in amplitude from threshold up to approximately 6.0 log q.deg-2.s-1. The potential during illumination then became nearly flat, and the negative OFF response was exaggerated. At higher intensities, positive-going PII (DC-component and b-wave) and the c-wave emerged, whereas the a-wave (negative-going) was usually below threshold. 4. The slow negative ERG response was generated in neural retina, rather than by the retinal pigment epithelium. The response was positive-going in the transretinal recordings obtained in subretinal space. It was not, however, related to two positive-going responses from distal retina previously described as contributing negative components to the ERG: the neural retina component of the c-wave, termed slow PIII, and the rod-receptor potential. The slow negative response had a slower time course and lower threshold than slow PIII, and, more importantly, it was present in the absence of the [K+]o decrease in subretinal space that causes slow PIII. Furthermore, APB (1.2 mM vitreal concentration) blocked the entire negative-going ERG, whereas at higher intensities it blocked PII but not the c-wave in the ERG or slow PIII in transretinal recordings. These results indicate that the negative-going ERG components near threshold and at low intensities all originated proximal to the photoreceptors.(ABSTRACT TRUNCATED AT 400 WORDS)

scholarly journals Ba2+ unmasks K+ modulation of the Na+-K+ pump in the frog retinal pigment epithelium.

1985 ◽  
Vol 86 (6) ◽  
pp. 853-876 ◽  
Author(s):  
E R Griff ◽  
Y Shirao ◽  
R H Steinberg
Keyword(s):  
Retinal Pigment Epithelium ◽  
Channel Blocker ◽  
Apical Membrane ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
K Channel ◽  
Evoked Responses ◽  
Physiological Conditions ◽  
Transepithelial Potential ◽  
Slow Piii

This paper presents electrophysiological evidence that small changes in [K+]o modulate the activity of the Na+-K+ pump on the apical membrane of the frog retinal pigment epithelium (RPE). This membrane also has a large relative K+ conductance so that lowering [K+]o hyperpolarizes it and therefore increases the transepithelial potential (TEP). Ba2+, a K+ channel blocker, eliminated these normal K+-evoked responses; in their place, lowering [K+]o evoked an apical depolarization and TEP decrease that were blocked by apical ouabain or strophanthidin. These data indicate that Ba2+ blocked the major K+ conductance(s) of the RPE apical membrane and unmasked a slowing of the normally hyperpolarizing electrogenic Na+-K+ pump caused by lowering [K+]o. Evidence is also presented that [K+]o modulates the pump in the isolated RPE under physiological conditions (i.e., without Ba2+). In the intact retina, light decreases subretinal [K+]o and produces the vitreal-positive c-wave of the electroretinogram (ERG) that originates primarily in the RPE from a hyperpolarization of the apical membrane and TEP increase. When Ba2+ was present in the retinal perfusate, the apical membrane depolarized in response to light and the TEP decreased so that the ERG c-wave inverted. The retinal component of the c-wave, slow PIII, was abolished by Ba2+. The effects of Ba2+ were completely reversible. We conclude that Ba2+ unmasks a slowing of the RPE Na+-K+ pump by the light-evoked decrease in [K+]o. Such a response would reduce the amplitude of the normal ERG c-wave.

M-wave of the toad electroretinogram

1991 ◽  
Vol 66 (6) ◽  
pp. 1927-1940 ◽  
Author(s):  
B. J. Katz ◽  
R. Wen ◽  
J. B. Zheng ◽  
Z. A. Xu ◽  
B. Oakley
Keyword(s):  
Plexiform Layer ◽  
Müller Cell ◽  
Inner Plexiform Layer ◽  
Excitatory Effect ◽  
Inner Retina ◽  
M Wave ◽  
Threshold Response ◽  
Slow Piii ◽  
Muller Cell ◽  
Toad Bufo

1. In the retina, two distinct, light-evoked releases of K+ have been described. One takes place in the outer plexiform layer (OPL) and is termed the "distal K+ increase." The other takes place in the inner plexiform layer (IPL) and is termed the "proximal K+ increase." Although the distal K+ increase generates the electroretinogram (ERG) b-wave, the contribution of the much larger proximal K+ increase to the ERG is less well understood. In this paper we detail our investigation of the proximal K+ increase and its contribution to the ERG. We describe an ERG component, the M-wave, which had not heretofore been observed in the diffuse-flash, vitreal ERG. 2. We studied the proximal K+ increase and the ERG M-wave in the isolated retina preparation of the toad, Bufo marinus. We used K(+)-sensitive microelectrodes, as well as conventional intra- and extracellular microelectrodes, to record K+ changes, the local (or intraretinal) ERG, the vitreal ERG, and Muller cell responses. 3. As in earlier studies of the amphibian and cat M-wave, we readily observed an M-wave in the intraretinal, or local, ERG (LERG). The M-wave we studied had characteristics similar to those of M-waves that were previously described. Specifically, we found that the M-wave was generated by a Muller cell response to the proximal K+ increase and that both the proximal K+ increase and the LERG M-wave were spatially tuned. 4. We used the aspartate receptor agonist, N-methyl-DL-aspartate (NMA), to reveal that an M-wave is present in the vitreal ERG. Researchers who previously investigated the M-wave were unable to identify an M-wave in the vitreal ERG. We found that the toad ERG M-wave was a small, positive potential that was partially obscured by the much larger b-wave and slow PIII components. 5. We observed that picrotoxin (PTX) had an excitatory effect on inner retina, as evidenced by an enhanced proximal K+ increase and an enhanced M-wave. This result indicates that it is likely that GABAergic inhibition in inner retina plays an important role in retinal processing in the toad. 6. At threshold, we found that the ERG consisted mainly of an M-wave, indicating that the amphibian threshold ERG is driven by proximal retina. This result is analogous to previous observations of the threshold ERG in cat. However, in cat, the M-wave and threshold response have been described as distinct ERG components.(ABSTRACT TRUNCATED AT 400 WORDS)

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