Post-receptoral contributions to the rat scotopic electroretinogram a-wave

Dang, Trung M.; Tsai, Tina I.; Vingrys, Algis J.

doi:10.1007/s10633-011-9269-y

Cited by 21 publications

(17 citation statements)

References 18 publications

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“…Measurement of the a-wave can be influenced by inner retinal activity since the photoreceptoral response is not complete before inner retinal responses begin, an issue which is particularly pertinent at low stimulus intensities. We found delays of the ZDF b-wave, but the differences in a-wave amplitudes as compared to Leans were most significant at the higher intensities where the a-wave implicit time was under 14 ms and therefore complete before the intrusion of any positive deflection from the inner retina [25], [26]. It appears then that the difference measured in a-wave amplitudes between Leans and ZDFs reflects a change in photoreceptoral function.…”

Section: Discussionmentioning

confidence: 61%

Retinal Adaptation to Changing Glycemic Levels in a Rat Model of Type 2 Diabetes

2013

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PurposeGlucose concentrations are elevated in retinal cells in undiagnosed and in undertreated diabetes. Studies of diabetic patients suggest that retinal function adapts, to some extent, to this increased supply of glucose. The aim of the present study was to examine such adaptation in a model of type 2 diabetes and assess how the retina responds to the subsequent institution of glycemic control.MethodsElectroretinography (ERG) was conducted on untreated Zucker diabetic fatty (ZDF) rats and congenic controls from 8–22 weeks of age and on ZDFs treated with daily insulin from 16–22 weeks of age. Retinal sections from various ages were prepared and compared histologically and by immunocytochemistry.Principal Findings/ConclusionsAcute hyperglycemia did not have an effect on control rats while chronic hyperglycemia in the ZDF was associated with scotopic ERG amplitudes which were up to 20% higher than those of age-matched controls. This change followed the onset of hyperglycemia with a delay of over one month, supporting that habituation to hyperglycemia is a slow process. When glycemia was lowered, an immediate decrease in ZDF photoreceptoral activity was induced as seen by a reduction in a-wave amplitudes and maximum slopes of about 30%. A direct effect of insulin on the ERG was unlikely since the expression of phosphorylated Akt kinase was not affected by treatment. The electrophysiological differences between untreated ZDFs and controls preceded an activation of Müller cells in the ZDFs (up-regulation of glial fibrillary acidic protein), which was attenuated by insulin treatment. There were otherwise no signs of cell death or morphological alterations in any of the experimental groups. These data show that under chronic hyperglycemia, the ZDF retina became abnormally sensitive to variations in substrate supply. In diabetes, a similar inability to cope with intensive glucose lowering could render the retina susceptible to damage.

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Section: Discussionmentioning

confidence: 61%

Retinal Adaptation to Changing Glycemic Levels in a Rat Model of Type 2 Diabetes

2013

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“…The leading edge of the rat a-wave reflects photoreceptoral activity [29,30]. This was quantified by modelling the first 6 ms over an ensemble of the brightest luminous energies (1.50 and 2.07 log cd.s.m −2 ) using a delayed Gaussian function [31,32].…”

Section: Photoreceptor Responsementioning

confidence: 99%

Glial and neuronal dysfunction in streptozotocin-induced diabetic rats

Wong

Vingrys

Bui

2011

j ocul biol dis inform

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Neuronal dysfunction has been noted very soon after the induction of diabetes by streptozotocin injection in rats. It is not clear from anatomical evidence whether glial cell dysfunction accompanies the well-documented neuronal deficit. Here, we isolate the Müller cell driven slow-P3 component of the full-field electroretinogram and show that it is attenuated at 4 weeks following the onset of streptozotocin-hyperglycaemia. We also found a concurrent reduction in the sensitivity of the phototransduction cascade, as well as in the components of the electroretinogram known to indicate retinal ganglion cell and amacrine cell integrity. Our data support the idea that neuronal and Müller cell dysfunction occurs at the same time in streptozotocin-induced hyperglycaemia.

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“…However, the response of rat cones peaks at a much later time than the dark-adapted a-wave and therefore is likely to be of insignificant amplitude at the time of the a-wave peak (<5 μV at 10 ms, Bui and Fortune, 2006). An early negative post-receptoral component in the rat ERG that could be removed by pharmacologically blocking ionotropic glutamate receptors has been reported by Dang et al (2011), but extrapolation of their measurements suggests that the amplitude of this post-receptoral signal would be little more than 1/10 of the peak amplitude of the a-wave generated by our strongest stimuli.…”

Section: Comparison Of Trans-retinal Voltage Simulations With Recomentioning

confidence: 55%

The rod-driven a-wave of the dark-adapted mammalian electroretinogram

Robson

Frishman

2014

Progress in Retinal and Eye Research

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The a-wave of the electroretinogram (ERG) reflects the response of photoreceptors to light, but what determines the exact waveform of the recorded voltage is not entirely understood. We have now simulated the trans-retinal voltage generated by the photocurrent of dark-adapted mammalian rods, using an electrical model based on the in vitro measurements of Hagins et al. (1970) and Arden (1976) in rat retinas. Our simulations indicate that in addition to the voltage produced by extracellular flow of photocurrent from rod outer to inner segments, a substantial fraction of the recorded a-wave is generated by current that flows in the outer nuclear layer (ONL) to hyperpolarize the rod axon and synaptic terminal. This current includes a transient capacitive component that contributes an initial negative “nose” to the trans-retinal voltage when the stimulus is strong. Recordings in various species of the a-wave, including the peak and initial recovery towards the baseline, are consistent with simulations showing an initial transient primarily related to capacitive currents in the ONL. Existence of these capacitive currents can explain why there is always a substantial residual transient a-wave when post-receptoral responses are pharmacologically inactivated in rodents and nonhuman primates, or severely genetically compromised in humans (e.g. complete congenital stationary night blindness) and nob mice. Our simulations and analysis of ERGs indicate that the timing of the leading edge and peak of dark-adapted a-waves evoked by strong stimuli could be used in a simple way to estimate rod sensitivity.

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Post-receptoral contributions to the rat scotopic electroretinogram a-wave

Cited by 21 publications

References 18 publications

Retinal Adaptation to Changing Glycemic Levels in a Rat Model of Type 2 Diabetes

Retinal Adaptation to Changing Glycemic Levels in a Rat Model of Type 2 Diabetes

Glial and neuronal dysfunction in streptozotocin-induced diabetic rats

The rod-driven a-wave of the dark-adapted mammalian electroretinogram

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