Intraretinal isolation of PIII subcomponents in the isolated rabbit retina after treatment with sodium aspartate

Hanitzsch, Renate

doi:10.1016/0042-6989(73)90186-7

Cited by 42 publications

(18 citation statements)

References 32 publications

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“…An increase in cwave amplitude might also be caused by a decrease of a slow, negative component of the ERG. Bernhard & Skoglund (1941), recording from frog eyes, proposed that alcohol selectively suppressed P 111 of Granit's analysis ( and Hanitzsch (1973) indicate that P I11 consists of at least two subcomponents, both in cold-blooded vertebrates and in mammals: a distal part from the receptors and a proximal part from the inner nuclear layer. Bernhard, Knave & Persson (1973) recorded the low-intensity ERG of the sheep and noted that the receptor potential was unaffected by alcohol.…”

Section: Discussionmentioning

confidence: 98%

THE c‐WAVE OF THE HUMAN D.C. REGISTERED ERG. III. EFFECTS OF ETHYL ALCOHOL ON THE c‐WAVE

Skoog

1974

Acta Ophthalmologica

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The amplitude of the c-wave of the human d.c. registered ERG is known to oscillate with a frequency of about 2Jhour in response to repeated stimulations. A small oral dose of ethyl alcohol caused a marked increase in amplitude of the oscillations and also elevated their mean level. A first peak was reached 10-15 min after the intake of alcohol. The b-wave increased slightly in response to ethanol, but no significant effect on the a-wave was observed with the present doses and stimulus conditions. The results encourage further studies of drug influence on the c-wave with the intention of correlating ocular toxicity of a substance to c-wave changes.

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Section: Discussionmentioning

confidence: 98%

THE c‐WAVE OF THE HUMAN D.C. REGISTERED ERG. III. EFFECTS OF ETHYL ALCOHOL ON THE c‐WAVE

Skoog

1974

Acta Ophthalmologica

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“…That is, the time-to-peak was 203 Ϯ 26 msec after 1 hr and 175 Ϯ 28 msec after 3 hr, and the half-decay time was 204 Ϯ 4 msec after 1 hr and 208 Ϯ 8 msec after 3 hr (n ϭ 3). The amplitude of the sPIII, which is generated by Muller glial cells in response to light-induced, photoreceptor-mediated changes in the extracellular K ϩ concentration (Hanitzsch, 1973;Witkovsky et al, 1975), was 168 Ϯ 19 and 131 Ϯ 2 V, and the time constant of the sPIII was 1.85 Ϯ 0.03 and 1.92 Ϯ 0.17 sec at the same intensity and time points, respectively (data are from three retinas from three independent experiments). These measurements indicate that the sPIII-and b-waves generated by the intact neural rabbit retina had similar amplitude and kinetics as those typically obtained from the intact rabbit eye (Dong and Hare, 2002) and rabbit eyecup (Dick et al, 1985), and thus that the intact neural retinal preparation is physiologically viable.…”

Section: Methodsmentioning

confidence: 96%

A Circadian Clock and Light/Dark Adaptation Differentially Regulate Adenosine in the Mammalian Retina

Ribelayga¹,

Mangel²

2005

J. Neurosci.

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Although the purine adenosine acts as an extracellular neuromodulator in the mammalian CNS in both normal and pathological conditions and regulates sleep, the regulation of extracellular adenosine in the day and night is incompletely understood. To determine how extracellular adenosine is regulated, rabbit neural retinas were maintained by superfusion at different times of the regular light/dark and circadian cycles. The adenosine level in the superfusate, representing adenosine overflow from the retinas, and the adenosine level in retinal homogenates, representing adenosine content, were measured using HPLC with fluorescence detection in the absence or presence of blockers of adenosine transport and/or extracellular adenosine synthesis. We report that darkness, compared with illumination, increases the level of extracellular adenosine, and that a circadian clock also increases extracellular adenosine at night. In addition, we show that the darkness-evoked increase in the level of extracellular adenosine results primarily from an increase in the conversion of extracellular ATP into adenosine, but that the clock-induced increase at night results primarily from an increase in the accumulation of intracellular adenosine. We also show that a slightly hypoxic state increases adenosine content and overflow to an extent similar to that of the clock. Our findings demonstrate that the extracellular level of adenosine in the mammalian retina is differentially regulated by a circadian clock and the lighting conditions and is maximal at night under dark-adapted conditions. We conclude that adenosine is a neuromodulator involved in both circadian clock and dark-adaptive processes in the vertebrate retina.

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“…Since then it has been shown that the c-wave represents the hyperpolarization mainly of the apical membrane of the pigment epithelial cells in response to the rod initiated decrease in external potassium in the space surrounding the photoreceptors that occurs during light stimulation (Steinberg, Schmidt & Brown 1970;Schmidt & Steinberg 197 1 ;Steinberg & Miller 1973;Oakley & Green 1976). I n addition, it is very likely that the c-wave is affected by other neuroretinal activities, e. g. slow P 111, a slow negative potential (Granit 1947) with at least two subcomponents, from the distal part of the receptors and from the inner nuclear layer, respectively (Murakami & Kaneko 1966;Hanitzsch 1973). I n many cases there is a need of separating the pigment epithelial responses from the potentials of the neuroretina.…”

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confidence: 99%

CHANGES IN ULTRASTRUCTURE AND FUNCTION OF THE SHEEP PIGMENT EPITHELIUM AND RETINA INDUCED BY SODIUM IODATE¹

Nilsson

Knave

Persson

1977

Acta Ophthalmologica

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The present investigation shows that the membrane properties of the sheep pigment epithelial cells were very rapidly and severely affected by sodium iodate, whereas the effects concerning the neuroretina were delayed. The c-wave of the ERG was immediately abolished and replaced by a cornea-negative potential, but the a- and b-waves were preserved for about 80-100 min. Ultrastructurally the plasma membranes (particularly the basal plasma membrane) of the pigment epithelial cells were destroyed or less distinct than normally. The cell organelles were swollen and ruptured. There were indications that the pigment epithelium could no longer participate in the receptor outer segment turnover. The photoreceptor cells were morphologically undamaged, and few or no signs of injury were observed in the inner layers of the retina. The effects upon the neuroretinal functions seen after 80-100 min, consisting of a reduction of alpha- and beta-wave amplitudes, were most likely caused by an inability of the pigment epithelium to maintain in the long run its metabolic and barrier properties. It appears that at an early stage after sodium iodate injection, the present preparation may be useful for the study of the effects on the neuroretina proper of drugs and other agents.

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Intraretinal isolation of PIII subcomponents in the isolated rabbit retina after treatment with sodium aspartate

Cited by 42 publications

References 32 publications

THE c‐WAVE OF THE HUMAN D.C. REGISTERED ERG. III. EFFECTS OF ETHYL ALCOHOL ON THE c‐WAVE

THE c‐WAVE OF THE HUMAN D.C. REGISTERED ERG. III. EFFECTS OF ETHYL ALCOHOL ON THE c‐WAVE

A Circadian Clock and Light/Dark Adaptation Differentially Regulate Adenosine in the Mammalian Retina

CHANGES IN ULTRASTRUCTURE AND FUNCTION OF THE SHEEP PIGMENT EPITHELIUM AND RETINA INDUCED BY SODIUM IODATE¹

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Intraretinal isolation of PIII subcomponents in the isolated rabbit retina after treatment with sodium aspartate

Cited by 42 publications

References 32 publications

THE c‐WAVE OF THE HUMAN D.C. REGISTERED ERG. III. EFFECTS OF ETHYL ALCOHOL ON THE c‐WAVE

THE c‐WAVE OF THE HUMAN D.C. REGISTERED ERG. III. EFFECTS OF ETHYL ALCOHOL ON THE c‐WAVE

A Circadian Clock and Light/Dark Adaptation Differentially Regulate Adenosine in the Mammalian Retina

CHANGES IN ULTRASTRUCTURE AND FUNCTION OF THE SHEEP PIGMENT EPITHELIUM AND RETINA INDUCED BY SODIUM IODATE1

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CHANGES IN ULTRASTRUCTURE AND FUNCTION OF THE SHEEP PIGMENT EPITHELIUM AND RETINA INDUCED BY SODIUM IODATE¹