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G Niemeyer

Publications and source records attributed to G Niemeyer.

At least 19 recordsLinked to original sources
PubMed2001

Retinal research using the perfused mammalian eye.

The effort to isolate and maintain alive in vitro an intact mammalian eye is rewarded by the full control provided over the arterial input and exclusion of systemic regulatory or compensatory mechanisms. Electrical recording of typical light-evoked field potentials from retina and optic nerve can be complemented by single-cell recording. Thus, light-induced electrical activity reflects the function of the retinal pigment epithelium, of the layers of the retina and of the ganglion cells or their axons. Retinal function in vitro is documented by electrophysiological and morphological methods revealing subtle features of retinal information processing as well as optic nerve signals that approach-at threshold stimulus intensity-the human psychophysical threshold. Such sensitivity of third-order retinal neurons is described for the first time. This well controlled in vitro preparation has been used successfully for biophysical, metabolic and pharmacological studies. Examples are provided that demonstrate the marked sensibility of the rod system to changes in glucose supply. Moreover, histochemical identification of glycogen stores revealed labeling of the second- and third-order neurons subserving the rod system, in addition to labeling of Müller (glial) cells in the cat retina. The glycogen content of the cat retina is augmented by prolonged anesthesia, largely depleted by ischemia after enucleation and enhanced by insulin. Pharmacological experiments using agonists and antagonists of putative retinal neurotransmitters are summarized and outlined using the muscarinic cholinergic agonist QNB as an example. Actions and uptake of the neuromodulator adenosine are presented in detail, including inhibitory effects on physiologically characterized ganglion cells. Neuronal effects of adenosine are distinguished from those resulting from vasodilatation and from glycogenolysis induced by the neuromodulator. To open the blood-retina barrier, a hyperosmotic challenge can be applied transiently. This process is monitored histochemically using FITC-albumin and with electrophysiological parameters. Changes in vitreo-scleral resistance and in the amplitude of the EOG-light peak appear to reflect the open/closed status of the barrier. This overview of the uses of the isolated perfused mammalian eye in retinal research concludes with a discussion of potential implications for clinically relevant topics.

Animals↗
PubMed2000

c-fos controls the "private pathway" of light-induced apoptosis of retinal photoreceptors.

White light (5 klux for 2 hr) induces apoptosis of rod photoreceptors in wild-type mice (c-fos(+/+)) within 24 hr, whereas rods of c-fos knock-out mice (c-fos(-/-)) are protected (). The range of this protection was tested by analyzing retinas of c-fos(+/+) and c-fos(-/-) mice up to 10 d after exposure to threefold increased light intensities (15 klux for 2 hr). In c-fos(-/-) mice, rods were unaffected, whereas they were destroyed in c-fos(+/+) mice. After light exposure, mitochondrial damage in rods was observed exclusively in c-fos(+/+) mice. Electroretinograms recorded 48 hr after exposure revealed a decrease of all components in c-fos(+/+) mice but indicated no light-induced loss of function in c-fos(-/-) mice. Thus, in c-fos(-/-) mice, light-induced apoptosis is blocked or its threshold is elevated more than threefold. Increased activity of the transcription factor activator protein-1 (AP-1) in retinas of light-exposed c-fos(+/+) mice indicated an acute contribution of AP-1 to apoptosis induction. AP-1 activity increased already during exposure and peaked approximately 6 hr thereafter, coinciding with the appearance of major morphological signs of apoptosis. Activated AP-1 mainly consisted of c-Fos/Jun heterodimers. In c-fos(-/-) mice, AP-1 activity remained unchanged, indicating that no other Jun- or Fos-family member could substitute for c-Fos. Like damaging light, N-methyl-N-nitrosourea (MNU) induced AP-1 containing c-Fos in c-fos(+/+) mice and did not induce AP-1 in c-fos(-/-) mice. In contrast to light, however, MNU induced apoptosis in rods of c-fos(-/-) mice. Thus, c-Fos is essential for a specific premitochondrial "private apoptotic pathway" induced by light but not for the execution of apoptosis induced by other stimuli.

Alkylating Agents↗
PubMed2000

[Effect of insulin on retinal glycogen content].

BACKGROUND: The effect of insulin on glucose and glycogen metabolism in peripheral organs is well known. However, information about the action of this peptide in the retina is incomplete. We addressed the questions whether insulin influences glycogen content in the cat retina and whether glycogen breakdown is triggered by lack of glucose. MATERIAL AND METHODS: Eyes from adult cats were enucleated under deep barbiturate and fentanylanesthesia. Retinas were snap frozen either before or following arterial in vitro perfusion. Three conditions were studied: a) Perfusion with a glucose- and insulin-free medium; b) perfusion with the addition of physiologic glucose concentration; and c) in combination with insulin. Glycogen content was determined by in vitro measurement of glucose converted from glycogen. RESULTS: The reference value for retinal glycogen after enucleation (10 min of ischemia) is 2.4 micrograms glucose/mg protein. Glucose- and insulin-free perfusion for 80 min following "normoglycemia" reduced the amount of retinal glycogen by one third. Perfusion for 3 h with 5.5 mM glucose led to a small increase of the partly depleted glycogen stores. Insulin, in contrast, markedly augmented the glycogen content. CONCLUSIONS: Insulin led to an increase in retinal glycogen content, indicating an influence of this peptide on retinal glucose and glycogen metabolism. However, it appears that glycogen might play a dynamic role in retinal metabolism as a buffer between abrupt changes in focal metabolic demands that occur during normal glucose supply rather than acting solely as an emergency energy reserve for neural function during hypoglycemia.

Animals↗
PubMed2000

[Stargardt's disease and its intrafamilial variability].

BACKGROUND: Because of its considerable differential diagnosis and a wide range of phenotypic variation, Stargardt's disease (juvenile macular dystrophy) can cause diagnostic problems. Moreover, ample variability in course and outcome of the disease has been described. PATIENTS AND METHODS: The diagnosis and variable course of Stargardt's disease of three affected siblings have been documented by clinical manifestation, fluorescein angiography and Ganzfeld-ERG including the ISCEV standard protocol. RESULTS: All three siblings presented with retinal abnormalities. However, only the youngest brother revealed symptoms for more than 10 y in terms of reduced visual acuity. The two elder ones had preserved central vision. Classical findings of contact lens biomicroscopy, fluorescein angiography and changes in the Ganzfeld-ERG confirmed the diagnosis of Stargardt's disease. CONCLUSIONS: The diagnosis of Stargardt's disease can be made as late as in the 7th decade of life. Tremendous variability can occur in course and outcome even within the same family. Therefore, visual prognosis is uncertain and has to be made with caution. In most cases the diagnosis can be established with the above mentioned methods.

Age Factors↗
PubMed2000

The retina of c-fos-/- mice: electrophysiologic, morphologic and biochemical aspects.

PURPOSE: Mice without a functional c-Fos protein (c-fos-/- mice) do not exhibit light-induced apoptotic cell death of rods in contrast to their wild-type littermates (c-fos+/+ mice). To analyze the consequences of the absence of c-fos in the retina, we investigated whether the retinas of c-fos-/- mice have a reduced capacity to absorb and transduce light compared with c-fos+/+ mice. METHODS: Retinal function was evaluated in dark-adapted mice by full-field electroretinograms (ERGs) over more than 6 log units of intensity. Retinal morphology was studied by light- and electron microscopy. Arrestin and the heat shock protein 70 (Hsp70) were detected by Western blot analysis. The rhodopsin content and the kinetics of rhodopsin regeneration were determined in retinal extracts. RESULTS: Although the configuration of the ERGs was comparable in both groups of mice, c-fos-/- mice showed a marked variability in all quantitative ERG-measures with lower mean amplitudes, longer latencies, and a 0.9-log-unit lower b-wave sensitivity on average. Morphometry showed that c-fos-/- mice have 23% fewer rods on average, whereas the number of cones was comparable among c-fos+/+ and c-fos-/- mice. Arrestin levels appeared slightly reduced in c-fos-/- mice when compared with c-fos+/+ mice, whereas Hsp70 levels were comparable in both genotypes. The kinetics of rhodopsin regeneration were similar, but c-fos-/- mice had a 25% lower rhodopsin content on average. CONCLUSIONS: Compared with c-fos+/+ mice, retinal function in c-fos-/- mice is attenuated to a variable but marked degree, which may be, at least in part, related to the reduced number of rods and the reduced rhodopsin content. However, c-fos does not appear to be essential for the ability to absorb photons, nor for phototransduction or the function of second-order neurons. The resistance to light-induced apoptosis of photoreceptor cells in c-fos-/- mice may result from the acute deficit of c-fos in the apoptotic cascade rather than from developmental deficits affecting rod photoreceptor function.

Animals↗
PubMed1999

Effects of adenosinergic agents on the vascular resistance and on the optic nerve response in the perfused cat eye.

The function of A1- and A2a-adenosine receptors in the control of vascular resistance and in the modulation of light-evoked neuronal activity was investigated in the isolated perfused cat eye. The A1 agonist CCPA, the A1 antagonist CPT, the A2a agonist CGS 21680 and the A2 antagonist DMPX were used. The agents were applied intra-arterially at concentrations in the low nanomolar to micromolar range during rod-selective photic stimulation. The flow rate of perfusate, reflecting vascular resistance and the light-evoked optic nerve response (ONR) were recorded. Our results show a vasodilating effect of both A1 and A2 agonists and a vasoconstricting effect of the respective antagonists. The dose-effect relationships are suggestive, however, of an A2a receptor-mediated mechanism. The amplitude of the ONR-ON component was decreased during application of both adenosine-agonists. Analysis of the dose-effect relationships and the blockade of the CCPA-induced decrease by CPT suggests that inhibition is mediated by A1 receptors. However, CGS 21680-mediated inhibition cannot be explained by unspecific binding at A1 receptors alone and suggests the involvement of inhibitory A2a receptors.

Adenosine↗
PubMed1999

[The electroretinogram (ERG) of the mouse: normal values, optimal stimulation and recording].

PURPOSE: The electroretinogram (ERG) is an appropriate method to evaluate the retinal function in a variety of animal models. In this study we present suitable conditions of stimulation and recording in the dark-adapted mouse. METHODS: Mice (n = 15) were dark-adapted during 14 hours and anesthetized with a single intraperitoneal injection of xylazine/ketamine. Pupils were dilated and a d.c.-silk-silver electrode or a AgCl-contact-lens electrode was placed on the cornea. The electroretinogram (ERG) was obtained by Ganzfeld stimulation over a range of 6 log units of intensity (8 x 10(-2) - 8 x 104 cd/m2). Intensity, duration and the interval of the light stimuli were varied separately. RESULTS: Reproducible values of the intensity-response functions are obtained for the a-, b- and c-waves of the ERG under well controlled adaptation- and stimulus-conditions. C-wave amplitudes are best evaluated using d.c.-recording and a stimulus duration of 4 seconds. The position of the d.c.-silk-silver electrode on the cornea can affect the ERG-amplitudes. Using a contact-lens electrode, the recorded b-wave amplitudes are on average 20% below those recorded with a centrally positioned d.c.-silk-silver electrode. Stimulus-intervals of at least 60 seconds are recommended at high intensities. CONCLUSIONS: An unequivocal assessment of retinal function requires reproducible ERG-values over a wide range of intensities. To obtain these, well controlled and standardized experimental conditions are required.

Animals↗
PubMed1999

[From the symptom to electroretinography diagnosis].

Retinal function can be documented noninvasively and objectively by electroretinography, complementing clinical examinations. Symptoms of nightblindness and of dayblindness with photoaversion, nystagmus, poor vision in infants or unclear visual field defects are meaningful indications for ERG testing. We use standardized (ISCEV) full-field single flash ERGs to evaluate the function of the rod- and of the cone-system. In infants, general anesthesia is useful to combine an abbreviated ERG protocol with ophthalmoscopy and fundus photography. ERG testing facilitates to distinguish between functional deficits in the rod- and cone-system, between congenital-stationary retinal dysfunction and progressive retinal heredo-degenerations. Frequently a functional deficit of the retina without ophthalmoscopic changes can be assessed. These entities include achromatopsia, congenital stationary night blindness, early stages of retinitis pigmentosa (RP) or progressive cone dystrophy, as well as toxic retinal changes. Congenital amaurosis Leber (LCA), infantile RP, Usher's syndrome and retinal involvement in other neuropediatric or metabolic syndromes can be diagnosed or excluded by ERG recording early-on. Synoptic evaluation of the full-field ERG, pattern-ERG and VEP completes neuro-ophthalmological screening.

Adult↗
PubMed1999

Effect of verapamil enantiomers and metabolites on cardiac K+ channels expressed in Xenopus oocytes.

The effect of verapamil and its enantiomers and metabolites on cardiac action potential repolarizing potassium channels was tested. For this purpose, the potassium channels Kv1.1, Kv1.5, Kir2.1, and HERG, and the IsK subunit of the IKs-channel complex were expressed in Xenopus oocytes and two-electrode voltage-clamp experiments were performed. Verapamil induced a concentration-dependent block of Kv1. 1-, Kv1.5-, IKs-, and HERG-induced currents with IC50 values of 14.0 +/- 2.7 microM (n = 4), 5.1 +/- 0.5 microM (n = 6), 161.0 +/- 26.3 microM (n = 4), and 3.8 +/- 0.2 microM (n = 5), respectively. The same potency of HERG channel inhibition was observed for the optical enantiomers (+)-verapamil (IC50 = 3.5 +/- 0.4 microM, n = 5) and (-)-verapamil (IC50 = 4.0 +/- 0.7 microM, n = 4), as well as the derivatives norverapamil (D591; IC50 = 3.8 +/- 0.3 microM, n = 4) and D703 (IC50 = 2.2 +/- 0.4 microM, n = 4). The verapamil metabolites D620 and D617 did not block HERG-induced currents at concentrations of up to 30 microM (n = 3). These results demonstrate that cardiac delayed rectifier potassium currents are sensitive targets to calcium channel blockers.

Animals↗
PubMed1998

A simple and stable d.c.electrode for ocular electrophysiology.

We describe the fabrication of a simple silver-silk electrode which permits remarkably stable d.c.recording of the electroretinogram (ERG) and the optic nerve response (ONR). A saline soaked wick of surgical silk, guided into a polyethylene tube connects the tissue to a coil of Ag/AgCl wire placed in a small glass vial, which is filled with 0.9% NaCl. The vial that holds the tube and the wire is closed with a rubber cap allowing easy refilling with NaCl. Examples of the usefulness of the new silver-silk electrode are shown. We applied it in experimental work in the isolated arterially perfused cat eye for d.c.recordings of the ERG and the optic nerve response (ONR), and also in vivo, in anesthetized mice to record c-waves.

Animals↗
PubMed1998

[Leber congenital amaurosis: diagnosis, follow-up and differential diagnosis].

AIM OF THE STUDY: Leber's congenital amaurosis (LCA) had been diagnosed on/in 42 children between 1968 and 1996 at the Deptm. of Ophthalmology, University Hospital Zurich. We reexamined critically this rare diagnosis in retrospect and with new examinations where possible. PATIENTS AND METHODS: Clinical and electroretinographic (ERG) results, often obtained in general anesthesia, were re-evaluated and when possible repeated in new examinations. RESULTS: Thirty-three of the total 42 patients presented with an extinguished, 35 with markedly reduced, and 6 with minimal ERGs. A profound visual loss (from no light perception to 20/200), nystagmus and strabismus were the principal symptoms. The heterogeneity of retinal findings ranged from normal to salt and pepper or bone spicules pigmentation and pronounced chorioretinal atrophy. Vascular attenuation and rarification were frequent. Patients with nonocular findings such as mental retardation (n = 12), renal (n = 3) and skeletal (n = 4) abnormalities revealed no differing ERG- or retinal findings. The oculodigital sign (eye-poking) was found in 25%, and parental consanguinity was evident in 10% of the cases. In 16 patients that were reexamined, the progression of the disease was characterized by an increase in retinal pigmentary changes, attenuation of retinal vessel, and further diminuation of the visual acuity (n = 6). CONCLUSION: Upon review, the diagnosis had to be revised in 8 patients as juvenile retinitis pigmentosa and in one as infantile Refsum syndrome. Bilateral visual impairement in infants should be assessed clinically and electroretinographically within the first year. Neuropediatric and metabolic examinations meaningfully complement the diagnostic procedures.

Child↗
PubMed1998

Light-induced cell death of retinal photoreceptors in the absence of p53.

PURPOSE: Cell death by apoptosis is essential for normal development and tissue homeostasis, and it is involved also in a variety of pathologic processes. Apoptosis is the final common pathway of photoreceptor cell death in retinal dystrophies and degeneration. So far, little is known about genes regulating apoptosis in the retina. The tumor-suppressor gene product p53 is a potent regulator of apoptosis in numerous systems. However, p53-independent apoptotic pathways also have been described. In this study the authors investigated the role of p53 in the light-induced apoptosis of retinal photoreceptors using mice lacking p53. METHODS: Free-moving p53-/- and p53+/+ mice were dark adapted and were exposed to 8,500 or 15,000 lux of diffuse, cool, white fluorescent light for 2 hours. Animals were killed before and immediately after light exposure or at 12 hours in darkness after light exposure. Eyes were enucleated and processed for light and electron microscopy and histochemistry (TdT-dUTP terminal nick-end labeling method). Isolated retinas were subjected to the extraction of total retinal DNA. Electroretinogram (ERG) recordings were performed at all time points. RESULTS: Morphologic, biochemical, histochemical, and ERG analysis showed that the retinas of untreated p53-/- mice and wild-type control mice were structurally and functionally indistinguishable. After exposure to diffuse white fluorescent light, light-induced photoreceptor cell death was analyzed and was found to be the same in both groups of mice. CONCLUSIONS: These data suggest that light-induced apoptosis of photoreceptors is independent of functional p53.

Animals↗
PubMed1997

Effects of insulin under normal and low glucose on retinal electrophysiology in the perfused cat eye.

PURPOSE: To investigate the short-term effects of fast-acting insulin on the electroretinogram-b-wave, optic nerve response, standing potential, and flow rate in the arterially perfused cat eye under normal conditions and during low glucose levels. METHODS: Enucleated cat eyes were perfused with a glucose- and insulin-free tissue culture medium, to which glucose was applied at normal (5.5 mM) and reduced (2 and 1 mM) concentrations. Photic stimulation was performed in the rod-matched intensity range before, during, and after insulin application at postprandial (5 ng/ml) and at 10 and 20 x higher concentrations. RESULTS: Insulin failed to affect retinal signals at normal glucose levels. However, insulin enhanced the low glucose-induced decrease in rod-driven b-wave amplitude (P < 0.05 at 2 mM; P < 0.01 at 1 mM) without affecting the corresponding changes in the optic nerve response. The standing potential increased by as much as 0.75 mV in response to insulin. The perfusate flow rate was not altered by insulin. CONCLUSIONS: Insulin was not required for normal retinal function as observed during 10 hours of perfusion. The differential responsiveness to insulin under low glucose of the b-wave versus the optic nerve response is thought to reflect suppression of glucose use by Müller (glial) cells rather than neuromodulation, as the neuronal optic nerve response is unaffected. The postulated insulin sensitivity of Müller cells (changes in b-wave amplitude) indicates a possible difference in the mechanism of glucose metabolism of glia versus neurons. The electrophysiological effect of insulin under low glucose suggests its passage across the blood-retina barrier. The increase in the standing potential is likely to be a receptor-mediated retinal pigment epithelium effect. These results provide evidence in the retina for the reported multifunctional nature of the insulin receptor.

Animals↗
PubMed1997

Glucose concentration and retinal function.

The rod and cone systems of the mammalian retina differ in their structure and functional properties as well as in their metabolic characteristics. This article summarizes basic observations on retinal glucose metabolism reflected in retinal electrophysiology. Metabolic factors might be related to the complex pathogenesis of diabetic retinopathy. Effects of changing glucose concentration and, independently, of insulin on retinal responses obtained in an isolated mammalian eye preparation in vitro and also in vivo are presented. Electron microscopy (EM)-histochemical data reveal a distinctive distribution of glycogen in glia and in various subclasses of neurons in the cat retina. Low glucose, corresponding to hypoglycemia in vivo, affected the light-evoked electrical responses from the rod system, but not from the cone system in vitro. This could be confirmed in the anesthetized cat under glucose clamp conditions. Insulin had no influence on physiological retinal function, except under conditions of low glucose, where it enhanced the reduction in b-wave amplitude. This effect is interpreted as a sign of increased glucose utilization by the retinal Müller (glial) cells.

Animals↗
PubMed1996

Cholinergic effects on cat retina In vitro: changes in rod- and cone-driven b-wave and optic nerve response.

To identify cholinergically mediated components in the optic nerve response (ONR) we studied effects of cholinergic agonists and antagonists in the arterially perfused cat eye. Acetylcholine, carbachol, scopolamine, quinuclidinylbenzilate and mecamylamine were applied intra-arterially in micromolar concentrations. Recordings of rod- and cone-driven ERG accompanied those of the ONR and revealed: (i) cholinergic agonists enhanced the b-wave, particularly under photopic conditions, whereas scopolamine decreased the b-wave. Mecamylamine induced biphasic effects (decrease followed by increase) in the amplitudes of the rod- and cone-driven b-waves. The effects on the cone-driven ERG were more marked than those on the rod-driven ERG. (ii) The ON-component of the ONR was increased, then decreased by acetylcholine. The cholinergic antagonists exerted complex changes in the ONR-ON component depending on dosage and adaptation. Scopolamine increased, then decreased the rod-driven ON-component, but mainly increased the cone-driven ON-component. Mecamylamine tended to increase the cone-driven, but to decrease the rod-driven ON-component of the ONR. (iii) The configuration of the rod- as well as for the cone-driven ONR, in particular the early plateau and OFF-components, were consistently and reversibly changed by cholinergic agonists, as well as by both muscarinic and nicotinic antagonists. Agonists decreased, and antagonists increased the amplitude of the plateau-component. We conclude that the ERG b-wave was enhanced by acetylcholine, but decreased by cholinergic antagonists. Cholinergic agonists and antagonists affect the same specific components of the ONR in a dose-related and reversible fashion, indicating a major contribution of cholinergic mechanisms to information processing in the cat retina.

Acetylcholine↗
PubMed1996

Full characterization of the maculopathy associated with an Arg-172-Trp mutation in the RDS/peripherin gene.

The objective of this study was to fully characterize the macular dystrophy phenotype and genotype in a large family of the Zermatt area of Switzerland. Clinical and molecular studies of the family included a comprehensive eye examination and a mutational analysis of the RDS, rhodopsin, and TIMP-3 genes. In selected cases, fluorescein angiography, perimetry, and electroretinography were performed. Forty-two family members at risk of expressing the maculopathy were studied. Of these, 24 were found to be clinically affected. The severity of macular disease in these patients was clearly age-related and different stages of progression were identified. Central pigmentary alterations were seen in adolescent patients, while patients in their late teens and twenties exhibited drusen-like deposits. Later, these defects formed focal areas of atrophy which eventually led to central geographic atrophy with severe visual loss by the fifth decade and cone-rod dysfunction. The transmission of this condition is autosomal dominant with complete penetrance. The underlying genetic defect is a mutation in codon 172 of the RDS/peripherin gene, a gene expressed in both rods and cones, which results in the substitution of tryptophan for an arginine residue at that position. 'Zermatt macular dystrophy' is a dominant, age-related, progressive macular dystrophy which in later stages resembles atrophic age-related macular degeneration. The size of the family studied allowed definition of the clinical spectrum of this condition and identification of the related genetic defect which allows more precise diagnosis and counseling.

Adult↗
PubMed1996

Histochemical demonstration of glycogen in neurons of the cat retina.

PURPOSE: To demonstrate histochemically the cellular distribution of particulate glycogen in the cat retina and to correlate it with glucose sensitivity of neuronal electrical activities. METHODS: Free-floating, ultrathin sections of cat eyes (without glucose challenges) were stained by the periodic acid-thiocarbohydrazide-silver proteinate procedure and examined by electron microscopy. RESULTS: Muller cells were filled uniformly with fine-grain glycogen throughout all retinal layers. Particle density was higher in Muller cells of the peripheral retina than in those of central retina. Astrocytes contained little, if any, particulate glycogen. Alpha and beta ganglion cells had a heavy content of clumped glycogen granules. Rod bipolar and A17 amacrine cells of the rod pathway were stained intensely with particulate glycogen. No glycogen was seen in photoreceptor cells, cone bipolar cells, and the majority of amacrine cells, including AII cells of the rod pathway. However, one type of cone bipolar-driven amacrine cell was intensely glycogen positive. Its ultrastructural morphology, stratification pattern, and synaptology suggest that is a wide-field, axon-bearing type called A22. CONCLUSIONS: Except for the cone bipolar-driven ON-OFF A22 amacrine cell, it appears that glycogen staining preferentially labels neurons of the rod pathway. These observations are compatible with the reported sensitivity of the rod-driven electroretinogram and optic nerve response to glucose in the cat retina.

Animals↗