Biomedical subjects

E Zrenner

Publications and source records attributed to E Zrenner.

At least 181 records · Page 10Linked to original sources

PubMed1993

The spectral sensitivity of dark- and light-adapted cat retinal ganglion cells.

The spectral sensitivity of cat retinal ganglion neurons (RGNs) was determined by means of extracellular recordings under scotopic and photopic conditions, in both receptive field center and surround. Test stimuli were presented either as square-wave single flashes or as flicker stimuli. Chromatic adaptation was achieved by a large steady monochromatic background field. In the dark-adapted state the spectral sensitivity of the majority of ganglion cells (92%) was rod mediated (peak sensitivity at 501 nm). Under photopic conditions all neurons received input from a long-wavelength-sensitive (L-cone) system with a peak sensitivity of 550 nm. Input from a short-wavelength-sensitive (S-cone) system (peak sensitivity at 450 nm), however, was found only in 15% of the ganglion cells. A small cell population (8%) located within the area centralis revealed a different receptive field organization. In these cells, spectral sensitivity in the field center peaked at 520 nm in the dark-adapted state and response threshold was about 1 log unit higher than in cells with a peak sensitivity of 501 nm. Critical flicker fusion was reached at 60-70 Hz, a frequency that usually is mediated by cones. We therefore postulate an additional input of a midspectral receptor system (M-system) other than rods in cat retinal ganglion cells. This input was found only in the receptive field center of some ganglion cells in the dark-adapted state, whereas the surround sensitivity was mediated in all cells by rod signals under scotopic and predominantly by L-cone signals under photopic conditions.

Adaptation, Physiological↗

PubMed1993

[Differential diagnostic strategies in uncertain vision disorders].

The differential diagnosis of visual disturbances of unclear origin can cause major problems in ophthalmology, especially if there are no functional defects or if functional defects cannot be explained by morphological findings after an extensive regular ophthalmological investigation. The aim of this paper is to present strategies that allow subtle visual disturbances to be related to certain groups of functional defects. Especially simple investigations are emphasized that lead quickly to a well-founded possible diagnosis that helps both the ophthalmologist and patient save time and cost-consuming deviations. The key investigations are: (1) a symptom-oriented case history; (2) exclusion of refractive problems by pin-hole test, retinoscopy and ophthalmometry; (3) the swinging flashlight test; (4) ophthalmoscopy of the macula and optic disc; (5) visual field. A flow chart is presented that explains the strategy of additional special investigations based on the results of the key findings in order to approach quickly the cause of a visual disturbance. Some of the more common causes of visual disturbances of unclear origin are discussed, including some major therapeutic principles.

Humans↗

PubMed1992

Deletions in exon 5 of the human rhodopsin gene causing a shift in the reading frame and autosomal dominant retinitis pigmentosa.

By screening patients with autosomal dominant retinitis pigmentosa for mutations in the rhodopsin gene, two deletions (8 bp and 1 bp) have been identified in exon 5; these deletions cause a shift in the reading frame. The predicted proteins should be radically altered with translation continuing past the normal stop signal and resulting in a rhodopsin molecule that is, respectively, 1 and 10 amino acids longer. The clinical phenotype of the patients is described and is compared with that associated with other mutations in the same region of the gene.

Adult↗

PubMed1992

Wavelength discrimination as a function of field intensity, duration and size.

Wavelength discrimination was measured in 8 normal observers as a function of test field intensity (2.5-63 td), duration (0.5-5 sec) and dia (0.5-2 degrees) to determine the conditions under which the just noticeable difference (JND) is smallest. The wavelengths of the standard and comparison hemifields were always equated for the observer's sensation luminance. For field intensity and duration, the wavelength JND was found to decrease until these parameters were increased beyond a certain value--25 td and 1.0 sec, respectively--and to remain constant thereafter. For field diameter, however, the JND was smallest only within a very limited range of values--between 1.0 and 1.5 degrees--and increased sharply with smaller and larger values.

Adult↗

PubMed1992

Dose-dependent effects of 6-hydroxy dopamine on deprivation myopia, electroretinograms, and dopaminergic amacrine cells in chickens.

We found that a single intravitreal injection of 6-hydroxy dopamine (6-OHDA) is highly efficient in blocking the development of deprivation-induced myopia in young chickens. To investigate the effects of 6-OHDA on retinal function, we studied electroretinograms (ERGs) in chickens aged 15-25 days, 4 days subsequent to the injection. Both spectral sensitivity and oscillatory potentials were tested. In addition, a histological examination was performed of dopaminergic amacrine cells labeled by a monoclonal antibody against tyrosine hydroxylase. We found that, at doses of 6-OHDA sufficient to suppress deprivation myopia entirely, no effect could be detected on either the ERGs or on the density and appearance of dopaminergic amacrine cells. For higher doses, spectral sensitivity and the number of dopaminergic amacrine cells declined gradually. In contrast, as doses increased, oscillatory potentials 1 and 2 grew in amplitude only to decline at the highest doses. The results indicate that (1) development of deprivation myopia requires normal retinal function and that (2) slight changes in the gains of dopaminergic pathways are sufficient to block the development of deprivation myopia.

Animals↗

PubMed1992

["Glare vision". I. Physiological principles of vision change with increased test field luminance].

Clinical tests of visual acuity are an important measure of visual function. However visual acuity is usually determined only in narrow range of luminance levels between 160 and 320 cd/m2; therefore losses of visual acuity in other ranges of light intensity can not be detected. In a distance of 80 cm from the patients eyes, Landolt rings of varying sizes were presented on a small test field whose light intensity can be varied between 0.1 and 30,000 cd/m2. Thereby an acuity-luminance-function can be obtained. We studied such functions under different conditions of exposure time both with constant and with increasing luminance of the test field. We found that persons with normal vision can increase their visual acuity with increasing test field luminance up to a range of 5000 cd/m2. The maximum values of visual acuity under optimal lightening conditions lie (varying with age) between 2.2 and 0.9. Under pathological conditions visual acuity falls at high luminances accompanied by sensations of glare. Tests of glare sensitivity as a function of exposure time showed 4 sec to be a critical time of exposure since after 4 sec normal persons just reach their maximum visual acuity at high luminances. The underlying physiological mechanisms lead us to suppose that patients with neuronal light adaptation disturbances display a greater visual loss as a result of decreased time of exposure than those with disturbances in the ocular media. Visual acuity as well as the capacity to increase the patients visual acuity under optimal conditions of lighting were both found to be strongly age-dependent.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1992

["Glare vision". II. Study of visual acuity of glare sensitive patients in increasing test field luminance].

Sensitivity to glare is an unspecific ophthalmological symptom that can be caused by different anatomical structures; it can be related to optical and to cortical structures, it also can be due to defects in the neuronal mechanisms of the retina that control adaptation processes. In many cases the exact mechanisms are still unknown. Tests of visual acuity in glare sensitive patients with increasing test field luminance reveal-depending on the underlying disease-several types of variations from the normal visual-acuity-function that was determined over a wide range of light intensity from 0.1 to 30,000 cd/m2. Marked changes in the visual acuity-luminance-function at high test field intensities were found primarily in patients with retinal diseases, particularly in disturbances of the cone system. These visual acuity losses at high test field luminances can be explained by major functional impediments of the neuronal adaptive mechanisms at the retinal level. Less apparent were the changes in visual acuity-luminance-function in cases of optic nerve diseases. According to our studies changes in the visual acuity-luminance-function accompanied with high glare sensitivity are most often due to pathological changes in neuronal circuitry of the retina, less often to the effects of stray light. This test therefore can provide an important criterion for establishing the correct diagnosis.

Adolescent↗

PubMed1992

Longitudinal chromatic aberration and emmetropization: results from the chicken eye.

1. Due to the chromatic dispersion of the ocular media, the focal length of the optics of the eye is about 3 diopters longer for red light than for blue light. Because emmetropization in the chicken (Gallus domesticus) does not require colour cues and operates properly in monochromatic light, one can, therefore, expect that chickens raised in red light become more myopic (with longer eyes) than chicks raised in short wavelength light. Prior to conducting this experiment, we matched the brightness of both light conditions by means of flicker electroretinograms such that equiluminance was obtained for the chickens. 2. Unexpectedly, refractive development was not different from controls in white light for either red or near-ultraviolet light. 3. We tested whether the visual mechanisms guiding refractive development were still sensitive to defocus under both illuminations by treating the chicks with spectacle lenses. 4. Similar to a previous experiment in white light, the growth of the eye in red light also changed such that it compensated for the imposed defocus. It failed to do so, however, in near-ultraviolet light. 5. A histological analysis of the sampling intervals for the ultraviolet receptor system revealed that its spatial resolving power was too low to detect the defocus imposed by the lenses, whereas the long wavelength receptors provided sufficiently good visual acuity. 6. The results show that, during emmetropization, the chicken eye elegantly bypasses the problem of multiple chromatic focal planes by having a low sensitivity to defocus in the blue end of the spectrum. Because the chromatic dispersion function is steep in the blue range but flat at the red end of the spectrum, the remaining chromatic defocus in the spectral range of high visual acuity is low and may match the depth of field of the eye.

Animals↗

PubMed1992

Horner's syndrome: a retrospective analysis of 90 cases and recommendations for clinical handling.

The records of 90 cases of oculosympathetic paresis (1982-1991), 39 women and 51 men aged between 3 months and 82 years, were evaluated. The mean baseline anisocoria was 0.92 mm but did not exceed 2.4 mm. The mean difference in the position of the upper eyelid was 2.3 mm. Enophthalmus of 1 mm or more was found in only 25% and exophthalmus of 1 mm or more, in 18%. Exophthalmus or enophthalmus of more than 2 mm was not encountered. The cocaine test (5% solution in most cases) was performed in 85 cases and could be quantified in 65 cases. The average dilation of the involved pupil was 0.52 mm, whereas the normal pupil dilated 2.14 mm. The average postcocaine anisocoria was 2.54 mm. Hydroxyamphetamine 1% dilated the involved pupil in cases with presumed preganglionic lesions slightly more than the normal fellow pupil (2.39 mm and 2.09 mm respectively). The difference was significant (P < 0.05). In postganglionic lesions, the hydroxyamphetamine dilation was 0.57 mm. The hydroxyamphetamine test had a specificity of 90% for postganglionic lesions and 88% for preganglionic. An underlying acquired disease could be identified in 53 cases; 6 cases were congenital. In 37 cases (including the congenital ones), no cause was found. Among the 33 preganglionic lesions, only one malignant tumor was found, whereas 6 malignant tumors were encountered among the 20 postganglionic cases. Additional ocular motor palsies or other local signs were present in these 6 cases. Goiter was frequently associated with preganglionic Horner's syndrome.

Adolescent↗

PubMed1992

Diffuse loss of rod function in autosomal dominant retinitis pigmentosa with pro-347-leu mutation of rhodopsin.

There is considerable variety among the clinical features of autosomal dominant retinitis pigmentosa (ADRP). This is probably at least in part due to genetic heterogeneity. Recently, various mutations of the rhodopsin gene have been detected in some ADRP families. We report on six patients from two families with ADRP who were investigated by means of psychophysical and electrophysiological methods. All displayed the same rhodopsin gene mutation at codon 347, which exchanges the amino acid proline for leucine (pro-347-leu). The patients had early-onset night blindness and impaired side vision as of the end of their second life decade. They produced monophasic dark-adaptation curves, showing a lack of rod function and elevated cone thresholds. Dark-adapted two-color threshold perimetry using 500- and 650-nm stimuli revealed a diffuse loss of rod function and centrally preserved cone function. The electroretinogram was nonrecordable at the age of about 30 years. A certain variability of visual function loss was noted among patients in the overall severe course of the disease, but the clinical findings of this genotype corresponded to type 1 ADRP of Massof and Finkelstein in all cases.

Adult↗

PubMed1992

Human tritanopia associated with two amino acid substitutions in the blue-sensitive opsin.

Tritanopia is an autosomal dominant genetic disorder of human vision characterize by a selective deficiency of blue spectral sensitivity. The defect is manifested within the retina and could be caused by a deficiency in function or numbers (or both) of blue-sensitive cone photoreceptors. We have used PCR, denaturing gradient gel electrophoresis, and DNA sequencing of amplified exons to detect in four of nine unrelated tritanopic subjects two different point mutations in the gene encoding the blue-sensitive opsin, each leading to an amino acid substitution. Segregation analysis within pedigrees and hybridization of oligonucleotides specific for each allele to DNA samples from control subjects support the hypothesis that these mutations cause tritanopia. These results complete the genetic evidence for the trichromatic theory of human color vision.

Arginine↗

PubMed1992

[Retinitis pigmentosa. Clinical findings, results of molecular genetic techniques and research perspectives].

In recent years, research efforts in the basic and clinical sciences have yielded numerous new findings. The review given here outlines clinical findings, research results, and perspectives on the origin of hereditary retinal degeneration as far as molecular genetics, biochemistry, morphology, and clinical research are concerned: genotype-phenotype correlation, electroretinography, color perimetry, blue cone function, exogenous factors, refraction problems, fat metabolism, immunological aspects, retinal transplantation, and phenocopies of retinitis pigmentosa and related syndromes. The consequences for ophthalmological practice are pointed out and comprehensive, improved diagnostic procedures are recommended, using a checklist proposed here (see appendix).

Adult↗

PubMed1992

Detection and characterization of point mutations in the choroideremia candidate gene by PCR-SSCP analysis and direct DNA sequencing.

By making use of positional cloning strategies we recently isolated a candidate gene for choroideremia (CHM), which is transcribed in retina, choroid, and/or retinal pigment epithelium. The gene contains an open reading frame that is structurally altered in 10 CHM patients with sizable deletions and in a female patient with a balanced translocation involving the Xq21 band. Employing PCR-SSCP analysis and direct DNA sequencing we have now detected and characterized different point mutations in five patients with CHM. Each of these mutations introduces a termination codon into the open reading frame of the CHM candidate gene, thereby predicting a distinct truncated protein product. Together these findings provide convincing evidence for the candidate gene being identical with the choroideremia gene.

Amino Acid Sequence↗

PubMed1991

Is colour vision possible with only rods and blue-sensitive cones?

At night all cats are grey, but with the approach of dawn they take on colour. By starlight, a single class of photoreceptors, the rods, function, whereas by daylight, three classes, the blue-, green- and red-sensitive cones, are active and provide colour vision. Only by comparing the rates of quantal absorption in more than one photoreceptor class is colour vision possible. Although the comparisons generally take place between the cones, they can involve the rods as well. Here we investigate the wavelength discrimination of an extremely rare group of individuals, blue-cone monochromats, who have only rods and one class of cones. We find that these individuals can distinguish wavelengths (440 to 500 nm) in the twilight region where the rods and blue-sensitive cones are simultaneously active.

Color Perception↗

PubMed1991

Mizuo phenomenon in X-linked retinoschisis. Pathogenesis of the Mizuo phenomenon.

Four unrelated males with X-linked retinoschisis and a golden fundus reflex had Mizuo-Nakamura phenomenon, which, to our knowledge, has been described only in Oguchi's disease and X-linked cone dystrophy. These findings, together with experimental observations and data from the literature, led us to hypothesize that the Mizuo-Nakamura phenomenon is caused by an excess of extracellular potassium in the retina as a result of a decreased potassium scavenging capacity of retinal Müller cells.

Adult↗

PubMed1991

Effects of D-1 and D-2 dopamine antagonists on ERG and optic nerve response of the cat.

Various concentrations of three dopamine antagonists (fluphenazine, haloperidol and sulpiride) with different affinities to the receptor subtypes were applied in order to test their effect on responses from outer (isolated PIII-component of the ERG), middle (b-wave) and inner (optic nerve response, ONR) retinal layers, recorded from dark-adapted, isolated, arterially-perfused cat eyes. In the range of concentrations tested (e.g. from 4 nmol ml-1 to 16 mumols ml-1 for haloperidol) none of the drugs added to the perfusion medium had any effect on either slow or fast PIII-amplitude or on the temporal characteristics of the response. All dopamine antagonists increased the rod b-wave with a comparable molar efficacy. The rod b-wave latency and implicit time showed no drug-induced changes. In the rod ONR the D-1 antagonist fluphenazine increased the fast transient on-component while it simultaneously strongly decreased the off-component. IN contrast, concentrations of the D-2 antagonists sulpiride that had a comparable effect on the ONRs fast transient on-component influenced neither the slow transient on-component nor the off-component. These findings indicate that the D-1 and D-1 receptors play different roles in the transmission of rod signals at the border of middle and inner retina.

Animals↗

PubMed1991

Angiotensin-like immunoreactive cells in the chicken retina.

The cellular distribution of Angiotensin II (ANGII) in the chicken retina was studied by immunocytochemical methods. Three different antibodies directed against ANGII revealed a distinct subpopulation of ANGII-positive amacrine cells. Their cell bodies were located in the innermost rows of the inner nuclear layer (INL). ANGII-positive cell bodies also were found in the ganglion cell layer (GCL). Faint labelling in the centre of the INL was visible, probably related to Müller cell bodies. Single ANGII-positive fibres, each arising from an amacrine cell body, ran to sublayer 3 or 5 of the INL, forming narrow plexi. In addition, small fibres connecting sublayer 3 with sublayer 5 could be observed. ANGII-positive fibres could neither be detected in the optic nerve nor in the outer parts of the retina. Incubation of the tissue in ANGII or angiotensin I (ANGI) dissolved in Ringer solution prior to fixation, increased number and intensity of labelled cells and resulted in better labelling of sublayers 3 and 5 of the inner plexiform layer (IPL). Blockage of the conversion of ANGI to ANGII by adding captopril to the ANGI containing pre-incubation medium reduced the ANGII induced staining enhancement. All three ANGII-antibodies showed corresponding results. These results indicate that a subpopulation of amacrine cells contains angiotensin II in chicken retina. This subpopulation is apparently able to take up ANGII and ANGI, to convert ANGI to ANGII and to store ANGII.

Angiotensin II↗

PubMed1991

Diurnal control of rod function in the chicken.

We studied rod function in the chicken by recording corneal electroretinograms (ERGs). The following experiments were performed to demonstrate rod function during daytime: (1) determining the dark-adaptation function; (2) measuring the spectral sensitivity by a a-b-wave amplitude criterion in response to monochromatic flickering light of different frequencies ranging from 6.5-40.8 Hz (duty cycle 1:1); (3) analyzing the response vs. log stimulus intensity (V-log I) function in order to reveal a possible two phase process; and (4) determining the spectral sensitivity function either in a non-dark adapted state or after dark adaptation of the animals for 1 and 24 h. None of these experiments demonstrated clear evidence of rod function during daytime. On the other hand, we found rods histologically by light- and electron microscopy. Therefore, we repeated our ERG recordings during the night (between midnight and 3:00 A.M.). Without previous dark adaptation, rod function could be seen immediately in the same experiments described above. The result shows that, in the chicken, rods are turned on endogenously during the night but are scarcely functional during the day.

Animals↗