[Intake of 18 g dietary fiber daily for every citizen?].
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Biomedical subjects
Publications and source records attributed to B Rohrer.
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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.
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.
The influence of neural activity on the morphology of retinal-axon-terminal arbors and the precision of the developing retinotectal projection in zebrafish embryos was explored. Terminal-arbor morphology and their distribution in the tectum was determined with anatomical fiber-tracing methods using the fluorescent dyes dil and diO. To allow development under activity-deprived conditions, TTX was injected into the eyes of 30-38-hr-old zebrafish embryos at concentrations that effectively blocked neural activity both in retinal ganglion cells and throughout the CNS. Much like axons with normal neural-activity patterns, activity-deprived axons from dorsal and ventral and from temporal and nasal regions in the retina terminated over retinotopically appropriate and nonoverlapping regions of the tectum. Even after ablation of 1 hemiretina at the time of axonal outgrowth, activity-deprived axons from the remaining hemiretina grew directed toward and arborized selectively within their retinotopically appropriate tectal half in the same way as would nondeprived axons. Besides being retinotopic, the area over which small populations of activity-deprived axons from neighboring ganglion cells arborize is as small as that of active axons. The size of terminal arbors of retinal ganglion cell axons was unaffected by blockade of neural activity. The mean terminal-arbor size was 27 x 18 microns for the TTX-injected and 31 x 22 microns for the control embryos. The tectal coverage of TTX-blocked and control axons was equally small, with values of 1.4% and 1.6%, respectively. These data show that a precisely organized retinotopic map in developing zebrafish forms independent of neural-impulse activity.
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Studies of form-deprivation myopia (FDM) in animal models have shown that postnatal ocular growth is regulated by the quality of patterned images on the retina. One of the major challenges in myopia research is to identify the biochemical mechanisms which translate retinal visual responses into signals that regulate scleral growth. Dopamine (DA) has been implicated in this process, since retinal DA levels decline in FDM and subconjunctival injections of apomorphine (Apo, a nonspecific DA agonist) prevent FDM in a dose-dependent way (Stone et al., 1989). To gain insight into where and how DA ligands act to regulate ocular elongation, we compared the action and distribution of DA receptor ligands injected intravitreally vs. subconjunctivally in young chicks. Ocular length was measured by A-scan ultrasound. We found that daily intravitreal injections of Apo block FDM at a 50% effective dose (ED50) of 5 pg per day, or a peak concentration in the vitreous humor of 108 pM, compared to an ED50 of 2.5 ng for subconjunctival injections as reported by Stone et al. (1989, 1990). [3H]-spiperone, a D2-receptor antagonist, reached average maximum retinal concentrations of 160 pM and 260 pM, during the first hour after intravitreal and subconjunctival administration, respectively, at the ED50 dose. In contrast, the maximum spiperone concentrations in the retinal pigment epithelium (RPE) were 30 pM and 410 pM, respectively, after intravitreal or subconjunctival ED50 doses. Spiperone concentrations in sclera after ED50 doses to the two sites differed by 4 x 10(4) (0.4 pM vs. 1.7 nM, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)
In this study, the possible role of the retinal enkephalin system in form-deprivation myopia (FDM) in the chick eye was investigated. Daily intravitreal injection of the nonspecific opiate antagonist naloxone blocked development of FDM in a dose-dependent manner, while injection of the opiate agonist morphine had no effect at any dose tested. The ED50 for naloxone (calculated maximum concentration in the vitreous) was found to be in the low picomolar range. The results using receptor-subtype-specific drugs were contradictory. Drugs specific for mu and delta receptors had no effect on FDM. The kappa-specific antagonist nor-binaltorphimine (nor-BNI) reduced FDM by about 50% at maximum daily retinal doses ranging between 4 x 10(-10) and 4 x 10(-7) M, while the kappa-specific agonist U50488 blocked FDM in a dose-dependent manner with an ED50 between 5 x 10(-8) and 5 x 10(-7) M. Met-enkephalin immunoreactivity (ME-IR) was localized immunocytochemically to a subset of amacrine cells (ENSLI cells) and their neurites in the inner plexiform layer (IPL). As reported previously, ENSLI cells from untreated chick retinas showed a cyclical pattern of immunoreactivity, with increased immunoreactivity in the light compared to the dark. Form-deprivation did not appear to change this pattern. Amounts of preproenkephalin mRNA from normal or form-deprived eyes were approximately the same under all conditions. Daily injection of naloxone, however, did increase ME-IR in the dark. These results suggest that naloxone may affect release of enkephalin from the ENSLI cells. The results as presented are inconclusive with regards to the role of the enkephalin system in FDM. While the kappa receptor may participate, there is no conclusive evidence here for a direct effect of opiate receptors. The effect of naloxone on form-deprived eyes may be due to its effect on release of peptides from the ENSLI cells.