Search PubMed⌕ Search

Biomedical subjects

H Ripps

Publications and source records attributed to H Ripps.

At least 73 records · Page 4Linked to original sources
PubMed1987

Photoreceptor processes in visual adaptation.

In this paper we have stressed two experimental results in need of explanation: (i) the reduced efficacy with which (remaining, abundant) rhodopsin in the light-adapted receptor mediates the flash response; and (ii) the disparity in conditions of irradiation (weak background vs. extensive bleaching) leading to equivalent conditions of threshold. The model discussed above suggests, in molecular terms, a possible basis for both properties of receptor adaptation. On the view developed here, property (i) derives from the ability of photoactivated or bleached pigment (R or B) to restrict dramatically the availability of a substance required for phototransduction. Property (ii) derives in large part from the pronounced disparity in the effectiveness of R (during illumination) and B (remaining after illumination) in reducing the availability of this substance. On this view, the "equivalence" of threshold elevation in states of light- vs. dark-adaptation derives from an overall equality of a product of factors (Q, Etot/Es, and J of equation 2). Under all but extreme conditions, this aggregate of factors is dominated by the term Etot/Es, reflecting the functional state of E.

Animals↗
PubMed1987

Progressive cone dystrophy.

Psychophysical, reflectometric, and electrophysiologic studies were done on four members of a dominant pedigree with progressive cone dystrophy. The two youngest individuals were asymptomatic at the initial examination, and none of the subjects complained of problems associated with night vision. Nevertheless, absent or grossly reduced cone-mediated electroretinographic (ERG) responses showed the widespread loss of cone function, and moderate elevations (less than 1 log unit) in absolute threshold together with reductions in rhodopsin levels in the mid-peripheral retina provided evidence of impairment of the rod system. The progressive nature of the disease was apparent from the case histories and the changes in visual performance that occurred on re-test after a 5-year interval. Moreover, the results of increment threshold measurements at several retinal loci suggested that peripheral cones may be affected earlier and more severely than those in the central retina.

Adolescent↗
PubMed1987

Variable expressivity in fundus albipunctatus.

A healthy, 14-year-old girl presented with nyctalopia, good vision, and multiple, irregular, yellowish lesions of the fundus. Dark adaptometry showed prolonged cone and rod branches, elevated thresholds, and the cone-rod transition occurring after 50 minutes in darkness. Her scotopic electroretinogram (ERG) b-wave attained normal amplitudes after 45 minutes of dark adaptation. The half-time for regeneration of rhodopsin after an extensive bleach was 16 minutes, four times longer than normal, and the maximum density difference measured by fundus reflectometry was at the lower limit of the normal range. Although photopigment kinetics were significantly faster than observed in other reported cases of fundus albipunctatus, it appears likely that there is a wide spectrum of functional and funduscopic abnormalities in this disorder. However, fundus appearance, adaptometric findings, and rhodopsin determinations serve to distinguish fundus albipunctatus from other flecked retina diseases.

Adolescent↗
PubMed1987

Progressive cone dystrophy.

Psychophysical, reflectometric, and electrophysiological studies were performed on four members of a dominant pedigree with progressive cone dystrophy. The two youngest individuals were asymptomatic at the initial examination, and none of the subjects complained of problems associated with night vision. Absent or grossly reduced cone-mediated ERG responses revealed the widespread loss of cone function. Moderate elevations (1 log unit) in absolute threshold together with reductions in rhodopsin levels in the midperipheral retina provided evidence of a mild impairment of the rod system also, although not to the degree seen in a cone-rod dystrophy. The progressive nature of the disease was apparent from the case histories and the changes in visual performance that occurred on re-test after a 5-year interval. Likewise, the results of incremental threshold measurements at several retinal loci suggested that peripheral cones may be affected earlier and more severely than those in the central retina.

Adolescent↗
PubMed1985

Pharmacological modification of the light-induced responses of Müller (glial) cells in the amphibian retina.

The light-evoked responses of Müller (glial) cells were monitored by intracellular recording in the isolated, superfused retina of Xenopus laevis. Müller cells had dark resting potentials of -88.5 +/- 6.9 mV and small 1-2 mV light responses of variable waveform in normal Ringer's solution. Exposure to picrotoxin (0.5-1.0 mM) greatly enhanced the light response which then consisted of depolarizing transients (Vmax 5-15 mV) at stimulus onset and offset. GABA (5-10 mM) antagonized the picrotoxin effect and suppressed the light response, whereas 2-amino 4-phosphonobutyrate (0.10-0.15 mM) blocked selectively the 'on' transient. None of these agents appreciably modified the glial cells resting potential level. On the other hand, veratrine (6-9 micrograms/ml) depolarized the Müller cell by 4-13 mV and slowed and greatly reduced the light response. These effects were antagonized by tetrodotoxin (1-4 microM) which itself reduced the light response by 30-50% without altering its shape. On the basis of these findings, we suggest that alterations in the activity of the inner retinal neurons, i.e. amacrine and ganglion cells, are primarily responsible for the drug-induced changes in the membrane potential and light-evoked responses of the Müller cell.

Aminobutyrates↗
PubMed1985

Light-induced potassium fluxes in the skate retina.

Changes in the extracellular concentration of potassium [K+]0 in response to photic stimulation were studied in the skate retina with the aid of ion-selective electrodes. The results confirm earlier studies in demonstrating that the light-evoked changes originate at three intraretinal sites; an efflux of K+ was recorded in the regions of the two plexiform (synaptic) layers, whereas a decrease in [K+]0 occurred in the extracellular space surrounding the photoreceptors. Prolonged illumination induced long-term alterations in the levels of [K+]0 which, depending upon the retinal depth of the recording electrode, contained contributions from the various sinks and sources of [K+]0. In addition, the marked undershoot of the baseline level of [K+]0 that followed termination of the stimulus suggested the activity of a metabolically driven process for the uptake of extracellular potassium.

Animals↗
PubMed1984

Pharmacological properties of isolated horizontal and bipolar cells from the skate retina.

Retinal neurons were enzymatically and mechanically dissociated from adult skate retinas and maintained in cell culture for up to 14 days. Intracellular recordings were made from isolated horizontal and bipolar cells while neurotransmitters were applied via pressure ejection. L-Glutamate, quisqualate, kainate, and gamma-amino-butyric acid (GABA), when applied to horizontal cells, produced large (60 to 70 mV), long-lasting depolarizations. These responses appear to consist of at least two components: a graded depolarization and a Ca++-dependent regenerative component. As regards bipolar cells, L-glutamate and its analogues depolarized about 30% of the cells tested, while GABA hyperpolarized most of these neurons. Both agents acted on bipolar cells by increasing conductance. Repeated applications of L-glutamate, quisqualate, kainate, and GABA to horizontal cells produced no desensitization, but in these circumstances the glutamate analogues, kainate and quisqualate, induced certain morphological changes, most notably a retraction of cell processes and the appearance of blebs on the cell surface.

Animals↗
PubMed1984

Functional abnormalities in vincristine-induced night blindness.

Various noninvasive test procedures were used to evaluate retinal function in a patient who had become night blind following vincristine chemotherapy. The results obtained were strikingly similar to those reported previously in subjects with recessively inherited stationary night blindness; the dark-adaptation curve was monophasic (ie, no evidence of a scotopic branch), rhodopsin kinetics were entirely normal, and spectral threshold data revealed the presence of residual rod-mediated vision. Also like the heritable condition, the b-wave of the ERG was depressed grossly despite normal a-wave potentials. These findings, and the fact that vincristine is known to disrupt the structural integrity of neuronal microtubules, suggest that the drug-induced defect involves the process of synaptic transmission between the photoreceptors and their second-order neurons.

Adaptation, Ocular↗
PubMed1983

The visual cells of the skate retina: structure, histochemistry, and disc-shedding properties.

Earlier studies have shown that visual function in skate is subserved solely by the rod mechanism and that the retina of this elasmobranch contains only rod photoreceptors. Nevertheless, the skate retina is capable of responding to levels of illumination that extend well into the photopic range, and we have detected in histological sections (usually from younger animals) small, proximally displaced, conelike photoreceptors which possibly represent another class of visual cell. However, ultrastructural and histochemical studies showed that the membranous discs of the outer segments of these cells were isolated from the plasma membrane, and that their synaptic terminals appeared immature and unlike those usually associated with cone receptors. In addition, the pattern of incorporation of 3H-fucose, as revealed by radioautography, was similar for both the rods and the smaller visual cells; i.e., the label was concentrated along the basal discs of the outer segment. When we examined the disc-shedding behavior of the visual cells in skates entrained for 2 weeks or longer to a 12-hour light:12-hour dark cycle, enhanced phagocytic activity was seen only following light onset; there was no significant increase following light offset. On the available evidence, it seems reasonable to conclude that the small visual cells are rods that have recently differentiated, and are growing and being incorporated into the photoreceptor layer of the retina.

Animals↗
PubMed1982

Night blindness revisited: from man to molecules. Proctor lecture.

Night blindness is a frequent concomitant of retinal disorders, many of which are of genetic origin. Through the use of quantitative noninvasive test procedures it has been possible to study patients with these hereditary conditions and to show that the visual abnormalities often result from defects in the functional properties of the rod photoreceptors. More important, the uniqueness of the functional disturbance in the various types of night-blinding disorders suggests that each involves a specific aspect of the rod's internal machinery, i.e., the molecular processes devoted to transduction, intercellular communication, and the renewal of cellular components. Knowledge gained from the study of these clinical entities and from the investigation of experimental animals regarding the cellular events involved in these vital processes have enabled us to formulate tentative hypothesis as to the molecular bases of the hereditary defects.

Genetic Diseases, Inborn↗
PubMed1981

Changes in ERG b-wave and Müller cell structure induced by alpha-aminoadipic acid.

The role of the Müller cell in the generation of the ERG b-wave was studied in the skate eye by examining the effects of a gliotoxic agent (alpha-aminoadipic acid; alpha-AAA) on retinal structure and function. Superfusing the eyecup for 1 h in 50 mM alpha-AAA resulted in the loss of the b-wave and extensive damage to glial cells, i.e. disruption of the cells' plasma membranes, and a marked loss of cytoplasmic substance. Of the other retinal elements, only the horizontal cells showed some signs of injury in alpha-AAA. On returning the retina to a normal Ringer solution, the widespread loss of cytoplasmic electron density persisted, but the Müller cell membranes appeared to have undergone repair, and the b-wave recovered fully its normal amplitude and waveform.

Adipates↗
PubMed1981

Flash photolysis of rhodopsin in the cat retina.

The bleaching of rhodopsin by short-duration flashes of a xenon discharge lamp was studied in vivo in the cat retina with the aid of a rapid, spectral-scan fundus reflectometer. Difference spectra recorded over a broad range of intensities showed that the bleaching efficacy of high-intensity flashes was less than that of longer duration, steady lights delivering the same amount of energy. Both the empirical results and those derived from a theoretical analysis of flash photolysis indicate that, under the conditions of these experiments, the upper limit of the flash bleaching of rhodopsin in cat is approximately 90%. Although the fact that a full bleach could not be attained is attributable to photoreversal, i.e., the photic regeneration of rhodopsin from its light-sensitive intermediates, the 90% limit is considerably higher than the 50% (or lower) value obtained under other experimental circumstances. Thus, it appears that the duration (approximately 1 ms) and spectral composition of the flash, coupled with the kinetic parameters of the thermal and photic reactions in the cat retina, reduce the light-induced regeneration of rhodopsin to approximately 10%.

Animals↗
PubMed1981

Rhodopsin kinetics in the cat retina.

The bleaching and regeneration of rhodopsin in the living cat retina was studied by means of fundus reflectometry. Bleaching was effected by continuous light exposures of 1 min or 20 min, and the changes in retinal absorbance were measured at 29 wavelengths. For all of the conditions studied (fractional bleaches of from 65 to 100%), the regeneration of rhodopsin to its prebleach levels required greater than 60 min in darkness. After the 1-min exposures, the difference spectra recorded during the first 10 min of dark adaptation were dominated by photoproduct absorption, and rhodopsin regeneration kinetics were obscured by these intermediate processes. Extending the bleaching duration to 20 min gave the products of photolysis an opportunity to dissipate, and it was possible to follow the regenerative process over its full time-course. It was not possible, however, to fit these data with the simple exponential function predicted by first-order reaction kinetics. Other possible mechanisms were considered and are presented in the text. Nevertheless, the kinetics of regeneration compared favorably with the temporal changes in log sensitivity determined electrophysiologically by other investigators. Based on the bleaching curve for cat rhodopsin, the photosensitivity was determined and found to approximate closely the value obtained for human rhodopsin; i.e., the energy Ec required to bleach 1-e-1 of the available rhodopsin was 7.09 log scotopic troland-seconds (corrected for the optics of the cat eye), as compared with approximately 7.0 in man.

Animals↗
PubMed1981

"Rapid regeneration" in the cat retina: a case for spreading depression.

Fundus reflectometry of the cat retina showed that under certain circumstances a rapid increase in density may follow intense bleaching exposures. The spectral characteristics of the density changes indicated that neither rhodopsin nor its bleach products could be responsible for this effect. The poor condition of the animals in which the phenomenon was observed and its conspicuous absence in the majority of the experimental runs suggested that the effect was associated with a process other than the resynthesis of rhodopsin. It was shown that an extrareceptoral event, spreading depression (SD) of the retina, is the most likely source of the rapid spectral change. The well-known tissue alterations associated with SD were induced in the retina independently of pigment density change. The resultant difference spectra resembled those produced when the rapid density increase occurred spontaneously. It seems likely that the abnormal physiological condition of those cats in which the phenomenon is more frequently observed primes the retina for the light-induced generation of spreading depression.

Animals↗
PubMed1981

Pigmentary abnormalities of the macula in rhesus monkeys: clinical observations.

In a survey of 546 rhesus monkeys of various ages, 6.1% of the animals showed ophthalmoscopically visible hypopigmented spots in their maculas. There was a statistically significant correlation between the age of the animal and the degree of hypopigmentation. Electroretinographic responses and visually evoked potentials were evaluated in a selected group of monkeys with and without hypopigmented macular spots. No significant change in retinal function as a result of the macular abnormalities could be detected.

Age Factors↗