6 results on '"Rosenstein, Ruth E."'
Search Results
2. Effect of retinal ischemia on the non-image forming visual system.
- Author
-
González Fleitas, María Florencia, Bordone, Melina, Rosenstein, Ruth E., and Dorfman, Damián
- Subjects
RETINAL injuries ,ISCHEMIA ,VISION disorders ,RETINAL ganglion cells ,PHOTOSYNTHETIC pigments ,MELANOPSIN ,OPTICAL reflection - Abstract
Retinal ischemic injury is an important cause of visual impairment. The loss of retinal ganglion cells (RGCs) is a key sign of retinal ischemic damage. A subset of RGCs expressing the photopigment melanopsin (mRGCs) regulates non-image-forming visual functions such as the pupillary light reflex (PLR), and circadian rhythms. We studied the effect of retinal ischemia on mRGCs and the non-image-forming visual system function. For this purpose, transient ischemia was induced by raising intraocular pressure to 120 mm Hg for 40 min followed by retinal reperfusion by restoring normal pressure. At 4 weeks post-treatment, animals were subjected to electroretinography and histological analysis. Ischemia induced a significant retinal dysfunction and histological alterations. At this time point, a significant decrease in the number of Brn3a(+) RGCs and in the anterograde transport from the retina to the superior colliculus and lateral geniculate nucleus was observed, whereas no differences in the number of mRGCs, melanopsin levels, and retinal projections to the suprachiasmatic nuclei and the olivary pretectal nucleus were detected. At low light intensity, a decrease in pupil constriction was observed in intact eyes contralateral to ischemic eyes, whereas at high light intensity, retinal ischemia did not affect the consensual PLR. Animals with ischemia in both eyes showed a conserved locomotor activity rhythm and a photoentrainment rate which did not differ from control animals. These results suggest that the non-image forming visual system was protected against retinal ischemic damage. [ABSTRACT FROM AUTHOR]
- Published
- 2015
- Full Text
- View/download PDF
3. Effect of Experimental Diabetic Retinopathy on the Non-Image-Forming Visual System.
- Author
-
Fernandez, Diego C., Sande, Pablo H., de Zavalía, Nuria, Belforte, Nicolás, Dorfman, Damián, Casiraghi, Leandro P., Golombek, Diego, and Rosenstein, Ruth E.
- Subjects
DIABETIC retinopathy ,BLINDNESS ,RETINAL ganglion cells ,MELANOPSIN ,CIRCADIAN rhythms ,SUPRACHIASMATIC nucleus ,STREPTOZOTOCIN - Abstract
Diabetic retinopathy is a leading cause of blindness. Intrinsically photosensitive retinal ganglion cells (ipRGCs), which express the photopigment melanopsin, are involved in non-image-forming visual responses such as photoentrainment of circadian rhythms and pupilary light reflex. Since several reports indicate that retinal ganglion cells are affected by diabetes, we investigated the non-image-forming visual system in an advanced stage of experimental diabetes in rats induced by streptozotocin. After 15 wks of diabetes induction, clear alterations in the visual function were observed and all animals developed mature cataracts. At this time point, concomitantly with a significant decrease in the number of Brn3a(+) retinal ganglion cells, no differences in the number of melanopsin-containing cells, melanopsin levels, and retinal projections to the suprachiasmatic nuclei and the olivary pretectal nucleus were observed. At high light intensity, afferent pupil light reflex appears to be conserved in diabetic animals. After 15 wks of diabetes induction, a significant decrease in light-induced c-Fos expression in the suprachiasmatic nuclei was found. In diabetic animals, the locomotor activity pattern was conserved, although a delay in the time needed for re-entrainment after a phase delay was observed. In diabetic animals, lensectomy reversed the alterations in c-Fos expression and in the locomotor activity rhythm. These results suggest that the neuronal substrate of the non-image-forming visual system remained largely unaffected at advanced stages of diabetes, and that lensectomy, a relatively easy and safe surgery, could partially restore circadian alterations induced by diabetes. (Author correspondence: ) [ABSTRACT FROM AUTHOR]
- Published
- 2013
- Full Text
- View/download PDF
4. Alterations of Locomotor Activity Rhythm and Sleep Parameters in Patients With Advanced Glaucoma.
- Author
-
Lanzani, María Florencia, de Zavalía, Nuria, Fontana, Héctor, Sarmiento, María Ines Keller, Golombek, Diego, and Rosenstein, Ruth E.
- Subjects
GLAUCOMA ,CIRCADIAN rhythms ,MELANOPSIN ,RETINAL ganglion cells ,SLEEP ,ACTIGRAPHY ,HUMAN locomotion ,PATIENTS - Abstract
The aim of this study was to evaluate the effect of advanced glaucoma on locomotor activity rhythms and related sleep parameters. Nine normal subjects and nine age-matched patients with bilateral advanced primary open-angle glaucoma, >10 yrs since diagnosis, were included in this observational, prospective, case-control study. Patients were required to record the timing and duration of their sleep and daily activities, and wore an actigraph on the wrist of the nondominant arm for 20 d. Activity rhythm period, MESOR (24-h time-series mean), amplitude (one-half peak-to-trough variation), and acrophase (peak time), plus long sleep episodes during the wake state, sleep duration, efficiency, and latency, as well as mean activity score, wake minutes, and mean wake episodes during the sleep interval were assessed in controls and glaucomatous patients. Glaucomatous patients exhibited significant decrease in nighttime sleep efficiency, and significant increase in the mean activity score, wake minutes, and mean wake episode during the night. These results suggest that alterations of circadian physiology could be a risk to the quality of life of patients with glaucoma. (Author correspondence: ) [ABSTRACT FROM AUTHOR]
- Published
- 2012
- Full Text
- View/download PDF
5. Characterization of 2-[125I]-Iodomelatonin Binding Sites in the Golden Hamster Retina by Autoradiography.
- Author
-
Rosenstein, Ruth E. and Dubocovich, Margarita L.
- Subjects
- *
AUTORADIOGRAPHY , *RETINA , *MELATONIN - Abstract
The characterization of 2-[125I]-iodomelatonin binding sites was performed in the golden hamster retina using in vitro quantitative autoradiography. The specific binding of the radioligand fulfills all the criteria for binding to a receptor site, being stable, reversible, saturable and of high affinity. 2-[125I]-iodomelatonin labels a single class of sites in the sections of whole eyes as well as in isolated retinas with a similar affinity, whereas the total number of receptors was higher in sections of whole eyes than in isolated retinas. Melatonin and related analogues competed for 2-[125I]-iodomelatonin binding with the following order of affinities: 2-iodomelatonin > 6-hydroxymelatonin > melatonin > 6-chloromelatonin >>> N-acetyl-5-hydroxytryptamine (NAS) > 5-methoxytryptamine > 5-hydroxytryptamine (serotonin). Micro-molar concentrations of GTP and GDP dose-dependently and specifically inhibited agonist binding, suggesting coupling of the binding sites to a Gi protein. These results suggest the participation of melatonin in the regulation of retinal physiology trough activation of melatonin receptor subtypes. [ABSTRACT FROM AUTHOR]
- Published
- 2001
- Full Text
- View/download PDF
6. GABA RELEASE MECHANISM IN THE GOLDEN HAMSTER RETINA.
- Author
-
Lopez-costa, Juan J., Goldstein, Jorge, Pecci-saavedra, Jorge, Della Maggiore, Valeria M., De Las Heras, Marcelo A., Sarmiento, Maria I. Keller, and Rosenstein, Ruth E.
- Subjects
GABA ,GOLDEN hamster ,RETINA physiology ,SECRETION ,PHYSIOLOGY - Abstract
Studies the GABA release mechanism in the golden hamster retina. Observation of GABA-like immunoreactivity in amacrine cells, in neurons localized in ganglion cell layer and in fibers at the inner plexiform layer; Existence of at least two pools of GABA in the hamster retina; Compatibility with both vesicular and carrier-mediated mechanisms of transmitter release.
- Published
- 1999
- Full Text
- View/download PDF
Catalog
Discovery Service for Jio Institute Digital Library
For full access to our library's resources, please sign in.