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PubMed2003

Identification of novel genes and altered signaling pathways in the retinal pigment epithelium during the Royal College of Surgeons rat retinal degeneration.

Shed photoreceptor outer segments (POS) are phagocytosed by RPE cells in a circadian manner. The homozygous deletion of the c-mer gene abolishes the ingestion phase of this phagocytosis in the Royal College of Surgeons (RCS) rat strain, which in turn leads to the death of photoreceptor cells. We identified RPE transcripts for which the expression is modulated by the abrogation of POS phagocytosis. A microarray approach and the differential display (DDRT-PCR) technique revealed 116 modulated known genes, 4 modulated unknown genes, and 15 expressed sequenced tags (ESTs) corresponding to unknown genes. The microarray and DDRT-PCR analyses detected alterations in signaling pathways such as the phosphatidylinositol 3-kinase-Akt-mTOR pathway and the DLK/JNK/SAPK pathway. The abrogation of POS phagocytosis caused a decrease in endomembrane biogenesis and altered endocytosis, exocytosis, transcytosis, and several metabolic and signaling pathways in RCS RPE cells. We also found differential levels of transcripts encoding proteins involved in phagocytosis, vesicle trafficking, the cytoskeleton, retinoic acid, and general metabolism.

Animals↗
PubMedDate not supplied

The retinal targets of centrifugal neurons and the retinal neurons projecting to the accessory optic system.

In birds, neurons of the isthmo-optic nucleus (ION), as well as "ectopic" neurons, send axons to the retina, where they synapse on cells in the inner nuclear layer (INL). Previous work has shown that centrifugal axons can be divided into two anatomically distinct types depending on their model of termination: either "convergent" or "divergent" (Ramon y Cajal, 1889; Maturana & Frenk, 1965). We show that cytochrome-oxidase histochemistry specifically labels "convergent" centrifugal axons and target neurons which appear to be amacrine cells, as well as three "types" of ganglion cells: two types found in the INL (displaced ganglion cells) and one in the ganglion cell layer. Labeled target amacrine cells have distinct darkly labeled "nests" of boutons enveloping the somas, are associated with labeled centrifugal fibers, and are confined to central retina. Lesions of the isthmo-optic tract abolish the cytochrome-oxidase labeling in the centrifugal axons and in the target amacrine cells but not in the ganglion cells. Cytochrome-oxidase-labeled ganglion cells in the INL are large; one type is oval and similar to the classical displaced ganglion cells of Dogiel, which have been reported to receive centrifugal input; the other type is rounder. Rhodamine beads injected into the accessory optic system results in retrograde label in both types of cells, showing that two distinct types of displaced ganglion cells project to the accessory optic system in chickens. The ganglion cells in the ganglion cell layer that label for cytochrome oxidase also project to the accessory optic system. These have proximal dendrites that ramify in the outer inner plexiform layer.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMedDate not supplied

Induction of retinal degeneration in a crab by light and okadaic acid in vitro: comparison with the Drosophila light-dependent retinal degeneration mutant w rdgBKS222.

Retinae of the crab Leptograpsus which had been maintained on a 12-h light/12-h dark cycle were cultured in vitro and exposed to 1 microM okadaic acid (OKA) at 0.75 h before light onset. Control retinae were subjected to the same routine and sampled at the same times without OKA treatment. At the concentration used, OKA totally inhibits types 1 and 2A protein phosphatases, minimally inhibits type 2B, and does not affect type 2C. 1 microM OKA provoked a diminution of rhabdom diameter measured at the level of the photoreceptor nuclei in the dark, some ommatidial cartridges being stripped of rhabdomeral microvilli altogether. After 1-h illumination (225-320 lux), further reduction of rhabdom diameter was modest in control retinae but precipitate in those treated with OKA. After 2 h, control rhabdom diameters showed a further, not significant, decline, but OKA had induced a resynthesis of massive structures with the light-microscopic appearance of rhabdoms. Electron microscopy revealed that they were heterogeneous and of the following kinds: (1) a minority of rhabdoms with normally disposed but distorted microvilli; (2) rhabdoms in the throes of events that parody normal assembly; and (3) rhabdomal volumes occupied by saccular organelles or by pleats or ruffles of irregular architecture. The cytoplasm of all such receptors was packed with free and bound ribosomes and endomembranes. The sequence of events parallels that seen during light-induced degeneration of photoreceptors of the Drosophila mutant w rdgBKS222. Preliminary experiments show that a protein kinase activator SC-9 mimics many of these effects in the dark in the presence of 1 microM OKA. As a working hypothesis, it is proposed that light activates protein kinases via diacylglycerols generated by the phototransduction cascade, and that in both crab retinas challenged with OKA and retinas of rdg BKS222 activation of a nuclear regulatory protein by hyperphosphorylation provokes a runaway transcription whose selectivity and extent remain to be determined.

Animals↗
PubMed2003

Evaluation of retinal haemodynamics and retinal function after application of dorzolamide, timolol and latanoprost in newly diagnosed open-angle glaucoma patients.

PURPOSE: The purpose of this prospective, randomized, cross-over study was to investigate and compare the microcirculatory effects of timolol, dorzolamide and latanoprost in newly diagnosed primary open-angle glaucoma (POAG) patients. Haemodynamics were assessed using fluorescein angiography by means of a scanning laser ophthalmoscope (SLO). Visual function and visual field indices were evaluated during all drug treatment phases. METHODS: Fourteen patients with newly diagnosed POAG (age 55 +/- 7 years; 10 male, four female) were recruited for the study. At baseline examination, blood pressure, heart rate, intraocular pressure (IOP), SLO angiograms, and contrast sensitivity (CS) were analysed. Patients then randomly received timolol, dorzolamide or latanoprost treatment for 4 weeks. Patients then returned and all procedures were repeated and assessed. Arteriovenous passage times (AVPs), peripapillary arterial and venous diameters were assessed from SLO angiograms, using digital image processing. Calculated ocular perfusion pressure was determined for each treatment phase. RESULTS: Intraocular pressure was significantly lowered by each drug compared to baseline (p < 0.0001). Arteriovenous passage times were significantly shortened after dorzolamide application compared to baseline (p = 0.009), whereas neither timolol nor latanoprost treatment resulted in significant AVP changes. Peripapillary arterial and venous diameters, systolic and diastolic blood pressure, heart rate and ocular perfusion pressures were not significantly altered during any treatment phase. Contrast sensitivity testing at 6 cycles/degree (c.p.d.) revealed a significant rise after dorzolamide compared to timolol (p = 0.007). CONCLUSION: Our results suggest that dorzolamide treatment significantly shortened AVP times in newly diagnosed open-angle glaucoma patients, whereas timolol and latanoprost had no significant effect. Given that prolonged AVP times have been associated with disease progression in glaucoma; dorzolamide treatment may benefit optic nervehead preservation by increasing ocular perfusion.

Adrenergic beta-Antagonists↗