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Retinal Function (retinal + function)
Selected AbstractsIntravitreal treatment with Erythropoietin (EPO) preserves visual function following ocular ischemia in ratsACTA OPHTHALMOLOGICA, Issue 2007R DERSCH Purpose: Erythropoetin (EPO) is a promising neuroprotective drug. It is known that EPO reduces apoptosis of retinal ganglion cells following axotomy or glaucoma in rats. Until now, functional aspects of this neuroprotective effect have not been addressed. We investigated effects of EPO on retinal and optic nerve function and on the survival of retinal ganglion cells following ocular ischemia. Methods: Ocular ischemia was induced by increase of the IOP to 120mmHg for 55 min in Brown-Norway rats. Animals were treated intravitreally with 4U/eye (n=12) during the time of ischemia, controls (n=16) recieved BSS instead. Visual pathway was investigated by VEP 4 days after ischemia. Potentials were evoked by frequency and luminance modulated flicker stimuli and recorded in awake freely-moving rats. Retinal function was evaluated by ERG 7 days after ischemia. Retinal ganglion cells were labelled retrogradelly 4 days after ischemia and were quantified 6 days later in retinal flatmounts. Results: Both frequency and luminance modulated evoked potentials increased due to the application of EPO from 6±2% (mean in percent of the non-ischemic eye ± standard error) in control to 46±8% in treated animals and from 26±5% to 69±6% respectively. EPO increased responses of ischemic eyes from 31±6,V to 96±8,V (a-wave) and from 34±6,V to 110±15,V (b-wave). Morphologically, the intravitreal administration of EPO increased the number of surviving ganglion cells from 32±4% to 92±11%. Conclusions: We found a sizable functional benefit of intravitreal injection of EPO following interruption of ocular blood supply. This suggests that administration of EPO is a viable therapeutic option in ischemic retinal diseases. [source] Color vision and macular recovery time in epileptic adolescents treated with valproate and carbamazepineEUROPEAN JOURNAL OF NEUROLOGY, Issue 7 2006A. Verrotti Visual dysfunction has been reported in patients diagnosed with epilepsy. Some of these visual disturbances may be attributable to either the disease process, or the anticonvulsant therapy prescribed to control the seizures. The aims of our study were to evaluate whether color vision and macular function are impaired in epileptic adolescents, to study if the monotherapy with valproic acid (VPA) and carbamazepine (CBZ) can affect color vision and macular function and to determine the possible relationship between color vision, retinal function and antiepileptic drugs (AEDs) dosage and their serum concentrations. We examined 45 (16 male and 29 female, mean age ± SD, 15.71 ± 2.01 years) Caucasian epileptic patients suffering from various types of cryptogenic epilepsy before the beginning of therapy and after 1 year of VPA or CBZ monotherapy and 40 sex- and age-matched healthy controls. Color vision was assessed by Farnsworth Munsell (FM) 100-hue test and total error score (TES) was evaluated. This test consists of colored caps: the testee has to arrange the caps according to their colors macular function was assessed by nyctometry evaluating initial recovery time (IRT) and summation method (SM). This test evaluates visual acuity after a period of intense illumination of macula. Analysis of variance was used to evaluate the difference between controls and patients; moreover, Pearson's correlation test have been performed. Before the beginning of therapy, there were no differences in color vision and macular function between controls and epileptic patients. After 1 year, the patients, treated with VPA or CBZ, showed a deficit in FM 100-hue test. At nyctometry, all patients showed no significant variation of macular function between baseline evaluation and second evaluation at end of the follow-up. Our study demonstrates that, in our group of epileptic patients, epilepsy per se does not affect color vision and retinal function. In contrast, after 1 years of therapy with VPA and CBZ these patients showed a deficit in FM 100-hue test although nyctometry evaluation continued to be normal allowing to exclude an impairment in macular function. Further investigations are required to determine the pathophysiological alteration(s) that are at the basis of color perception defects. [source] Evidence for the involvement of purinergic P2X7 receptors in outer retinal processingEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 1 2006Theresa Puthussery Abstract Extracellular ATP mediates fast excitatory neurotransmission in many regions of the central nervous system through activation of P2X receptors. Although several P2X receptor subunits have been identified in the mammalian retina, little is known about the functional role of these receptors in retinal signalling. The purpose of the present study was to investigate whether purinergic P2X7 receptors are involved in outer retinal processing by assessing receptor localization, degradation of extracellular ATP and the effect of functional activation of P2X7 receptors on the electroretinogram (ERG). Using light and electron microscopy, we demonstrated that P2X7 receptors are expressed postsynaptically on horizontal cell processes as well as presynaptically on photoreceptor synaptic terminals in both the rat and marmoset retina. Using an enzyme cytochemical method, we showed that ecto-ATPases are active in the outer plexiform layer of the rat retina, providing a mechanism by which purinergic synaptic transmission can be rapidly terminated. Finally, we evaluated the role of P2X7 receptors in retinal function by assessing changes to the ERG response of rats after intravitreal delivery of the P2X7 receptor agonist benzoyl benzoyl ATP (BzATP). Intravitreal injection of BzATP resulted in a sustained increase (up to 58%) in the amplitude of the photoreceptor-derived a-wave of the ERG. In contrast, BzATP caused a transient reduction in the rod- and cone-derived postreceptoral responses. These results provide three lines of evidence for the involvement of extracellular purines in outer retinal processing. [source] Prognosis for splicing factor PRPF8 retinitis pigmentosa, novel mutations and correlation between human and yeast phenotypes,HUMAN MUTATION, Issue 5 2010Katherine V. Towns Abstract PRPF8 -retinitis pigmentosa is said to be severe but there has been no overview of phenotype across different mutations. We screened RP patients for PRPF8 mutations and identified three new missense mutations, including the first documented mutation outside exon 42 and the first de novo mutation. This brings the known RP-causing mutations in PRPF8 to nineteen. We then collated clinical data from new and published cases to determine an accurate prognosis for PRPF8 -RP. Clinical data for 75 PRPF8 -RP patients were compared, revealing that while the effect on peripheral retinal function is severe, patients generally retain good visual acuity in at least one eye until the fifth or sixth decade. We also noted that prognosis for PRPF8 -RP differs with different mutations, with p.H2309P or p.H2309R having a worse prognosis than p.R2310K. This correlates with the observed difference in growth defect severity in yeast lines carrying the equivalent mutations, though such correlation remains tentative given the limited number of mutations for which information is available. The yeast phenotype is caused by lack of mature spliceosomes in the nucleus, leading to reduced RNA splicing function. Correlation between yeast and human phenotypes suggests that splicing factor RP may also result from an underlying splicing deficit. © 2010 Wiley-Liss, Inc. [source] The role of early neural activity in the maturation of turtle retinal functionJOURNAL OF ANATOMY, Issue 4 2001EVELYNE SERNAGOR In the developing vertebrate retina, ganglion cells fire spontaneous bursts of action potentials long before the eye becomes exposed to sensory experience at birth. These early bursts are synchronised between neighbouring retinal ganglion cells (RGCs), yielding unique spatiotemporal patterns: ,waves' of activity sweep across large retinal areas every few minutes. Both at retinal and extraretinal levels, these embryonic retinal waves are believed to guide the wiring of the visual system using hebbian mechanisms of synaptic strengthening. In the first part of this review, we recapitulate the evidence for a role of these embryonic spontaneous bursts of activity in shaping developing complex receptive field properties of RGCs in the turtle embryonic retina. We also discuss the role of visual experience in establishing RGC visual functions, and how spontaneous activity and visual experience interact to bring developing receptive fields to maturation. We have hypothesised that the physiological changes associated with development reflect modifications in the dendritic arbours of RGCs, the anatomical substrate of their receptive fields. We demonstrate that there is a temporal correlation between the period of receptive field expansion and that of dendritic growth. Moreover, the immature spontaneous activity contributes to dendritic growth in developing RGCs. Intracellular staining of RGCs reveals, however, that immature receptive fields only rarely show direct correlation with the layout of the corresponding dendritic tree. To investigate the possibility that not only the presence of the spontaneous activity, but even the precise spatiotemporal patterns encoded in retinal waves might contribute to the refinement of retinal neural circuitry, first we must clarify the mechanisms mediating the generation and propagation of these waves across development. In the second part of this review, we present evidence that turtle retinal waves, visualised using calcium imaging, exhibit profound changes in their spatiotemporal patterns during development. From fast waves sweeping across large retinal areas and recruiting many cells on their trajectory at early stages, waves become slower and eventually stop propagating towards hatching, when they become stationary patches of neighbouring coactive RGCs. A developmental switch from excitatory to inhibitory GABAA responses appears to mediate the modification in spontaneous activity patterns while the retina develops. Future chronic studies using specific spatiotemporal alterations of the waves will shed a new light on how the wave dynamics help in sculpting retinal receptive fields. [source] Cell-penetrating peptide TAT-mediated delivery of acidic FGF to retina and protection against ischemia,reperfusion injury in ratsJOURNAL OF CELLULAR AND MOLECULAR MEDICINE, Issue 7 2010Yi Wang Abstract The development of non-invasive ocular drug delivery systems is of practical importance in the treatment of retinal disease. In this study, we evaluated the efficacy of transactivator of transcription protein transduction domain (TAT-PTD, TAT49,57) as a vehicle to deliver acidic FGF (aFGF) to retina in rats. TAT-conjugated aFGF-His (TAT-aFGF-His) exhibited efficient penetration into the retina following topical administration to the ocular surface. Immunochemical staining with anti-His revealed that TAT-aFGF-His proteins were readily found in the retina (mainly in the ganglion cell layer) at 30 min. and remained detectable for at least 8 hrs after administration. In contrast, His+ proteins were undetectable in the retina after topical administration of aFGF-His, indicating that aFGF-His cannot penetrate the ocular barrier. Furthermore, TAT-aFGF-His, but not aFGF-His, mediated significant protection against retinal ischemia,reperfusion (IR) injury. After IR injury, retina from TAT-aFGF-His-treated rats showed better-maintained inner retinal layer structure, reduced apoptosis of retinal ganglion cells and improved retinal function compared to those treated with aFGF-His or PBS. These results indicate that conjugation of TAT to aFGF-His can markedly improve the ability of aFGF-His to penetrate the ocular barrier without impairing its biological function. Thus, TAT49,57 provides a potential vehicle for efficient drug delivery in the treatment of retinal disease. [source] Increased expression of glial cell line-derived neurotrophic factor protects against oxidative damage-induced retinal degenerationJOURNAL OF NEUROCHEMISTRY, Issue 3 2007Aling Dong Abstract Oxidative damage contributes to retinal cell death in patients with age-related macular degeneration or retinitis pigmentosa. One approach to treatment is to identify and eliminate the sources of oxidative damage. Another approach is to identify treatments that protect cells from multiple sources of oxidative damage. In this study, we investigated the effect of increased expression of glial cell line-derived neurotrophic factor (GDNF) in three models of oxidative damage-induced retinal degeneration. Double transgenic mice with doxycycline-inducible expression of GDNF in the retina were exposed to paraquat, FeSO4, or hyperoxia, all sources of oxidative damage and retinal cell death. Compared to controls, mice with increased expression of GDNF in the retina showed significant preservation of retinal function measured by electroretinograms, reduced thinning of retinal cell layers, and fewer TUNEL-positive cells indicating less retinal cell death. Mice over-expressing GDNF also showed less staining for acrolein, nitrotyrosine, and 8-hydroxydeoxyguanosine, indicating less oxidative damage to lipids, proteins, and DNA. This suggests that GDNF did not act solely to allow cells to tolerate higher levels of oxidative damage before initiation of apoptosis, but also reduced damage from oxidative stress to critical macromolecules. These data suggest that gene transfer of Gdnf should be considered as a component of therapy for retinal degenerations in which oxidative damage plays a role. [source] Ocular phenotype in a mouse gene knockout model for infantile neuronal ceroid lipofuscinosisJOURNAL OF NEUROSCIENCE RESEARCH, Issue 5 2006Bo Lei Abstract Mutations in the human protein palmitoyl thioesterase-1 (PPT-1) gene result in an autosomal recessive neurodegenerative disorder designated neuronal ceroid lipofuscinosis (NCL), type CLN1, or infantile NCL. Among the symptoms of the CLN1 disease are accumulation of autofluorescent lysosomal storage bodies in neurons and other cell types, seizures, motor and cognitive decline, blindness, and premature death. Development of an effective therapy for this disorder will be greatly assisted by the availability of suitable animal models. A mouse PPT-1 gene knockout model has recently been generated. Studies were performed to determine whether the mouse model exhibits ocular features of the human CLN1 disorder. A progressive accumulation of autofluorescent storage material in all layers of the retina was observed in the PPT-1 knockout mice. Accompanying the storage body accumulation was a modest loss of cells with nuclei in the outer and inner nuclear layers. As indicated by electroretinogram (ERG) responses, retinal function was only mildly impaired at 4 months of age but was severely impaired by 8 months, despite only modest changes in retinal morphology. The pupillary light reflex (PLR), on the other hand, was exaggerated in the knockout mice. The apparent anomaly between the ERG and the PLR findings suggests that disease-related PLR changes may be due to changes in extraocular signal processing. The pronounced ocular phenotype in the PPT-1 knockout mice makes these animals a good model for testing therapeutic interventions for treatment of the human CLN1 disorder. © 2006 Wiley-Liss, Inc. [source] Ethanol Consumption Alters Electroretinograms and Depletes Neural Tissues of Docosahexaenoic Acid in Rhesus Monkeys: Nutritional Consequences of a Low n-3 Fatty Acid DietALCOHOLISM, Issue 12 2001Robert J. Pawlosky Background: Alcohol amblyopia is a rare neuropathy characterized by the development of blurred vision and a reduction in visual acuity. Further diagnostic details of this condition have shown abnormalities in the electroretinogram (ERG) that include an increase in implicit times in the a- and b-waves and a depression of b-wave amplitude. Methods: Periodically, the ERGs and the fatty acyl composition of nervous tissue were analyzed from alcohol-consuming rhesus monkeys (Macaca mulatta) (mean consumption 2.6 g kg/day over a 5-year period) and controls that were maintained on a nutritionally sufficient diet that had low, yet adequate, amounts of linoleic acid but very low ,-linolenic acid. Results: Animals consuming alcohol had increased a- and b-wave implicit times and decreased b-wave amplitudes in their electroretinograms compared with those of the dietary control group at 2.5 and 5 years. The fatty acyl composition of brain specimens obtained by surgical biopsy at baseline, 2.5 years, and 5 years demonstrated that docosahexaenoic acid (DHA) had decreased in both groups of animals compared with baseline values. In the brains of the alcohol-treated animals, DHA was even further decreased (2.5 years: ,20%; 5 years: ,33%) compared with the diet controls. In the retinas of the alcohol-consuming animals at 5 years, there was a similar decrease in DHA (-35%) compared with controls. Generally, the n-6 fatty acid, docosapentaenoic acid (DPAn-6) increased in these tissues, apparently compensating for the loss of DHA. Conclusions: A reciprocal change in the DHA/DPAn-6 ratio is known to be associated with abnormal electroretinograms in a number of species. Thus, a marginal intake of n-3 fatty acids in some alcohol abusers may, in part, be responsible for the biochemical changes that underlie the diminished retinal function associated with the visual abnormalities observed in alcohol-amblyopic patients. [source] Retinal organization in the retinal degeneration 10 (rd10) mutant mouse: A morphological and ERG studyTHE JOURNAL OF COMPARATIVE NEUROLOGY, Issue 2 2007Claudia Gargini Abstract Retinal degeneration 10 (rd10) mice are a model of autosomal recessive retinitis pigmentosa (RP), identified by Chang et al. in 2002 (Vision Res. 42:517,525). These mice carry a spontaneous mutation of the rod-phosphodiesterase (PDE) gene, leading to a rod degeneration that starts around P18. Later, cones are also lost. Because photoreceptor degeneration does not overlap with retinal development, and light responses can be recorded for about a month after birth, rd10 mice mimic typical human RP more closely than the well-known rd1 mutants. The aim of this study is to provide a comprehensive analysis of the morphology and function of the rd10 mouse retina during the period of maximum photoreceptor degeneration, thus contributing useful data for exploiting this novel model to study RP. We analyzed the morphology and survival of retinal cells in rd10 mice of various ages with quantitative immunocytochemistry and confocal microscopy; we also studied retinal function with the electroretinogram (ERG), recorded between P18 and P30. We found that photoreceptor death (peaking around P25) is accompanied and followed by dendritic retraction in bipolar and horizontal cells, which eventually undergo secondary degeneration. ERG reveals alterations in the physiology of the inner retina as early as P18 (before any obvious morphological change of inner neurons) and yet consistently with a reduced band amplification by bipolar cells. Thus, changes in the rd10 retina are very similar to what was previously found in rd1 mutants. However, an overall slower decay of retinal structure and function predicts that rd10 mice might become excellent models for rescue approaches. J. Comp. Neurol. 500:222,238, 2007. © 2006 Wiley-Liss, Inc. [source] Comparisons of structural and functional abnormalities in mouse b-wave mutantsTHE JOURNAL OF PHYSIOLOGY, Issue 18 2008Maureen A. McCall In the most simplistic view, the retinal circuit can be divided into vertical excitatory pathways that use glutamate as their neurotransmitter and lateral inhibitory pathways in the outer and inner synaptic layers that modulate excitation via glycine and GABA. Within the vertical excitatory pathways, the visual signal is initiated in the rod, cone or both photoreceptors, depending on the adaptation state of the retina. This signal is transmitted to the rest of the retina through the bipolar cells, which can be subdivided based on: the photoreceptor that provides their input, their dendritic and axonal morphology, and the polarity of their response evoked by a luminance increment, e.g. depolarizing or hyperpolarizing responses. The polarity of this response is controlled by the type of glutamatergic postsynaptic receptor that is expressed on their dendritic terminals. Hyperpolarizing bipolar cells express AMPA/kainate receptors, whereas depolarizing bipolar cells (DBCs) express the metabotropic glutamate receptor 6 (Grm6). The electroretinogram (ERG) is a non-invasive method used to assess overall retinal function. The initiation of the visual signal in the photoreceptors is reflected in the ERG a-wave and the ensuing depolarization of DBCs in the b-wave. When there is failure of signal transmission from photoreceptors to DBCs or signalling within DBCs, the ERG a-wave is present, while the b-wave is absent or significantly reduced. This ERG phenotype has been found in the human population and is referred to as congenital stationary night blindness. Until recently, it had been assumed that the absence of a b-wave was indicative of a lack of signalling through the On pathway, leaving the Off pathway unaffected. Here we review recent findings that demonstrate that many mouse mutants share a no b-wave ERG phenotype but their retinal morphology and RGC responses differ significantly, suggesting very different effects of the underlying mutations on output from the DBCs to the rest of the retinal circuit. [source] Contribution of voltage-gated sodium channels to the b-wave of the mammalian flash electroretinogramTHE JOURNAL OF PHYSIOLOGY, Issue 10 2008Deb Kumar Mojumder Voltage-gated sodium channels (Nav channels) in retinal neurons are known to contribute to the mammalian flash electroretinogram (ERG) via activity of third-order retinal neurons, i.e. amacrine and ganglion cells. This study investigated the effects of tetrodotoxin (TTX) blockade of Nav channels on the b-wave, an ERG wave that originates mainly from activity of second-order retinal neurons. ERGs were recorded from anaesthetized Brown Norway rats in response to brief full-field flashes presented over a range of stimulus energies, under dark-adapted conditions and in the presence of steady mesopic and photopic backgrounds. Recordings were made before and after intravitreal injection of TTX (,3 ,m) alone, 3,6 weeks after optic nerve transection (ONTx) to induce ganglion cell degeneration, or in combination with an ionotropic glutamate receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX, 200 ,m) to block light-evoked activity of inner retinal, horizontal and OFF bipolar cells, or with the glutamate agonist N -methyl- d -aspartate (NMDA, 100,200 ,m) to reduce light-evoked inner retinal activity. TTX reduced ERG amplitudes measured at fixed times corresponding to b-wave time to peak. Effects of TTX were seen under all background conditions, but were greatest for mesopic backgrounds. In dark-adapted retina, b-wave amplitudes were reduced only when very low stimulus energies affecting the inner retina, or very high stimulus energies were used. Loss of ganglion cells following ONTx did not affect b-wave amplitudes, and injection of TTX in eyes with ONTx reduced b-wave amplitudes by the same amount for each background condition as occurred when ganglion cells were intact, thereby eliminating a ganglion cell role in the TTX effects. Isolation of cone-driven responses by presenting test flashes after cessation of a rod-saturating conditioning flash indicated that the TTX effects were primarily on cone circuits contributing to the mixed rod,cone ERG. NMDA significantly reduced only the additional effects of TTX on the mixed rod,cone ERG observed under mesopic conditions, implicating inner retinal involvement in those effects. After pharmacological blockade with CNQX, TTX still reduced b-wave amplitudes in cone-isolated ERGs indicating Nav channels in ON cone bipolar cells themselves augment b-wave amplitude and sensitivity. This augmentation was largest under dark-adapted conditions, and decreased with increasing background illumination, indicating effects of background illumination on Nav channel function. These findings indicate that activation of Nav channels in ON cone bipolar cells affects the b-wave of the rat ERG and must be considered when analysing results of ERG studies of retinal function. [source] 2244: Update on genetics in inherited retinal diseaseACTA OPHTHALMOLOGICA, Issue 2010BP LEROY Purpose To provide an overview of the recent developments in genetics of inherited retinal dystrophies and dysfunctions. Methods A systematic approach, supported by case presentations, will be used to illustrate an overview of new insights into genotypes and phenotypes of generalised dystrophies and dysfunctions of the retina. Results Much progress has been made in recent years in unravelling the molecular mechanisms underlying generalised retinal dystrophies and dysfunctions, with a wide variety of functions attributed to proteins encoded by causative genes. Identification of new genes such as PDE6C in achromatopsia and TRPM1 in autosomal recessive cCSNB provide further insight in retinal function. In addition, proven and confirmed success of gene therapy for Leber congenital amaurosis in man is leading the way for further treatment trials in humans suffering from different inherited retinal diseases. Conclusion Rapid progress is being made in the field of genetic retinal disease, with novel developments both in genotyping and improved detailed phenotyping. In addition, gene therapy is becoming a potentially feasible treatment option for several inherited retinal conditions. [source] 2245: Electrodiagnosis in inherited retinal diseaseACTA OPHTHALMOLOGICA, Issue 2010GE HOLDER Purpose To describe the roles of electrophysiology in the diagnosis and counselling of patients with inherited retinal disease. Methods Electrophysiological testing performed to incorporate and extend the recommendations of the International Society for Clinical Electrophysiology of Vision. Results Using a case-based presentation, it will be shown that electrophysiological testing can objectively assess the function of the different cell types and layers within the retina of the patient with inherited retinal dysfunction, which enables accurate diagnosis and counselling when placed in clinical context. The roles of pattern and multi-focal ERG in the assessment of macular function will be discussed. The electrophysiological findings will be discussed in relation to imaging studies when appropriate. It will shown that distinctive electrophysiological findings can direct appropriate and therefore cost-effective mutational screening in patients with atypical fundus changes. Conclusion Electrophysiological testing is fundamental to the successful management of patients with inherited disorders of retinal function. [source] Correlation of fundus autofluorescence with photoreceptor morphology and functional changes in eyes with retinitis pigmentosaACTA OPHTHALMOLOGICA, Issue 5 2010Taku Wakabayashi Abstract. Purpose:, To assess and correlate fundus autofluorescence (FAF) characteristics with photoreceptor morphology and functional features in eyes with retinitis pigmentosa (RP). Methods:, Thirty-four eyes of 17 patients with RP were examined. We compared FAF images obtained by confocal scanning laser ophthalmoscopy with Spectral-domain optical coherence tomography (SD-OCT) and retinal function assessed by microperimetry. Results:, Normal FAF surrounded by a ring of increased FAF at the macular area was detected in 32 (94%) eyes. The diameter of the normal FAF was correlated significantly with the preserved area of the photoreceptor inner segment and outer segment (IS/OS) junction on SD-OCT (R = 0.939, p < 0.001). The area outside the ring was associated with loss of IS/OS junction and external limiting membrane (ELM). The ring of increased FAF demarcated the border between the central retina with preservation of the IS/OS junction and ELM, and the adjacent eccentric retina with loss of these bands. In two eyes of one patient, there was no preservation of normal FAF at the macula and the photoreceptor IS/OS junction was not detected on SD-OCT. The mean retinal sensitivity derived from microperimetry was correlated significantly with the area of normal FAF (R = 0.929, p = 0.007) and the preserved area of the IS/OS junction (R = 0.851, p = 0.032). Ten eyes had progressive reduction in size of the normal FAF inside the ring accompanied by decreased area of preserved IS/OS during 3.1 years. Conclusion:, FAF appears to reflect the integrity of the photoreceptor layer. It may serve as a secondary outcome measure for novel therapeutic strategies for RP. [source] Multifocal electroretinography amplitudes increase after photocoagulation in areas with increased retinal thickness and hard exudatesACTA OPHTHALMOLOGICA, Issue 2 2010Monica Lövestam-Adrian Abstract. Purpose:, This study aimed to evaluate local response on multifocal electroretinography (mfERG) and to assess retinal thickness with optical coherence tomography (OCT) after focal laser treatment in areas with retinal oedema and exudates in patients with diabetic retinopathy. Methods:, Twelve diabetes patients (aged 60 ± 14 years, diabetes duration 16 ± 8 years) treated with focal or grid photocoagulation in areas with retinal oedema and/or exudates underwent mfERG and OCT before and 3 months after treatment. The average thickness (in ,m) in any of the nine sectors (defined according to the ETDRS) treated with photocoagulation was measured. Amplitudes and implicit times were analysed in corresponding areas on the mfERG. Results:, Mean mfERG amplitudes increased after photocoagulation (21.5 ± 8.0 nV/deg2 versus 16.8 ± 6.1 nV/deg2; p = 0.012), whereas no difference was seen in implicit times. Mean OCT values in the treated regions were lower at follow-up (272 ± 23 ,m versus 327 ± 79 ,m; p = 0.013). No correlation was seen between changes in mfERG response and changes in OCT values. The decrease in retinal thickness was correlated with the number of laser spots applied (p = 0.002). Conclusions:, Focal argon laser treatment is effective in reducing retinal thickness. In addition, treated areas tend to show improved retinal function as demonstrated by increased amplitudes on mfERG. [source] Electrophysiological evaluation and visual outcome in patients with central retinal vein occlusion, primary open-angle glaucoma and neovascular glaucomaACTA OPHTHALMOLOGICA, Issue 1 2010Elisabeth Wittström Abstract. Purpose:, To evaluate patients with central retinal vein occlusion (CRVO) and neovascular glaucoma (NVG) using electrophysiology in order to gain better understanding of visual outcome and risk factors, such as previously diagnosed primary open-angle glaucoma (POAG). Methods:, Eighty-three patients (83 eyes) initially presenting with CRVO and examined with full-field electroretinography (ERG) within 3 months of the thrombotic event were analysed retrospectively regarding treatment, risk factors and visual outcome. In addition, 30 patients initially presenting with NVG caused by CRVO were also investigated regarding risk factors using electrophysiology in order to determine the cause of their visual impairment. Results:, Nineteen (23%) of the 83 patients initially presenting with CRVO had been diagnosed previously with POAG. Ninety-five per cent (18/19) of all the patients with previously diagnosed glaucoma developed ischaemic CRVO. Thirty-four per cent of the patients initially presenting with CRVO (28/83) developed NVG. Sixty-eight per cent (13/19) of the patients with previous glaucoma developed NVG, compared to 23% (15/64) of the patients without previous POAG. In the patients who initially presented with NVG, full-field ERG demonstrated a remaining retinal function of both cones and rods, indicating that the main cause of visual impairment is ischaemia of the ganglion cell layer. Conclusion:, Glaucoma is a significant risk factor for developing ischaemic CRVO and subsequent NVG. The presence of POAG in CRVO worsens visual outcome. NVG is associated with preserved photoreceptor function, thus indicating ischaemia of the ganglion cell layer as the primary cause of visual impairment. This emphasizes the importance of prompt treatment of ischaemia and elevated intraocular pressure in these patients. [source] Subfoveal choroidal blood flow and central retinal function in retinitis pigmentosaACTA OPHTHALMOLOGICA, Issue 2009B FALSINI [source] Tolerance and safety of ocular use of recombinant human erythropoietin (rhEPO).ACTA OPHTHALMOLOGICA, Issue 2009Neuroprotective effects in ocular hypertension/glaucoma Purpose The purpose of this study was to evaluate the long-term effects of monthly intravitreal injections of rhEPO in a rabbit model. Methods Sixteen New Zealand rabbits were divided into 4 groups: control (no injection), saline injection, or rhEPO injections of 500 U and 1000 U (N=4 per group). The right eye of each animal was injected monthly over a period of 7 months. Fundus examination and electroretinography (ERG) were performed at 1 day prior, and 1 week, 1 month, and 6 months after the initial injection. After the final ERG, animals underwent fluorescein angiography and sacrifice one week later. Scotopic and photopic ERG amplitude and implicit times were analyzed by calculating a ratio between the right and the left eyes. Angiograms were graded for the presence of neovascularization or leakage. Statistical analysis was carried out using two-way ANOVA. Results Fifteen animals were used for this experiment (1 developed a traumatic cataract and was excluded). Between all groups and time points, there were no statistically significant differences in the computed right eye:left eye ratios for the scotopic or photopic ERG components (p>0.05). No evidence of neovascularization or fluorescein leakage was seen on angiography. There were no visible differences in retinal architecture or thickness in the rhEPO groups when compared to uninjected controls. Conclusion Monthly 0.1 ml intravitreal injections of rhEPO at a dose of up to 1000 U over 7 months is well-tolerated and does not cause adverse effects on retinal function, architecture, or vasculature in a rabbit model. A review of published data on rhEPO and Glaucoma will also be presented. [source] Transthyretin levels in the vitreous correlate with change in visual acuity after vitrectomyACTA OPHTHALMOLOGICA, Issue 2009E VAN AKEN Purpose Little is known about biochemical markers related to change in visual acuity after vitrectomy. We investigated the potential use of transthyretin (TTR), a carrier of the retinol/retinol-binding protein, as a biochemical marker protein. Methods We measured TTR using immunonephelometry in a group of patients (n=77) in longstanding (> 1 week) retinal detachment (n=29), fresh (< 1 week) retinal detachment (n=17), macular holes (n=20), or diabetic retinopathy (n=11). Vitreous samples were taken at the start of every vitrectomy procedure. For reference values, cadaver specimens (n=73) were used. Results Reference values for vitreous TTR (median 18 mg/l; IQR 4-24 mg/l) comprised 2.2% of reference values for vitreous protein levels (median 538 mg/l; IQR 269-987 mg/l). Vitreous TTR values of patients were comparable in all disorders. Vitreous TTR values were higher in phakic (median 22.5 mg/l; IQR 10-27 mg/l) than in pseudophakic patients (median 12 mg/l; IQR 8-19 mg/l)(p=0.06). Postoperative change in visual acuity correlated well with vitreous TTR values found peroperatively (rs=0.408; p=0.012). Both change in visual acuity and lens status were the only variables which proved to explain the variance of TTR (multiple correlation coefficient: 0.494; phakic status: t=2.767; p=0.0084; and change in visual acuity t=2.924: p=0.0056). Conclusion Vitreous fluid concentrations of TTR can be regarded as a biochemical marker for retinal function. [source] Consequences of dietary omega-3 polyunsaturated fatty acid deficiency on retinal function and intraocular pressure in the ratACTA OPHTHALMOLOGICA, Issue 2009B BARDET Purpose Omega-3 polyunsaturated fatty acids (,3) are key components in nervous structures but their dietary intakes in the overall population are often below nutritional requirements. A chronic deficiency in ,3 is recognized to be associated with functional impairment of the retina. At the opposite, ,3 supplementation is associated with a reduced risk for AMD. The consequences of ,3 deficiency on other eye structures than the retina, such as ciliary bodies, are scarce. The purpose of our study was to compare the response of the retina and ciliary bodies to dietary ,3 deficiency in terms of fatty acid profile and eye functionality. Methods Two successive generations of Lewis rats (G1 and G2) were obtained under either a standard or ,3-deficient diet. Intraocular pressure (IOP) was measured by rebound tonometry throughout the experiment. Retinal functionality was assessed by scotopic electroretinography (ERG). Gas chromatography was used to determine the fatty acid profile of the ciliary bodies and retina. Results A 2-fold fall in DHA content of the retina was observed in ,3-deficient G1 animals. This decrease was accentuated in G2 (-66%) and counterbalanced by an increase in DPA,6 in the retina. The b-wave amplitude of the ERG was decreased by 50% at 9mcds/m² in ,3-deficient rats. In ciliary body DHA was reduced by 80% in ,3-deficient in G1 animals but not in G2. Meanwhile, animals from the ,3-deficient diet had increased IOP (18 vs 12mmHg, p<0.0001). Conclusion The crucial role of ,3 in retinal function was confirmed. The most relevant finding from our study is the rise in IOP, the major risk factor for glaucoma, which was observed in animals reared under dietary deficiency in ,3. [source] Effect of intravitreal injection of indocyanine green, triamcinolone acetonide and trypan blue on the electroretinographic response in the ratACTA OPHTHALMOLOGICA, Issue 2007C GARCHER CREUZOT Purpose: The purpose of this study was to evaluate the effects of intravitreal injection of ICG (indocyanine green), TB (trypan blue) and TA (triamcinolone acetonide) on the visual function assessed by electroretinogram (ERG) in the rat. Methods: Three groups of 12-week-old Sprague Dawley rats (n=6) received intravitreal injection in one eye of 0.1mL of either ICG 0.5mg/mL, TB 3mg/mL or TA 40mg/mL followed by a rinse with 1mL of saline solution. The controlateral eye was used as a control and was injected similarly with saline only. The scotopic ERG was recorded at different intensities (10mcds/m², 2500mcds/m² and 25000mcds/m²) before injection and 28 days after treatment. Results: No effect of the treatment was observed on the ERG amplitudes and wave latencies in control eyes and in eyes treated with TB and TA. The ERG b-wave amplitudes and latencies were significantly reduced in eyes treated with ICG at 10mcds/m² and 2500mcds/m² but not at 25000mcds/m² (amplitude means: t0=174.8,V versus t28=55.0,V at 10mcds/m² p<0.05; t0=176.5,V versus t28=70.0,V at 2500mcds/m² p<0.05; t0=140.3,V versus t28=40.0,V at 25000mcds/m² p=0.057). The ERG a-wave amplitudes and latencies were also significantly lowered at 2500mcds/m² in eyes treated with ICG (amplitude means: t0=45.0,V versus t28=23,V p<0.05; latency means: t0=7.6msec versus t28=9.5msec p<0.01). Conclusions: This study shows a side effect of ICG on retinal function four weeks after a transient retinal exposure. TA and TB could be considered as interesting alternatives to ICG for macular surgery. [source] Circadian proteomics of the mouse retinaPROTEINS: STRUCTURE, FUNCTION AND BIOINFORMATICS, Issue 19 2007Takahiro Tsuji Abstract The circadian clock in the retina regulates a variety of physiological phenomena such as disc shedding and melatonin release. Although these events are critical for retinal functions, it is almost unknown how the circadian clock controls the physiological rhythmicity. To gain insight into the processes, we performed a proteomic analysis using 2-DE to find proteins whose levels show circadian changes. Among 415 retinal protein spots, 11 protein spots showed circadian rhythmicity in their intensities. We performed MALDI-TOF MS and NanoLC-MS/MS analyses and identified proteins contained in the 11 spots. The proteins were related to vesicular transport, calcium-binding, protein degradation, metabolism, RNA-binding, and protein foldings, suggesting the clock-regulation of neurotransmitter release, transportation of the membrane proteins, calcium-binding capability, and so on. We also found a rhythmic phosphorylation of N -ethylmaleimide-sensitive fusion protein and identified one of the amino acid residues modified by phosphorylation. These findings provide a new perspective on the relationship between the physiological functions of the retina and the circadian clock system. [source] | |||||||||||||