Central Retinal Lesions Research Articles

Von Hippel-Lindau disease: A case report.

Introduction and importanceVon Hippel-Lindau (VHL) disease is a rare autosomal dominantly inherited genetic condition. Von Hippel characterized the illness independently in 1911, and Lindau in 1926. Its prevalence is estimated to be about 1 in every 36,000 live births. VHL is characterized by the production of several benign and malignant tumors, as well as cysts in other organs. For proper prognosis, good clinical judgement and timely diagnosis is warranted.Case presentationHerein, we report a case of a 50-year-old man with several central nervous system (CNS) lesions, retinal lesions, and renal cortical cysts with a diagnosis of VHL disease who was surgically treated. At a 3-month follow-up, he improved drastically with a marked alleviation of his signs and symptoms.DiscussionVHL is characterized by the creation of various benign and malignant tumors, as well as cysts in multiple organs, and is passed down through generations in an autosomal dominant pattern with near-complete penetrance. CNS lesions are surgically treated. Regular follow-up should be ensured.ConclusionsVHL disease is an extremely complicated disease with the need for diagnosis and genetic tests in the patient and family members, as well as intensive supervision of carriers of the mutated gene, thereby improving early diagnosis and successful treatment of the malignancies. The high cost of diagnostics and surgical therapies is a severe issue. Government care and financial assistance are critical considerations.

Comparison of Two Ultra-Widefield Cameras With High Image Resolution and Wider View for Identifying Diabetic Retinopathy Lesions.

PurposeTo compare the effectiveness of the Optos P200dTx and Zeiss Clarus 500 fundus cameras in detecting diabetic retinopathy (DR) lesions.MethodsA cross-sectional study was conducted among 243 patients with clinically diagnosed diabetes mellitus who were referred for an eye examination from two tertiary eye care centers in Chennai, India. Patients underwent DR screening based on mydriatic fundal images acquired by both fundal cameras. Fundal images from the two separate devices for each eye were compared based on accurately identified pathological retinal lesions with respect to type and location.ResultsWhen studying lesions of the central retina, they were better identified by the Zeiss Clarus compared with the Optos P200dTx, with six out of eight being statistically significant (P < 0.05). However, lesions of the mid-peripheral retina and peripheral retina were better identified by the Optos P200dTx than the Zeiss Clarus, with three out of eight lesions and five out of eight lesions being statistically significant (P < 0.05), respectively. Based on the color and size of lesions, the Optos P200dTx had a higher chance (59.6%) of missing white lesions than did the Zeiss Clarus (17%) (P < 0.0001). Consequently, small- and medium-sized lesions were missed more by the Optos P200dTx (30.72% and 32.63%, respectively) than the Zeiss Clarus (22.3% and 19.30%, respectively).ConclusionsThe capability of detecting or missing a particular DR lesion among diabetics differed between the two cameras based on effective field of view, resolution, and the retinal zone being imaged.Translational RelevanceThe choice of which ultra-widefield camera to be used for screening DR can be based on the greater prevalence of central versus peripheral retinal lesions noted in the patient population seen in a clinical practice.

Plasticity Beyond V1: Reinforcement of Motion Perception upon Binocular Central Retinal Lesions in Adulthood.

Induction of a central retinal lesion in both eyes of adult mammals is a model for macular degeneration and leads to retinotopic map reorganization in the primary visual cortex (V1). Here we characterized the spatiotemporal dynamics of molecular activity levels in the central and peripheral representation of five higher-order visual areas, V2/18, V3/19, V4/21a,V5/PMLS, area 7, and V1/17, in adult cats with central 10° retinal lesions (both sexes), by means of real-time PCR for the neuronal activity reporter gene zif268. The lesions elicited a similar, permanent reduction in activity in the center of the lesion projection zone of area V1/17, V2/18, V3/19, and V4/21a, but not in the motion-driven V5/PMLS, which instead displayed an increase in molecular activity at 3 months postlesion, independent of visual field coordinates. Also area 7 only displayed decreased activity in its LPZ in the first weeks postlesion and increased activities in its periphery from 1 month onward. Therefore we examined the impact of central vision loss on motion perception using random dot kinematograms to test the capacity for form from motion detection based on direction and velocity cues. We revealed that the central retinal lesions either do not impair motion detection or even result in better performance, specifically when motion discrimination was based on velocity discrimination. In conclusion, we propose that central retinal damage leads to enhanced peripheral vision by sensitizing the visual system for motion processing relying on feedback from V5/PMLS and area 7.SIGNIFICANCE STATEMENT Central retinal lesions, a model for macular degeneration, result in functional reorganization of the primary visual cortex. Examining the level of cortical reactivation with the molecular activity marker zif268 revealed reorganization in visual areas outside V1. Retinotopic lesion projection zones typically display an initial depression in zif268 expression, followed by partial recovery with postlesion time. Only the motion-sensitive area V5/PMLS shows no decrease, and even a significant activity increase at 3 months post-retinal lesion. Behavioral tests of motion perception found no impairment and even better sensitivity to higher random dot stimulus velocities. We demonstrate that the loss of central vision induces functional mobilization of motion-sensitive visual cortex, resulting in enhanced perception of moving stimuli.

Analysis of blue light pixels for detection of preferred retinal locus

Detection of ‘Preferred Retinal Locus’ (PRL) in human eyes is one of the important tests duringclinical assessment for treatment of certain retinal lesions. Significance of blue light has beenanalyzed in this paper using simple image processing algorithm in detecting PRL. Fundusphotographs of 19 patients, (eleven normal and eight central retinal lesions) were taken for theanalyses of RGB pixel intensities. Along with Red Maximum (Rmax), Green Maximum (Gmax)and Red Green maximum (R + Gmax), Blue Minimum (Bmin) pixel intensity values were alsoobtained for all the images. Blue pixel values were found to be minimum in fovea for all 100% of the normal retinal images. For PRL retinal images, Bmin method matched the location in 88% of images. This method signifies that the analysis of blue light for patients with eccentric fixationis a good alternative compared to scanning laser ophthalmoscope (SLO) and microperimetry

Recovery from Retinal Lesions: Molecular Plasticity Mechanisms in Visual Cortex Far beyond the Deprived Zone

In cats with central retinal lesions, deprivation of the lesion projection zone (LPZ) in primary visual cortex (area 17) induces remapping of the cortical topography. Recovery of visually driven cortical activity in the LPZ involves distinct changes in protein expression. Recent observations, about molecular activity changes throughout area 17, challenge the view that its remote nondeprived parts would not be involved in this recovery process. We here investigated the dynamics of the protein expression pattern of remote nondeprived area 17 triggered by central retinal lesions to explore to what extent far peripheral area 17 would contribute to the topographic map reorganization inside the visual cortex. Using functional proteomics, we identified 40 proteins specifically differentially expressed between far peripheral area 17 of control and experimental animals 14 days to 8 months postlesion. Our results demonstrate that far peripheral area 17 is implicated in the functional adaptation to the visual deprivation, involving a meshwork of interacting proteins, operating in diverse pathways. In particular, endocytosis/exocytosis processes appeared to be essential via their intimate correlation with long-term potentiation and neurite outgrowth mechanisms.

Retinal lesions induce layer-specific Fos expression changes in cat area 17

Quantitative analysis of the neuronal activity marker Fos revealed activity-dependent and lamina-specific changes in adult cat area 17, 14 days to 1 month after the induction of central retinal lesions. The supra- and infragranular layers were clearly differently engaged in the response to the visual deprivation, both inside and outside the lesion projection zone. The center of the LPZ exhibited an activity decrease in the extragranular layers, which was mainly reflected by an intracellular down-regulation of Fos rather than a decline in the number of Fos-immunoreactive nuclei. Interestingly, the infragranular layers displayed more Fos-immunoreactive neurons in experimental animals. This recruitment of an additional population of Fos expressing neurons in the subcortically projecting infragranular layers might have a protective function against neurodegeneration in the direct retinal target structures.

What can we learn about the visual cortex from retinal lesions?

Event Abstract Back to Event What can we learn about the visual cortex from retinal lesions? Ulf T. Eysel1* and Dimitrios V. Giannikopoulos1 1 Ruhr University, Department of Neurophysiology, Germany Binocular central retinal lesions induce a lesion projection zone (LPZ) with complete loss of visual excitability followed by extensive reorganization in the cat primary visual cortex. In how far can functional single cell properties be restored during the lesion-induced reorganization process in adulthood? We studied the dynamics of reorganization in the LPZ by single cell recordings with special emphasis on receptive field size (RF), orientation (OS) and direction selectivity (DS) over a period of one year in adult cats. Inside the LPZ the percentage of reactivated cells increased with time, and after 1 year reactivation spanned a total distance of more than 3.5 mm from the border towards the center of the LPZ. New visually responsive single cells had exceptionally large RFs, reduced sharpness of OS and supernormal DS surprisingly biased to directions centrifugal from the center of the LPZ. The initially very large RFs recovered to sizes as normally present at the border of the central retinal lesion, while the fine grain resolution obtained in controls with normal input from the central retina was never reestablished. OS did not recover at all, it decreased in quality inside the LPZ with distance from the border (Giannikopoulos and Eysel, 2006). The centrifugal bias of DS remained up to 12 months, however, after 2 weeks the strength of DS returned to and stayed normal inside the LPZ close to the border (up to 0.5 mm). 2 mm further inside normal values were observed at 12 weeks, but subnormal DS strength prevailed within the LPZ after 1 year. In summary, the long-ranging reactivation of single cells inside the LPZ in cat visual cortex is accompanied by reductions of functional specificity that can only partially or not at all be compensated by the adult plasticity of lateral connections and intracortical computations. Subcortical input appears most crucial for OS. RF can be restored best and appears most robust after reorganization. Supported by the DFG (SFB 509). Conference: IBRO International Workshop 2010, Pécs, Hungary, 21 Jan - 23 Jan, 2010. Presentation Type: Oral Presentation Topic: Vision: from the evolution of retinas to the evolution of ideas Citation: Eysel UT and Giannikopoulos DV (2010). What can we learn about the visual cortex from retinal lesions?. Front. Neurosci. Conference Abstract: IBRO International Workshop 2010. doi: 10.3389/conf.fnins.2010.10.00250 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 05 May 2010; Published Online: 05 May 2010. * Correspondence: Ulf T Eysel, Ruhr University, Department of Neurophysiology, Bochum, Germany, eysel@rub.de Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers Ulf T Eysel Dimitrios V Giannikopoulos Google Ulf T Eysel Dimitrios V Giannikopoulos Google Scholar Ulf T Eysel Dimitrios V Giannikopoulos PubMed Ulf T Eysel Dimitrios V Giannikopoulos Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.

Analysis of c-fos and zif268 Expression Reveals Time-Dependent Changes in Activity Inside and Outside the Lesion Projection Zone in Adult Cat Area 17 after Retinal Lesions

Retinal lesions induce a topographic reorganization in the corresponding lesion projection zone (LPZ) in the visual cortex of adult cats. To gain a better insight into the reactivation dynamics, we investigated the alterations in cortical activity throughout area 17. We implemented in situ hybridization and real-time polymerase chain reaction to analyze the spatiotemporal expression patterns of the activity marker genes zif268 and c-fos. The immediate early gene (IEG) data confirmed a strong and permanent activity decrease in the center of the LPZ as previously described by electrophysiology. A recovery of IEG expression was clearly measured in the border of the LPZ. We were able to register reorganization over 2.5-6 mm. We also present evidence that the central retinal lesions concomitantly influence the activity in far peripheral parts of area 17. Its IEG expression levels appeared dependent of time and distance from the LPZ. We therefore propose that coupled changes in activity occur inside and outside the LPZ. In conclusion, alterations in activity reporter gene expression throughout area 17 contribute to the lesion-induced functional reorganization.

Effect of binocular retinal lesions on CRMP2 and CRMP4 but not Dyn I and Syt I expression in adult cat area 17

Removal of retinal input from a restricted region of adult cat visual cortex leads to a substantial reorganization of the retinotopy within the sensory-deprived cortical lesion projection zone (LPZ). Still little is known about the molecular mechanisms underlying this cortical map reorganization. We chose two members of the collapsin response mediator protein (CRMP) family, CRMP2 and CRMP4, because of their involvement in neurite growth, and compared gene and protein expression levels between normal control and reorganizing visual cortex upon induction of central retinal lesions. Parallel analysis of Dynamin I (Dyn I) and Synaptotagmin I (Syt I), two molecules implicated in the exocytosis-endocytosis cycle, was performed because changes in neurotransmitter release have been implicated in cortical plasticity. Western blotting and real-time polymerase chain reaction revealed a clear time-dependent effect of retinal lesioning on CRMP2 and CRMP4 expression, with maximal impact 2 weeks post-lesion. Altered CRMP levels were not a direct consequence of decreased visual activity in the LPZ as complete surgical removal of retinal input to one hemisphere had no effect on CRMP2 or CRMP4 expression. Thus, CRMP expression is correlated to cortical reorganization following partial deafferentation of adult visual cortex. In contrast, Dyn I and Syt I were not influenced and thereby do not promote exocytosis-endocytosis cycle modifications in adult cat cortical plasticity.

Reorganization of Visual Processing in Macular Degeneration

Macular degeneration (MD), the leading cause of visual impairment in the developed world, damages the central retina, often obliterating foveal vision and severely disrupting everyday tasks such as reading, driving, and face recognition. In such cases, the macular damage eliminates the normal retinal input to a large region of visual cortex, comprising tens of square centimeters of surface area in each hemisphere, which is normally responsive only to foveal stimuli. Using functional magnetic resonance imaging, we asked whether this deprived cortex simply becomes inactive in subjects with MD, or whether it takes on new functional properties. In two adult MD subjects with extensive bilateral central retinal lesions, we found that parts of visual cortex (including primary visual cortex) that normally respond only to central visual stimuli are strongly activated by peripheral stimuli. Such activation was not observed (1) with visual stimuli presented to the position of the former fovea and (2) in control subjects with visual stimuli presented to corresponding parts of peripheral retina. These results demonstrate large-scale reorganization of visual processing in MD and will likely prove important in any effort to develop new strategies for rehabilitation of MD subjects.

Differential display implicates cyclophilin A in adult cortical plasticity.

Removal of retinal input from a restricted region of adult cat visual cortex leads to a substantial reorganization of the retinotopy within the sensory-deprived cortical zone. Little is known about the molecular mechanisms underlying this reorganization. We used differential mRNA display (DDRT-PCR) to compare gene expression patterns between normal control and reorganizing visual cortex (area 17-18), 3 days after induction of central retinal lesions. Systematic screening revealed a decrease in the mRNA encoding cyclophilin A in lesion-affected cortex. In situ hybridization and competitive PCR confirmed the decreased cyclophilin A mRNA levels in reorganizing cortex and extended this finding to longer postlesion survival times as well. Western blotting and immunocytochemistry extended these data to the protein level. In situ hybridization and immunocytochemistry further demonstrated that cyclophilin A mRNA and protein are present in neurons. To exclude the possibility that differences in neuronal activity per se can induce alterations in cyclophilin A mRNA and protein expression, we analyzed cyclophilin A expression in the dorsal lateral geniculate nucleus (dLGN) of retinally lesioned cats and in area 17 and the dLGN of isolated hemisphere cats. In these control experiments cyclophilin A mRNA and protein were distributed as in normal control subjects indicating that the decreased cyclophilin A levels, as observed in sensory-deprived area 17 of retinal lesion cats, are not merely a reflection of changes in neuronal activity. Instead our findings identify cyclophilin A, classically considered a housekeeping gene, as a gene with a brain plasticity-related expression in the central nervous system.

Retinotopic map plasticity in adult cat visual cortex is accompanied by changes in ca 2+/calmodulin-dependent protein kinase ii α autophosphorylation

In adult cats, the induction of homonymous binocular central retinal lesions causes a dramatic reorganization of the topographic map in the sensory-deprived region of the primary visual cortex. To investigate the possible involvement of the α-subunit of the calcium/calmodulin dependent protein kinase type II (αCaMKII) in this form of brain plasticity, we performed in situ hybridization and Western blotting experiments to analyze mRNA, protein and autophosphorylation levels of this multifunctional kinase. No differences in the mRNA or protein levels were observed between the central, sensory-deprived and the peripheral, non-deprived regions of area 17 of retinal lesion animals or between corresponding cortical regions of normal control animals. Western blotting with an αCaMKII threonine-286 phosphorylation-state specific antiserum consistently showed a small, albeit not significant, increase of αCaMKII autophosphorylation in the central versus the peripheral region of cortical area 17, and this both in normal subjects as well as in retinal lesion animals with a 3-day post-lesion survival time. In contrast, a post-lesion survival time of 14 days resulted in a αCaMKII autophosphorylation level that was four times higher in visually-deprived area 17 than in the non-deprived cortical region. This increased phosphorylation state is not a direct consequence of the decrease in visual activity in these neurons, because we would have expected to see a similar change at shorter or longer post-lesion survival times or in the visually deprived visual cortex of animals in which the left optic tract and the corpus callosum were surgically cut. No such changes were observed, leading to the conclusion that the phosphorylation changes observed at 14 days are related to a delayed reorganization of the retinotopic map of the striate cortex.

Glutamate levels and transport in cat (Felis catus) area 17 during cortical reorganization following binocular retinal lesions.

Glutamate is known to play a crucial role in the topographic reorganization of visual cortex after the induction of binocular central retinal lesions. In this study we investigated the possible involvement of the glial high-affinity Na+/K+-dependent glutamate transporters in cortical plasticity using western blotting and intracortical microdialysis. Basal extracellular glutamate levels and the re-uptake activity for glutamate have been determined by comparing the extracellular glutamate concentration before and during the blockage of glutamate removal from the synaptic cleft with the potent transporter inhibitor l-trans-pyrrolidine-3,4-dicarboxylic acid. In cats with central retinal lesions we observed increased basal extracellular glutamate concentrations together with a decreased re-uptake activity in non-deprived, peripheral area 17, compared with the sensory-deprived, central cortex of the same animal as well as the topographically matching regions of area 17 in normal subjects. Western blotting experiments revealed a parallel decrease in the expression level of the glial glutamate transporter proteins GLT-1 and GLAST in non-deprived cortex compared with sensory-deprived cortex of lesion cats and the corresponding regions of area 17 of normal subjects. This study shows that partial sensory deprivation of the visual cortex affects the removal of glutamate from the synaptic cleft and implicates a role for glial-neuronal interactions in adult brain plasticity.

Molecular cloning and differential expression of the cat immediate early gene c-fos

Recently, the effect of binocular central retinal lesions on the expression of immediate early genes in the visual system of adult cats was demonstrated using in situ hybridization and immunocytochemistry [2]. The present study was undertaken to quantify cat c-fos mRNA expression differences in the cat primary visual cortex after sensory deafferentation. Prior to quantification, DNA fragments obtained using reverse transcription-polymerase chain reaction (RT-PCR) in combination with rapid amplification of complementary DNA ends (RACE) were cloned and sequenced. This provided us with the necessary sequence 1 1 Note: nucleotide sequence data reported are available in the Genbank database under the accession number AF540379. information to prepare cat-specific c-fos primers for the development of a new quantitative RT-PCR assay. We optimized a reverse transcription-competitive polymerase chain reaction (RT-cPCR) method with a heterologous DNA fragment (competitor) as external standard to quantify relative amounts of cat c-fos mRNA expression levels. Internal standardization was accomplished by quantifying, in a parallel RT-cPCR, a well-characterized housekeeping gene, glyceraldehyde-3-phosphate dehydrogenase (GAPDH). This cat-specific RT-cPCR assay allowed us to measure c-fos mRNA expression levels in central and peripheral regions of primary visual cortex in normal and retinal lesion cats.

Retinal lesions affect extracellular glutamate levels in sensory-deprived and remote non-deprived regions of cat area 17 as revealed by in vivo microdialysis

This study aimed at gaining insight into the role of the excitatory neurotransmitter glutamate in topographic map reorganization in the sensory systems of adult mammals after restricted deafferentations. Hereto, in vivo microdialysis was used to sample extracellular glutamate from sensory-deprived and non-deprived visual cortex of adult awake cats 18 to 53 days after the induction of restricted binocular retinal lesions, and in topographically corresponding cortical regions of control animals. A microbore HPLC-ED method was applied for the analysis of the microdialysates. In normal subjects, the visual cortex subserving central and peripheral vision showed similar extracellular fluid glutamate concentrations. In contrast, in animals with homonymous central retinal lesions, the extracellular glutamate concentration was significantly lower in central, sensory-deprived cortex compared to peripheral, non-deprived cortex. Compared to control regions in normal subjects, glutamate decreased in the extracellular fluid of deprived cortex but increased significantly in remote non-deprived visual cortex. These results not only suggest an activity-dependent regulation of the glutamate levels in visual cortex but also imply a role for perilesional cortical regions in topographic map reorganization following sensory deafferentation.

Cooperative changes in GABA, glutamate and activity levels: the missing link in cortical plasticity.

Different intracortical mechanisms have been reported to contribute to the substantial topographic reorganization of the mammalian primary visual cortex in response to matching lesions in the two retinas: an immediate expansion of receptive fields followed by a gradual shift of excitability into the deprived area and finally axonal sprouting of laterally projecting neurons months after the lesion. To gain insight into the molecular mechanisms of this adult plasticity, we used immunocytochemical and bioanalytical methods to measure the glutamate and GABA neurotransmitter levels in the visual cortex of adult cats with binocular central retinal lesions. Two to four weeks after the lesions, glutamate immunoreactivity was decreased in sensory-deprived cortex as confirmed by HPLC analysis of the glutamate concentration. Within three months normal glutamate immunoreactivity was restored. In addition, the edge of the unresponsive cortex was characterized by markedly increased glutamate immunoreactivity 2-12 weeks postlesion. This glutamate immunoreactivity peak moved into the deprived area over time. These glutamate changes corresponded to decreased spontaneous and visually driven activity in unresponsive cortex and to strikingly increased neuronal activity at the border of this cortical zone. Furthermore, the previously reported decrease in glutamic acid decarboxylase immunoreactivity was found to reflect decreased GABA levels in sensory-deprived cortex. Increased glutamate concentrations and neuronal activity, and decreased GABA concentrations, may be related to changes in synaptic efficiency and could represent a mechanism underlying the retinotopic reorganization that occurs well after the immediate receptive field expansion but long before the late axonal sprouting.

Investigation of cortical reorganization in area 17 and nine extrastriate visual areas through the detection of changes in immediate early gene expression as induced by retinal lesions.

The effect of binocular central retinal lesions on the expression of the immediate early genes c-fos and zif268 in the dorsal lateral geniculate nucleus (dLGN) and the visual cortex of adult cats was investigated by in situ hybridization and immunocytochemistry. In the deafferented region of the dLGN, the c-fos mRNA level was decreased within 3 days. The dimensions of the geniculate region showing decreased amounts of c-fos mRNA matched the predictions based on the lesion size and the retinotopic maps of Sanderson ([1971] J. Comp. Neurol. 143:101-118). We did not detect zif268 mRNA in the dLGN. At the cortical level, both c-fos and zif268 mRNA expression decreased in the sensory-deprived region of area 17. In addition, the portions of areas 18, 19, 21a, 21b, and 7, as well as the posterior medial lateral suprasylvian area, the posterior lateral lateral suprasylvian area, the ventral lateral suprasylvian area, and the dorsal lateral suprasylvian area corresponding to the retinal lesions also displayed decreased c-fos and zif268 mRNA levels. Immunocytochemistry revealed similar changes for Zif268 and Fos protein. Three days post lesion, the dimensions of the lesion-affected cortical loci exceeded the predictions in relation to the size of the retinal lesions and the available retinotopic maps. Longer postlesion survival times clearly resulted in a time-dependent restoration of immediate early gene expression from the border to the center of the lesion-affected cortical portions. Our findings represent a new approach for investigating the capacity of adult sensory systems to undergo plastic changes following sensory deprivation and for defining the topographic nature of sensory subcortical and cortical structures.

Effect of sensory deafferentation on the GABAergic circuitry of the adult cat visual system

The effect of bilateral central retinal lesions on the GAD67 and GAD65 messenger RNA levels in the dorsal lateral geniculate nucleus, the perigeniculate nucleus and the visual cortex of the adult cat was investigated by in situ hybridization. Three days post-lesion, a decrease in the number of GAD67-expressing cells was apparent in the deafferented dorsal lateral geniculate nucleus. This decrease persisted until 7.5 months post-lesion and was more pronounced with longer survival times. The decrease in GAD67 mRNA was mirrored by a decrease in glutamate decarboxylase-immunoreactive cells. GAD65 messenger RNA expression levels were low in the dorsal lateral geniculate nucleus of both control and retinally-lesioned cats. In the perigeniculate nucleus the messenger RNA levels of both glutamate decarboxylase isoforms were clearly decreased over a restricted region. In the lesion-affected visual cortex, no changes at the messenger RNA level were observed for either GAD67 or GAD65 although changes in glutamate decarboxylase immunoreactivity have been previously described.[34]Hence, in the dorsal lateral geniculate nucleus, the perigeniculate nucleus and the visual cortex, different intracellular mechanisms seem to lead to decreased GABAergic inhibition in response to sensory deafferentation.

Relationship between retinal lesions and axial length, age and sex in high myopia.

We analysed the relationship between central and peripheral retinal lesions and axial length (AL), patient's age and sex with myopia greater than 6 diopters. A total of 212 eyes of 109 patients with high myopia underwent detailed funduscopy and A-scan ultrasonography. AL was measured, and central and peripheral retinal lesions were noted. Results were analysed using Student's t-test. Sixty-one patients (118 eyes) were female and 48 (94 eyes) male. Mean age was 31.00 +/- 13.67 years, and mean AL was 28.31 +/- 2.02 mm. Chorioretinal atrophy, Fuchs' spot, posterior staphyloma and posterior vitreous detachment increased significantly with AL and age. Fuchs' spot was more common in females. White-without-pressure (WWP) was inversely correlated with AL and age, and was more common in males. The high frequency of WWP in younger patients and moderate AL suggests that these lesions result from vitreoretinal tractions. Lattice degeneration was also a frequent finding in high myopia, and tended to increase with AL and age, though without reaching statistical significance.

Long-term effects of retinal lesions on growth-associated protein 43 (GAP-43) expression in the visual system of adult cats

We have investigated the role of growth-associated protein 43 (GAP-43) in synaptic reorganization in the visual system of adult cats that received binocular central retinal lesions. Different survival times between 3 and 8 months after induction of the lesion were chosen. In the deafferented part of the dorsal lateral geniculate nucleus (dLGN) we found a long-lasting increase in GAP-43 protein, while glial fibrillary acidic protein (GFAP) immunoreactivity, which initially increased due to the degeneration of retinal ganglion cells, slowly subsided over this period. In area 17, the pattern of GAP-43 expression did not provide indications for morphological changes in the cortical architecture following retinal lesions.