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BackgroundCongenital stationary night-blindness (CSNB) is a recessive autosomal defect in low-light vision in Appaloosa and other horse breeds. This condition has been mapped by linkage analysis to a gene coding for the Transient Receptor Potential cation channel Member 1 (TRPM1). TRPM1 is normally expressed in the ON-bipolar cells of the inner nuclear layer of the retina. Down-regulation of TRPM1 expression in CSNB results from a transposon-like insertion in intron 1 of the TRPM1 gene. Stop transcription signals in this transposon significantly reduce TRPM1 primary transcript levels in CSNB horses. This study describes additional contributions by a second mutation of the TRPM1 gene, the ECA1 108,249,293 C > T SNP, to down-regulation of transcription of the TRPM1 gene in night-blind horses. This TRPM1 SNP introduces a consensus binding site for neuro-oncological ventral antigen 1 (Nova-1) protein in the primary transcript. Nova-1 binding disrupts normal splicing signals, producing unstable, non-functional mRNA transcripts.ResultsRetinal bipolar cells express both TRPM1 and Nova-1 proteins. In vitro addition of Nova-1 protein retards electrophoretic migration of TRPM1 RNA containing the ECA1 108,249,293 C > T SNP. Up-regulating Nova-1 expression in primary cultures of choroidal melanocytes carrying the intron 11 SNP caused an average log 2-fold reduction of ~6 (64-fold) of TRPM1 mRNA expression.ConclusionsThese finding suggest that the equine TRPM1 SNP can act independently to reduce survival of TRPM1 mRNA escaping the intron 1 transcriptional stop signals in CSNB horses. Coexistence and co-inheritance of two independent TRPM1 mutations across 1000 equine generations suggests a selective advantage for the apparently deleterious CSNB trait.

Loewen, Matthew E., Nicola K. Smith, Don L. Hamilton, Bruce H. Grahn, and George W. Forsyth. CLCA protein and chloride transport in canine retinal pigment epithelium. Am J Physiol Cell Physiol 285: C1314-C1321, 2003. First published July 16, 2003; 10.1152/ajpcell.00210.2003.--Problems in ion and fluid transfer across the retinal pigment epithelium (RPE) are a probable cause of inappropriate accumulations of fluid between the photoreceptors of the retina and the RPE. The activities of [Cl.sup.-] transporters involved in basal fluid transfer across the RPE have been compared to determine whether [Ca.sup.2.sup.+] - or cAMP-dependent channels may be responsible for basal housekeeping levels of secretory activity in this tissue. The role of a candidate [Ca.sup.2.sup.+]-dependent CLCA protein in the basal RPE transport of [Cl.sup.-] has been investigated. Low concentrations of the [Cl.sup.-] conductance inhibitors glibenclamide and 5-nitro-2-(3-phenylpropylamino) benzoate reduced the short-circuit current in dog RPE preparations mounted in Ussing chambers and decreased the [Ca.sup.2.sup.+]-dependent [Cl.sup.-] efflux from fibroblasts expressing the pCLCA1 [Cl.sup.-] conductance regulator. However, these same agents did not inhibit the rate of [Cl.sup.-] release from cultured fibroblasts expressing the cystic fibrosis transmembrane regulator (CFTR) conductive [Cl.sup.-] channel. Addition of ionomycin to primary cultures of canine RPE cells or to fibroblasts expressing the pCLCA1 channel regulator increased the rate of release of [Cl.sup.-] from both types of cultured cells. However, the presence of pCLCA1 also increased cAMP-dependent [Cl.sup.-] release from fibroblasts expressing CFTR. We conclude that [Ca.sup.2.sup.+]-dependent [Cl.sup.-] transport may be more important than cAMP-dependent [Cl.sup.-] transport for normal fluid secretion across the RPE. Furthermore, CLCA proteins expressed in the RPE appear to regulate the activity of other [Cl.sup.-] transporters, rather than functioning as primary ion transport proteins. chloride channel; cystic fibrosis transmembrane conductance regulator, calcium; fluid secretion

A muskox neonate (Ovibos moschatus) that died of starvation was diagnosed with congenital lenticular anomalies that included spherophakia and hypermature cataract associated with probable lens-induced lymphocytic uveitis and neutrophilic keratitis. Impaired sight as a result of cataract and associated inflammation likely contributed to abandonment and starvation, although maternal death cannot be excluded definitively. Ocular lesions, such as congenital cataracts and spherophakia in neonates, may be important factors affecting survival in free-ranging animals. [ABSTRACT FROM AUTHOR]

Our objective was to investigate whether zinc interacts with taurine to influence the development of retinal structure and function. Virgin female Sprague-Dawley rats were bred overnight and assigned to one of four treatments in a 2 x 2 factorial design with two levels of zinc (50 [[micro]gram]/g through gestation and 50 [[micro]gram]/g after parturition; 15 [[micro]gram]/g through gestation and 7.5 [[micro]gram]/g after parturition) and two levels of taurine (2 or 0 [[micro]mol]/g). The control diet contained 50 [[micro]gram]/g zinc and 2 [[micro]mol]/g taurine. Guanidinoethyl sulfonate (10 g/L), a taurine transport inhibitor, was added to the drinking water of the rats receiving 0 [[micro]mol]/g taurine. At postnatal d 23, male pups (n = 10) were weaned onto their respective diets. Pup eyes were examined by biomicroscope and indirect ophthalmoscope at 4 and 7 wk; retinal folds and choroidal atrophy were detected in the pups deficient in zinc and taurine. Analysis of plasma zinc and tibial zinc concentrations revealed a significant interaction in these tissues (P < 0.05). Dark-adapted oscillatory potentials (OP) were recorded at 7.5-8.5 wk. Two-way ANOVA showed a significant interaction between zinc and taurine for O[P.sub.2] and O[P.sub.3] amplitudes; marginal zinc deficiency decreased the amplitude of the OP only when rats were also deficient in taurine. A significant depressing effect of marginal zinc deficiency was noted for O[P.sub.1] amplitude. Taurine deficiency significantly depressed the amplitude of O[P.sub.1] and O[P.sub.4]. Histological examination of the retinas from rats deficient in both zinc and taurine revealed photoreceptor degeneration and confirmed retinal dysplasia. These data provide evidence for an interaction between zinc and taurine in retinal morphology and function. KEY WORDS: * zinc deficiency * taurine deficiency * rats * oscillatory potential * retina

Purpose: To describe the optical coherence tomography (OCT) and fluorescein angiography changes in dogs with sudden acquired retinal degeneration syndrome (SARDS). Methods: Retinal OCT was performed on 10 SARDS dogs and eight control dogs. Tomograms were collected in four quadrants around the optic nerve. Measurements were collected from the photoreceptor layer, the outer nuclear layer, the outer retina, the inner retina and the whole retina thickness in all quadrants. Sodium fluorescein was injected intravenously and serial fundic photographs were collected for a 5 minute period post‐injection. Results: In all quadrants, the outer nuclear layer (dorsal temporal P = 0.0000, dorsal nasal P = 0.0001, ventral temporal P = 0.0002, ventral nasal P = 0.000) and outer retina (dorsal temporal P = 0.0001, dorsal nasal P = 0.0002, ventral temporal P = 0.0054, ventral nasal P = 0.0084) measurements were significantly decreased in SARDS dogs. The whole retina thickness was significantly decreased in the dorsal temporal (P = 0.0082) and ventral temporal (P = 0.0428) retina. There were no significant differences in the photoreceptor layer thickness or inner retinal thickness between SARDS and control dogs. All SARDS dogs had a loss of definition of all of the photoreceptor bands on OCT. Two SARDS dogs had multifocal small retinal detachments and one of these dogs exhibited fluorescein leaking at the detachment sites. Conclusions: The significant reduction in the outer nuclear layer and the loss of band signals in the photoreceptor layers in dogs with SARDS identified on OCT support the previous histopathology findings. Small detachments may occasionally be detected on OCT and they may leak fluorescein. [ABSTRACT FROM AUTHOR]

Abstract: A novel case of a canine odontogenic parakeratinized cyst (COPC) that resulted in exophthalmos and palatine, maxillary, and zygomatic bone erosion in a 5‐year‐old Chihuahua dog is reported. Final diagnosis was aided by cross‐sectional imaging (magnetic resonance imaging and computed tomography) and confirmed with histologic examination of the cyst wall. [ABSTRACT FROM AUTHOR]

Copyright of Canadian Veterinary Journal / Revue Vétérinaire Canadienne is the property of Canadian Veterinary Medical Association and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Canadian Veterinary Journal / Revue Vétérinaire Canadienne is the property of Canadian Veterinary Medical Association and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

A 15-year-old, neutered male, Shih Tzu cross developed progressive corneal stromal thickening and vascularization of the right eye, and 5 months later, of the left eye. Both eyes became blind due to extensive corneal opacification and were enucleated. Light microscopic examination revealed a diffuse corneal infiltrate of neoplastic mesenchymal cells, and immunohistochemistry revealed diffuse cytoplasmic vimentin immunoreactivity and variable cytoplasmic and nuclear immunoreactivity for S100 in the neoplastic cells. Transmission electron microscopy revealed desmosomes between contiguous cells, thread-like cytoplasmic processes coated with basement membrane, extracellular bundles of collagen, and axonal degeneration consistent with features of a nerve sheath neoplasm. This is the first report of primary, bilateral corneal nerve sheath sarcoma in a canine. [ABSTRACT FROM AUTHOR]

Objective The objective of this study is to investigate the structural and functional ocular changes that develop in turkeys exposed to a photoperiod of 23 h of light (23L) compared with a photoperiod of 14 h of light (14L). Procedures Ten-day-old Nicholas heavy strain poults were exposed to either a 14L or 23L photoperiod. Between 16 and 18 weeks of age, equal numbers of turkeys per treatment group underwent ophthalmic examination (biomicroscopy, indirect ophthalmoscopy) ( n = 14), refractometry ( n = 20), keratometry ( n = 20), tonometry ( n = 20), and full-field electroretinography ( ERG) ( n = 14). Postmortem analyses included orbital magnetic resonance imaging ( MRI) ( n = 10) and light microscopy ( n = 24) at 18 weeks of age. Results Autorefraction revealed a median of −0.13 for sphere in both groups ( P = 0.69), which is approximately emmetropia. The radius of curvature of the cornea was significantly higher ( P = 0.0001) and the refractive power of the cornea was significantly lower ( P = 0.0001) in the 23L group. The astigmatic power was significantly greater in the 23L group ( P = 0.0001). Mean intraocular pressure did not differ between groups ( P = 0.085). Turkeys from the 23L group had significantly larger globes in nasotemporal ( P = 0.0007), dorsoventral ( P = 0.015), and anterioposterior ( P = 0.021) directions, and anterior chambers were more shallow ( P = 0.0002). ERGs revealed the 23L group to have lower a- and b-wave amplitudes and significantly lower cone flicker amplitudes ( P = 0.0008). Light microscopic examination revealed 23L turkeys to have significantly decreased numbers of nuclei in the outer nuclear layer ( P = 0.0001) and inner nuclear layer ( P = 0.0186), and decreased choroidal thickness ( P = 0.0008). The prevalence of cataract in the 23L group was significantly higher ( P = 0.001). Conclusions Exposing turkeys to a prolonged photoperiod induces significant ocular disease. [ABSTRACT FROM AUTHOR]

An approximately six-month-old wild American black bear ( Ursus americanus) was found wandering in Saskatchewan and was presented to the Veterinary Medical Centre of the Western College of Veterinary Medicine for apparent blindness. Clinical examination confirmed an inability to navigate a photopic maze, bilateral tapetal hyper-reflectivity, fundi devoid of retinal vessels, and small pale optic nerve papillae. Single-flash electroretinography revealed A and B-wave amplitudes of approximately 40 and 140 microvolts, respectively, in both eyes. Histologic abnormalities included bilateral optic papillary mineralization and bilateral segmental optic nerve degeneration, with occasional intralesional lymphocytes confirmed with immunohistochemistry for CD3+. There was also bilateral multifocal retinal dysplasia, gliosis, lymphocytic retinitis, a complete lack of retinal blood vessels, an intravitreal vascular membrane, and a mild lymphocytic-plasmacytic uveitis with small pre-iridal cellular membranes. The presence of a positive ERG in a blind bear with numerous retinal ganglion cells and degenerative changes in the optic nerve are most consistent with vision loss due to optic nerve injury, which given the young age of the bear likely occurred during ocular development. The presence of ocular inflammation suggests this injury resulted from an inflammatory/infectious process. The etiology could not be determined. Hepatic concentrations of vitamin A were within the normal reference range for domestic species. Pan-herpesvirus PCR and immunohistochemistry for canine distemper virus and Toxoplasma gondii were negative, although this does not rule out these or other infectious etiologies. This represents the first case report of neonatal or congenital ocular abnormalities in an ursid species. [ABSTRACT FROM AUTHOR]