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PubMed2003

Optic cup morphogenesis requires pre-lens ectoderm but not lens differentiation.

The formation of the vertebrate optic cup is a morphogenetic event initiated after the optic vesicle contacts the overlying surface/pre-lens ectoderm. Placodes form in both the optic neuroepithelium and lens ectoderm. Subsequently, both placodes invaginate to form the definitive optic cup and lens, respectively. We examined the role of the lens tissue in inducing and/or maintaining optic cup invagination in ovo. Lens tissue was surgically removed at various stages of development, from pre-lens ectoderm stages to invaginating lens placode. Removal of the pre-lens ectoderm resulted in persistent optic vesicles that initiated neural retinal differentiation but failed to invaginate. In striking contrast, ablation of the lens placode gave rise to optic vesicles that underwent invagination and formed the optic cup. The results suggest that: (1) the optic vesicle neuroepithelium requires a temporally specific association with pre-lens ectoderm in order to undergo optic cup morphogenesis; and (2) the optic cup can form in the absence of lens formation. If ectopic BMP is added, a neural retina does not develop and optic cup morphogenesis fails, although lens formation appears normal. FGF-induced neural retina differentiation in the absence of the pre-lens ectoderm is not sufficient to create an optic cup. We hypothesize the presence of a signal coming from the pre-lens ectoderm that induces the optic vesicle to form an optic cup.

Animals↗
PubMed1995

Spatial discrimination against background with different optical systems for collection of fluorescence in laser-excited atomic fluorescence spectrometry with a graphite tube electrothermal atomizer.

A single 90 degrees off-axis ellipsoidal mirror fragment was used in a dispersive detection system for electrothermal atomization laser-excited atomic fluorescence spectrometry. The performance of the new optical arrangement was compared with those of optical arrangements that employed a plane mirror in combination with biconvex or plano-convex lenses. All the optical arrangements collected fluorescence in a scheme called front surface illustration. BEAM-4, an optical ray tracing program, was used for calculations of spatial ray distributions and optical collection efficiency for the various optical configurations. Experimentally, the best collection efficiency was obtained by use of the ellipsoidal mirror, in qualitative agreement with simulations done by use of the BEAM-4 software. The best detection limit for cobalt with the new optical arrangement was 20 fg, which was a factor of 5 better than that obtained with conventional optical arrangements with otherwise the same instrumentation. The signal-to-background ratio and the fluorescence collection efficiency were also studied as a function of position of the optical components for the various optical arrangements. For both cobalt and phosphorus, the signal-to-background ratio with the new optical arrangement remained stable within 10-20% during +/- 8 mm shifts in the position of the detection system from the focal plane of the optics. Overall, the new optical arrangement offered high collection efficiency, excellent sensitivity, and facile optical alignment due to efficient spatial separation between the fluorescence signal and the background radiation. The advantages of the new optical arrangement were particularly important during measurements in the presence of high levels of blackbody radiation.

Data Display↗
PubMed1999

Adenoviral gene therapy with catalase suppresses experimental optic neuritis.

OBJECTIVE: To determine if adenoviral-mediated transfer of the gene for catalase (CAT), the reactive oxygen species scavenger, suppresses experimental optic neuritis. CLINICAL RELEVANCE: Gene therapy with CAT delivered by an adeno-associated viral vector was previously shown to suppress experimental optic neuritis. Because the transduction of protein expression with recombinant adeno-associated viral vector is relatively slow, taking weeks to reach full levels, we studied the effects of replication-deficient adenovirus containing CAT in suppressing experimental optic neuritis. Transduction with adenovirus occurs within days of inoculation, thus, it may be more applicable for the treatment of patients with acute optic neuritis. MATERIALS AND METHODS: Replication-deficient adenovirus containing CAT was injected above the right optic nerve heads of SJL/J mice that were simultaneously sensitized for experimental allergic encephalomyelitis. For controls, the left eyes were injected with the replication-deficient adenovirus without CAT or no virus. The histological effects of CAT on the lesions of experimental allergic encephalomyelitis were measured by computerized analysis of the myelin sheath area (for demyelination), optic disc area (for optic nerve head swelling), the extent of the cellular infiltrate, extravasated serum albumin labeled with immunogold (for disruption of the blood-brain barrier), and the in vivo hydrogen peroxide reaction product. RESULTS: After 1 month, cell-specific catalase activity, evaluated by the quantitation of catalase immunogold, was increased about 2-fold each in endothelia, oligodendroglia, astrocytes, and axons of the CAT-inoculated right optic nerves compared with the control left optic nerves. The increased cellular levels of catalase reduced demyelination by 30%, optic nerve head swelling by 25%, cellular infiltration by 26%, disruption of the blood-brain barrier by 61%, and in vivo levels of hydrogen peroxide by 81%. CONCLUSIONS: Adenoviral-mediated gene transfer increased catalase levels in all optic nerve cell types, and it persisted for 1 month after inoculation. The increased cellular levels of catalase suppressed demyelination and blood-brain barrier disruption at the foci in the optic nerve where prior magnetic resonance imaging and histopathologic studies have demonstrated the demyelinating inflammation of experimental and human optic neuritis. Together, they suggest that gene therapy with CAT may be helpful in the treatment of patients with optic neuritis.

Adenoviridae↗
PubMed2001

[Conventional versus digital planimetry of optic disc photograph: a clinical comparative study].

BACKGROUND: The optic disc size is an important parameter for the diagnosis of glaucomatous and non-glaucomatous optic nerve damage. The aim of this study was to compare quantitative measurements of the optic disc with the established conventional planimetry and a new digital method using Soft imaging system analySIS(tm) for Ophthalmology and to determine the reproducibility of this new method. PATIENTS AND METHODS: Fifty color stereo optic disc photographs of 50 patients (mean age 41.7 +/- 13.4 y) were included in the retrospective, comparative study. Conventional and digital planimetry was taken from one skilled examiner in a masked fashion. According to patient's number measurement values obtained with both methods were matched. Digital planimetric measurements of 10 optic disc photographs were repeated on day 7 and day 14. Statistical analysis was done using linear regression analysis, reliability coefficient and U-test. RESULTS: The planimetric values did not vary significantly between the two methods for optic disc area (3.19 +/- 0.65 mm(2) vs. 3.03 +/- 0.64 mm(2), p=0.96), for cup area (1.36 +/- 0.62 mm(2) vs. 1.21 +/- 0.63 mm(2), p=0.96) or for neuroretinal rim area (1.83 +/- 0.39 vs. 1.82 +/- 0.41 mm(2), p=0.98). There was also no significant difference of horizontal and vertical diameter of optic disc and cup as well as the diameter of the superior temporal and inferior temporal retinal artery and vein at the optic disc border between both methods (p < 0.5). Differences between measured values for optic disc, optic cup area and neuroretinal rim area obtained with both methods were 0.16 +/- 0.10 mm(2) (range - 0.05 to 0.24), 0.15 +/- 0.10 mm(2) (range - 0.12 to 0.26) and 0.014 +/- 0.11 mm(2) (range - 0.26 to 0.26). A high correlation of all planimetric values was observed between both methods (r=0.9, p < 0.0001). Using digital planimetry differences between day 1, day 7 and day 14 were 0.05 +/- 0.03 (range 0.02 to 0.10 mm(2)) for optic disc, 0.05 +/- 0.04 (range 0.0 to 0.13 mm(2)) for optic cup area and 0.05 +/- 0.05 (range 0.01 to 0.14 mm(2)) for the neuroretinal rim area. The reliability coefficient of digital planimetry was 0.9 for optic disc parameters. CONCLUSIONS: The comparable results between both methods and a high reproducibility suggest that the digital planimetry could be used either for clinical routine or scientific evaluation of the optic nerve.

Adult↗
PubMed1985

Axonal and vascular changes following injury to the rat's optic nerve.

The optic nerve of the rat has been examined by light and electron microscopy, and also for vascular permeability to fluorescently labelled albumin, 2 days to 34 weeks after crushing in the orbit. The operation was usually followed by loss of 20-70% of the retinal ganglion cells. Axons could be followed from the retina into the optic nerve at all postoperative times, but they always ended anterior to the lesion. Evidence of feeble regenerative growth of optic axons was seen in the first few postoperative weeks: bifurcating fibres and fibres that turned back towards the eye were present within the optic nerve anterior to the lesion. At the site of crushing, the optic nerve eventually became a thin cord of astroglia, surrounded and partly infiltrated by collagenous connective tissue. Long argyrophilic fibres were conspicuous in the intracranial part of the crushed optic nerve from the seventh to the fourteenth postoperative week. These were shown by electron microscopy to be degenerating myelinated axons that had not been phagocytosed. It was conceivable that axons from the contralateral retina could have sprouted at the chiasma and grown into the degenerated optic nerve. This possibility was excluded by tracing anterograde axonal transport of horseradish peroxidase injected into the contralateral eye. Intravenously injected fluorescent protein entered the connective tissue of the orbit and the connective tissue trabeculae of the optic nerve, but it did not permeate into the central nervous tissue except at the lamina cribrosa, where the optic axons pierce the sclera. Permeability at this site was the same on the operated and unoperated sides. Abnormal permeability of the vasculature was seen at the site of crushing the optic nerve. Fluorescence there was strongest in the first two postoperative weeks and was not seen after the third week. A much less conspicuous defect of barrier function occurred in the intracranial portion of the crushed optic nerve, from the seventh to the fourteenth postoperative week. The responses of the optic nerve of the rat to axotomy contrast markedly with those of the goldfish, in which the blood vessels become permeable to protein throughout the optic pathway and the axons regenerate successfully. Various attempts were made to increase or prolong the opening of the blood-optic nerve barrier in the rat, in the hope of enhancing axonal regeneration, but these endeavours were all unsuccessful.

Animals↗
PubMed2005

The diagnostic yield of the evaluation for isolated unexplained optic atrophy.

PURPOSE: To report the diagnostic yield for the evaluation of isolated and unexplained optic atrophy. SETTING: Two tertiary care academic neuroophthalmology clinics. DESIGN: Retrospective case series. PARTICIPANTS: Patients with optic atrophy. METHODS: Retrospective review of all charts with the diagnosis of optic atrophy. Included patients were adults with isolated, but unexplained, optic atrophy. Patients were excluded if they were children, had incomplete or inadequate documentation of the findings, had nonneurologically isolated optic atrophy (e.g., other localizing findings), or had a history (e.g., prior neuroimaging study showed a compressive lesion, prior ischemic optic neuropathy) or examination (e.g., central retinal artery occlusion) evidence for an etiology for the optic atrophy. MAIN OUTCOME MEASURE: Results of diagnostic evaluation. RESULTS: A total of 1110 charts with the diagnosis of optic atrophy were reviewed from the 2 participating institutions (368 from the University of Cincinnati and 742 from the University of Iowa). Of these 1110 charts, 91 (8%) with isolated unexplained optic atrophy were included, and 1019 charts (92%) were excluded. Of 91 included patients, 18 (20%) had a compressive lesion causing optic atrophy, and 73 (80%) cases had no etiology for the optic atrophy on neuroimaging. Of the 18 patients with abnormal imaging (e.g., meningioma, pituitary adenoma, craniopharyngioma) studies, 11 had bilateral and 7 had unilateral optic atrophy. Five of the 18 patients had progressive visual loss, 3 had hemianopic visual field loss, and 11 were younger than 50 years old. CONCLUSIONS: Patients with optic atrophy in our study typically had historical or examination findings that led to an etiologic diagnosis. Neuroimaging showed an etiology in 20% of patients. Other laboratory testing did not produce an etiologic diagnosis in the absence of a suggestive history or examination. On the basis of our results, we recommend neuroimaging for all patients with unexplained optic atrophy and consideration for directed laboratory studies only.

Brain Neoplasms↗
PubMed2004

Optic nerve oxygenation.

The oxygen tension of the optic nerve is regulated by the intraocular pressure and systemic blood pressure, the resistance in the blood vessels and oxygen consumption of the tissue. The oxygen tension is autoregulated and moderate changes in intraocular pressure or blood pressure do not affect the optic nerve oxygen tension. If the intraocular pressure is increased above 40 mmHg or the ocular perfusion pressure decreased below 50 mmHg the autoregulation is overwhelmed and the optic nerve becomes hypoxic. A disturbance in oxidative metabolism in the cytochromes of the optic nerve can be seen at similar levels of perfusion pressure. The levels of perfusion pressure that lead to optic nerve hypoxia in the laboratory correspond remarkably well to the levels that increase the risk of glaucomatous optic nerve atrophy in human glaucoma patients. The risk for progressive optic nerve atrophy in human glaucoma patients is six times higher at a perfusion pressure of 30 mmHg, which corresponds to a level where the optic nerve is hypoxic in experimental animals, as compared to perfusion pressure levels above 50 mmHg where the optic nerve is normoxic. Medical intervention can affect optic nerve oxygen tension. Lowering the intraocular pressure tends to increase the optic nerve oxygen tension, even though this effect may be masked by the autoregulation when the optic nerve oxygen tension and perfusion pressure is in the normal range. Carbonic anhydrase inhibitors increase the optic nerve oxygen tension through a mechanism of vasodilatation and lowering of the intraocular pressure. Carbonic anhydrase inhibition reduces the removal of CO2 from the tissue and the CO2 accumulation induces vasodilatation resulting in increased blood flow and improved oxygen supply. This effect is inhibited by the cyclo-oxygenase inhibitor, indomethacin, which indicates that prostaglandin metabolism plays a role. Laboratory studies suggest that carbonic anhydrase inhibitors might be useful for medical treatment of optic nerve and retinal ischemia, potentially in diseases such as glaucoma and diabetic retinopathy. However, clinical trials and needed to test this hypotheses.

Animals↗
PubMed2001

[The dawn of neuroprotective therapy for glaucomatous optic neuropathy].

BACKGROUND: Neuroprotective therapy for glaucoma can be defined as treatment of the recalcitrant disease via direct modification of the molecular mechanism involving retinal ganglion cell death. I and my collaborators, at the dawn of the neuroprotective era, elaborated and conducted the following investigations in order to pursue our final goal, i.e., substantial improvement of the quality of life of glaucoma patients. METHODS AND RESULTS: 1. Investigation of in traocular pressure (IOP) independent prognostic factors in glaucomatous optic neuropathy. Clinical investigation along with multivariate analyses revealed that some IOP-independent factors including optic disc hemorrhage and compromised retrobulbar hemodynamics are associated with the development and progression of glaucomatous optic neuropathy. 2. Glaucoma therapy other than ocular hypotensive therapy. A long-term follow-up study demonstrated that calcium-channel blockers are efficacious in stabilizing the visual field in normal-tension glaucoma. 3. Establishment of animal models for glaucomatous optic neuropathy. Experimental animal models were created to conduct neuroprotective research for glaucomatous optic neuropathy: an IOP elevation model and an optic nerve crush model in the rat. In addition, a system was constructed for electrophysiological study in the rat to quantitatively investigate neuroprotective effect on the retina and the optic nerve. 4. Neuroprotective effects of several agents on experimental optic neuropathies. Several agents were studied for their neuroprotective effects on optic neuropathies induced in the rat. Some apoptosis-modifying agents were found to possess neuroprotective effects against optic neuropathy. CONCLUSIONS: IOP-independent prognostic factors exist in glaucomatous optic neuropathy. Glaucomatous optic neuropathy can be stabilized by IOP-unrelated therapy like calcium-channel blockers, at least in a subset of the disease. Modification of the apoptosis mechanism can protect retinal ganglion cells from damage caused by optic neuropathy in the rat models. All of the present studies suggest that neuroprotective therapy will probably become the treatment of choice in the near future for glaucomatous optic neuropathy.

Animals↗
PubMed1985

Fundus lesions in malignant hypertension. II. A pathologic study of experimental hypertensive optic neuropathy.

Accelerated renovascular hypertension produces optic nerve changes ranging from optic disc edema to optic atrophy. To elucidate the pathogenesis of hypertensive optic neuropathy, the optic nerves from 12 monkeys (23 eyes) with accelerated renovascular systemic hypertension were studied by electron and light microscopy. Within 21 months, the animals demonstrated the entire spectrum of pathologic changes. In the optic nerves with optic disc edema, the prelaminar optic nerve exhibited vasoconstriction with subsequent axonal hydropic swelling, axolemma disruption, and glial swelling. In retrolaminar myelinated optic nerve, vasoconstriction was more severe, with endothelial swelling and pericytic degeneration resulting in intramyelinic vacuoles and glial swelling. Optic disc edema appeared to result from axonal hydropic swelling secondary to ischemic infarct, followed by loss of axons and gliosis in the prelaminar optic nerve. The retrolaminar myelinated nerve showed prominent microglial reaction and eventual atrophy of axons and glia. Ischemia seemed to play a major role in hypertensive optic neuropathy, which represents anterior ischemic optic neuropathy.

Animals↗
PubMed2000

Atypical features prompting neuroimaging in acute optic neuropathy in adults.

BACKGROUND: Acute optic neuropathy due to an intracranial lesion may masquerade as optic neuritis or nonarteritic anterior ischemic optic neuropathy (NAION). We reviewed the records of patients who presented with acute unilateral optic neuropathy that was initially diagnosed as optic neuritis or NAION but who ultimately proved to have an underlying structural lesion. METHODS: Retrospective observational case series. We reviewed the records of patients with the initial diagnosis of optic neuritis or NAION in whom the diagnosis was changed to an intracranial etiology at four tertiary care neuro-ophthalmology centres between 1995 and 1998. RESULTS: Eight cases were identified in which atypical features prompted further investigation, including neuroimaging, leading to the diagnosis of an intracranial etiology for the optic neuropathy. Five patients were discovered to have neoplasms (a tuberculum sellae meningioma in two cases, an optic nerve sheath meningioma in two cases and a metastatic lesion in one case), and three patients had intracranial sarcoidosis. Atypical features for optic neuritis included a progressive course, absence of pain, optic atrophy at presentation, lack of significant visual improvement and age over 40 years. For NAION, the atypical features included progressive course, optic atrophy on presentation, absence of vasculopathic risk factors and preceding transient visual loss. INTERPRETATION: Clinicians should be aware that patients with intracranial lesions may present with acute optic neuropathy mimicking optic neuritis or NAION and that certain atypical features should warrant consideration for neuroimaging.

Acute Disease↗
PubMed2000

Discriminant analysis models for early detection of glaucomatous optic disc changes.

AIM: To evaluate and compare four different mathematical formulas for the early detection of morphometric optic nerve head changes in chronic open angle glaucoma. METHODS: The optic nerve heads of 161 patients with perimetrically defined glaucomatous optic nerve damage and of 194 normal subjects were examined by confocal laser scanning tomography. Using four formulas of linear discriminant analysis and the optic cup shape measure as the single optic disc variable, the predictive power of each of these methods was examined to differentiate between the normal eyes and the glaucoma eyes. RESULTS: The highest predictive power had an optic disc sector based formula, in particular in eyes with medium and large optic discs. This optic disc sector based formula was the one with the best agreement with the other formulas examined. It achieved a better predictability than any single optic disc variable evaluated. CONCLUSIONS: Combining quantitative optic disc variables by discriminant analysis functions, the predictive power of semiautomatic quantitative optic nerve head evaluation can be improved by providing the ophthalmologist with a diagnostic score for the detection of glaucomatous optic nerve damage. Because of the pattern of glaucomatous neuroretinal rim loss, an optic disc sector based discriminant formula may have a higher diagnostic precision than other formulas in detecting early glaucomatous damage.

Adult↗
PubMed1997

Efficacy of bidirectional fiber-optic phototherapy for neonatal hyperbilirubinemia.

OBJECTIVE: To evaluate the efficacy of fiber-optic phototherapy using the standard Ohmeda Biliblanket, a large version, double standard Biliblankets, and conventional phototherapy using daylight fluorescent lamps in full-term, healthy infants with nonhemolytic hyperbilirubinemia. METHODS: Full-term, healthy infants with nonhemolytic hyperbilirubinemia (bilirubin concentration, >255 micromol/L or 222 micromol/L at <48 hours of age) were allocated randomly to one of four modes of phototherapy: standard fiber-optic mat (Ohmeda Biliblanket), a large version, double standard Biliblankets, and conventional phototherapy. Bilirubin levels were monitored every 12 hours. Exposure was stopped when bilirubin levels were less than 185 micromol/L, the minimum duration being 24 hours. RESULTS: A total of 171 infants were studied; 42 were exposed to standard fiber-optic phototherapy, 43 to large fiber-optic phototherapy, 42 to double-fiber-optic phototherapy, and 44 to conventional phototherapy. Durations of exposure were 87.05 +/- 6.09 (SEM), 82.57 +/- 5.84, 64.85 +/- 5.43, and 62.61 +/- 3.74 hours, respectively; the 24-hour decline rates were 10.26% +/- 1.84%, 14. 50% +/- 1.53%, 21.82% +/- 1.71%, and 19.00% +/- 1.65%, respectively; the overall decline rates over the whole exposure period were 0.47% +/- 0.03%, 0.52% +/- 0.04%, 0.71% +/- 0.05%, and 0.75% +/- 0.04% per hour, respectively. The efficacy of double-fiber-optic phototherapy and conventional phototherapy was similar and significantly better than that of the large fiber-optic mat and the standard fiber-optic mat in duration, 24-hour decline rate, and overall decline rate. The large mat was slightly better than the standard-size mat with regard to 24-hour decline rate and overall decline rate, but this difference was not significant. Failure of phototherapy occurred only in the large fiber-optic mat group (3 of 43) and the standard fiber-optic mat group (4 of 42); none occurred in the other two groups, but differences not statistically significant. The nursing personnel were more comfortable with single fiber-optic phototherapy, which caused no initial disturbance to the swaddled infants as did conventional phototherapy, but found double-fiber-optic phototherapy difficult to use. CONCLUSION: For efficacy of fiber-optic phototherapy in full-term infants to be comparable to that of our conventional phototherapy, the light dose of the standard mats needs to be doubled.

Analysis of Variance↗
PubMed2004

Dose fractionation in stereotactic radiotherapy for parasellar meningiomas: radiobiological considerations of efficacy and optic nerve tolerance.

OBJECT: Benign meningiomas have been shown to be equally well controlled with single-dose radiosurgery (15 Gy) and fractionated doses of 54 Gy in 30 fractions after adequate follow up. For a subset of patients with meningioma, the optic apparatus is dose limiting when considering single-dose stereotactic radiosurgery, with tolerance estimated to be 8 to 10 Gy. Recently, hypofractionated regimens have been used to treat benign meningiomas with a small number of fractions. An analysis of the expected efficacy of hypofractionation compared with the estimated optic tolerance to fractionated radiotherapy was undertaken. METHODS: Using the assumption that 15 Gy in one fraction and 54 Gy in 30 fractions are isoeffective for control of benign meningioma, an alpha/beta for meningioma is calculated to be 3.28 Gy. Invoking a 10% error for these doses (15 Gy+/-10% is equivalent to 54 Gy+/-10%) results in upper and lower limits of the estimate for alpha/beta of 3.85 Gy and 2.7 Gy. Using these estimates, isoeffect curves for control of meningioma were constructed for fraction numbers of one to 45. Best estimates of optic nerve/chiasm tolerance to single doses of radiation are 8 to 10 Gy, with the reported incidence of optic neuropathy increasing significantly at higher doses. This is consistent with the optic ret model, which also predicts for optic tolerance following fractionated radiotherapy. Comparison of optic tolerance and estimates of efficacious doses at fraction numbers between one and 30 were made. Statistical estimates of patient numbers and duration of follow up required to rule out optic neuropathy following radiotherapy were made. Single doses of radiation required to treat benign meningioma optimally (13.5-16.5 Gy) clearly exceed the estimated and reported clinical tolerance of the optic nerves and chiasm. The application of equivalent biological doses in a small number of fractions continues to exceed optic tolerance until at least 25 fractions are applied. CONCLUSIONS: The use of small numbers of fractions to treat patients with meningioma when portions of optic nerve or chiasm receive full dose may result in undertreatment of the tumor and/or exceeding optic nerve tolerance. In such cases standard fractionation is recommended. Ruling out a low, yet unacceptable, risk of optic neuropathy may require the close study of many patients with long-term follow-up evaluation.

Dose Fractionation, Radiation↗
PubMed2006

[Guidance of regenerative axons in optic nerve regeneration in Bcl-2 overexpressing mice].

OBJECTIVE: To determine whether optic nerve can regenerate after optic nerve crush and weather the regenerating axon reaches the target in the brain in Bcl-2 overexpressing mice. METHODS: Left eye optic nerve crush was performed in wild-type (C57Bl/6J) and Bcl-2 transgenic mouse pups at 3 days after birth (P3), followed immediately by the opposite eyeball enucleated. Mouse pups were killed at 4 days post-surgery. Optic nerve regeneration was assessed at the sections of optic nerve and the brain. An anterograde tracer, cholera toxin B subunit conjugated with fluorescein (CTB-F), was applied intraocularly, immediately after optic nerve crush to label retinal ganglion cell axons. Immunofluorescence staining with anti-GAP-43 was carried out to reveal regenerating axons in optic nerve sections. RESULTS: In wild-type mice, severed optic nerves failed to regenerate. In contrast, in all of the Bcl-2 transgenic mice examined, optic nerves regenerated robustly over long distances, but the regenerating fibers were found to deviate from the optic pathway and grew into the forebrain to form aberrant projection. CONCLUSION: When the opposite eyeball is removed in P3 Bcl-2 overexpressing mice with optic nerve was crushed in one side, the guidance from the normal optic pathway is lost, the optic nerve could regenerate and reach the brain, but the regenerating axons could not reach both side of target in the midbrain, they grow into aberrant place of forebrain.

Animals↗
PubMed1989

Regeneration of axons from the adult rat optic nerve: influence of fetal brain grafts, laminin, and artificial basement membrane.

After transection of the optic nerve of adult rats, most of the axons in the proximal stump die and the surviving ones are unable to regenerate into the distal optic nerve. Since the fetal brain has an inherent capacity to regenerate axons, we investigated whether fetal (E16) target regions of optic axons (thalamus and tectum) transplanted to the completely transected optic nerve of adult rats would promote axon regeneration. In control operated rats, axon growth beyond the site of transection was restricted to a few fibers that grew irregularly within the connective tissue scar. By contrast, in grafted animals directed outgrowth of optic axons toward the transplant started at 6 days postoperation (p.o.) and reached its maximum 15 days p.o. and later, when numerous single optic fibers and small axon fascicles had grown toward and into the graft, where they formed arborizations and terminal varicosities. Regenerating optic axons were further advanced than GFAP-positive strands of astroglia that emanated from the proximal optic nerve stump. Laminin immunoreactivity appeared at 6 days p.o. in the zone of reactive astroglia in the terminal part of the optic nerve stump. Later it showed a distribution complementary to the pattern of GFAP immunoreactivity, which it seemd to circumscribe. There was no unequivocal codistribution of laminin immunoreactivity with regenerating axons. In further experiments, target regions from different ontogenetic stages (E14 to neonate and adult) and nontarget regions (E16, cerebral cortex or spinal cord) were grafted to the optic nerve stump. With the exception of the adult grafts, all transplants had effects on axon regeneration comparable to those of E16 target regions. In order to test the effects of extracellular matrix molecules on axon regeneration, a basement membrane gel reconstituted from individual components of the Engelbreth-Holm-Sarcoma (EHS) sarcoma was implanted between proximal and distal optic nerve stumps. No axons were induced to regenerate by this matrix. Likewise, laminin adsorbed to nitrocellulose paper and implanted at the lesion site did not stimulate axon growth from the proximal optic nerve stump. These results indicate that fetal brain is able to induce and direct regrowth of axons from the optic nerve toward the graft across a substrate that is not composed of astroglia or basement membrane components like laminin. The directed growth of axons in the absence of a preformed substrate implies a chemotactic growth response along a concentration gradient mediated by neurotropic molecules released from the graft.

Animals↗
PubMed1993

Development of myelin mosaicism in the optic nerve of heterozygotes of the X-linked myelin-deficient (md) rat mutant.

The oligodendrocyte population of the optic nerve has been suggested to arise either from a radial migration of neuroepithelial cells of the optic stalk or from the longitudinal migration of progenitor cells into the optic nerve from the brain, via the optic chiasm. Female heterozygotes of the X-linked myelin deficient (md) rat trait show a marked mosaic pattern of myelination of the optic nerves. This degree of mosaicism is not observed in other parts of the central nervous system. A total of 235 optic nerves from female rats of from 3 weeks to 24 months of age were examined by light microscopy. Nerves (104), from rats of all ages, showed defects in myelination consisting of distinct patches of non-myelination, often sharply demarcated from adjacent areas of normally myelinated axons. In some animals the abnormality was grossly apparent as areas of transparency within the intact optic nerves. In the majority of optic nerves showing mosaicism, defects in myelination were observed along the whole length of the nerve. However, a worsening of the defect toward the retinal end of the nerve was noted in 15 optic nerves, and an additional 11 nerves showed a defect in this region alone. It was also found that a number of rats had mosaicism in only one optic nerve. The preferential involvement of the retinal end of the optic nerves, and the asymmetrical involvement of the optic nerves within individual rats, is interpreted as indirect evidence in support of the proposed longitudinal migration of the oligodendrocyte precursor into the optic nerve.

Animals↗
PubMed1976

Tumors of the optic nerve.

This is a review of primary and secondary tumors of the optic nerve. The emphasis is an optic nerve gliomas and meningiomas. Optic nerve gliomas are slowly growing astrocytic neoplasms of the anterior visual pathways, the majority of which occur within the first two decades of life, with equal sex incidence in about 1 of 200,000 patients presenting with eye complaints. The incidence is greater in neurofibromatosis. The typical presentation is visual impairment in a verbal pre-school child with optic canal enlargement and optic atrophy. An intraorbital location of the tumor leads to axial, irreducible, non-pulsatile proptosis. An intracranial location may disturb hypothalamic and pituitary function and produce hydrocephalus. Ocular findings may also include limited motility on a mechanical-restrictive basis, a pupillary relative afferent defect, nystagmus, and variable, non-specific visual field defects. Roentgenographic studies may show concentric unilateral enlargement of the optic canal with preservation of a well corticated margin, a fossa under the anterior clinoid process in continuity with the optic canal ('J'-shaped sella), and findings of increased intracranial pressure. On pathologic examination the tumor is a smooth, fusiform, intradural enlargement of the optic nerve. Histologically there is proliferation of elongated (pilocytic) astrocytes in reticulated patterns with intervening microcystic spaces containing mucosubstance and surrounding reactive hyperplasia of the arachnoid. Mitoses are not found. The diagnosis is clinical X-ray studies and brain scan should be performed. The differential diagnosis is that of unilateral proptosis in a child and includes acute ethmoiditis, hyperthyrobidism, craniostenosis, other neoplasms, Hand-Schuller-Christian disease, and orbital hemorrhage due to trauma. Surgical resection is performed in cases with unilateral optic nerve involvement, the surgical approach being determined by tumor location. Bilateral or chiasmal cases are treated with radiotherapy when progression occurs. Malignant optic nerve gliomas and optic nerve hyperplasia are also discussed. Optic nerve meningiomas arise from the nerve sheath and are to be distinguished from orbital meningiomas arising from ectopic arachnoidal cells or those secondarily involving the orbit by extension from adjacent sites. Up to 80% of orbital meningiomas occur in females, in two age peaks, 25% in the first decade, and the rest in the 5th decade. Meningiomas present with visual loss and may produce proptosis, papilledema and/or optic atrophy, retinal striae, opticociliary shunts, limitation of extra-ocular movements, and lid edema, Signs of von Recklinghausen's disease should be sought. X-rays are the mainstay of diagnosis. Orbital meningiomas are composed of cells in sheets or in whorls with some spindle shaped cells. Calcifications are typical. Usually the dura is penetrated and the orbit invaded. Primary orbital meningiomas are locally infiltrating but do not metastasize. Complete local excision en bloc is recommended...

Adolescent↗
PubMed1990

Macromolecular structure of axon membrane and action potential conduction in myelin deficient and myelin deficient heterozygote rat optic nerves.

The macromolecular structure of the axon membrane in optic nerves from 25-day-old male littermate control and myelin deficient (md) rats and 16-month-old md heterozygotic rats was examined with quantitative freeze-fracture electron microscopy. The axon membrane of control optic nerves displayed an asymmetrical partitioning of intramembranous particles (IMPs); P-fracture faces of myelinated internodal axon membrane were more particulate than those of pre-myelinated axons (approximately 1600 v 1100 microns-2, respectively), while relatively few IMPs (approximately 150 microns-2) were present on external faces (E-faces) of internodal or pre-myelinated axon membrane. Amyelinated axons of md optic nerves also exhibited an asymmetrical partitioning of IMPs; protoplasmic membrane face (P-face) IMP densities, taken as a group, exhibited a wide range (approximately 600-2300 microns-2) and, in most regions, E-faces displayed a relatively low IMP density (approximately 175 microns-2). Axons of greater than 0.4 microns diameter exhibited significantly greater mean P-face IMP density than axons less than 0.4 microns diameter. Aggregations of E-face IMPs (approximately 350 microns-2) were occasionally observed along amyelinated axon membrane from md optic nerves. Optic nerves from md heterozygote rats exhibit myelin mosaicism, permitting examination of myelinated and amyelinated axon membrane along the same tract. The axon membrane exhibits different ultrastructure in these two domains. Myelinated internodal axon membrane from md heterozygote optic nerves exhibits similar P- and E-face IMP densities to those of control internodal axolemma (approximately 1800 and 140 microns-2, respectively). Amyelinated axons in the heterozygote exhibit a membrane structure similar to amyelinated axons in md optic nerve. P-face IMP density of large diameter (greater than 0.4 microns) amyelinated axons from md heterozygote optic nerves is significantly greater than that of small calibre (less than 0.4 microns) axons. In most regions, amyelinated axon membrane exhibits a relatively low E-face IMP density (approximately 200 microns-2); however, focal aggregations (approximately 400 microns-2) of E-face particles are present. Electrophysiological recordings demonstrate that amyelinated axons in md optic nerves support the conduction of action potentials. Compound action potentials in md optic nerves exhibit a monophasic configuration, even at 20-days postnatal, similar to that of pre-myelinated optic nerve of 7-day-old normal rats. Moreover, conduction velocities in the amyelinated 20-day-old md optic nerve are similar to those displayed by pre-myelinated axons from 7-day-old optic nerves.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗