Mass of the optic nerve, the optic chiasm and the optic tract of practical medical importance

The intraorbital, intracanalicular, and intracranial length of the optic nerve was measured. Also the length of the optic tract between chiasm and lateral geniculate body was estimated. Included are the ampulla of the optic sheaths, the course of the ophthalmic artery, and the distance of the ciliary ganglion to the lateral margin of the orbit.     

Models and treatments for traumatic optic neuropathy and demyelinating optic neuritis

Pathologies of the optic nerve could result as primary insults in the visual tract or as secondary deficits due to inflammation, demyelination, or compressing effects of the surrounding tissue. The extent of damage may vary from mild to severe, differently affecting patient vision, with the most severe forms leading to complete uni‐ or bilateral visual loss. The aim of researchers and clinicians in the field is to alleviate the symptoms of these, yet uncurable pathologies, taking advantage of known and novel potential therapeutic approaches, alone or in combinations, and applying them in a limited time window after the insult. In this review, we discuss the epidemiological and clinical profile as well as the pathophysiological mechanisms of two main categories of optic nerve pathologies, namely traumatic optic neuropathy and optic neuritis, focusing on the demyelinating form of the latter. Moreover, we report on the main rodent models mimicking these pathologies or some of their clinical aspects. The current treatment options will also be reviewed and novel approaches will be discussed.     

Fiber optic array biosensors

Optical fiber arrays provide a powerful substrate for creating high-density sensing systems that can address a variety of biological problems. The fiber substrate can be used to create femtoliter wells that can be loaded with individual beads to create high-density arrays for multiplexed screening and analysis. In addition, living cells can be loaded into the arrays, and their individual responses monitored over long time periods, enabling functional screening of biologically active compounds. Adherent cells can be attached to the fiber substrate to provide a rapid method for observing cell migration and for screening anti-migratory compounds. Finally, individual enzyme molecules can be loaded into the array wells enabling single molecule detection via enzyme-catalyzed signal amplification.     

Calpain inhibitor attenuated optic nerve damage in acute optic neuritis in rats

Optic neuritis (ON), which is an acute inflammatory autoimmune demyelinating disease of the central nervous system (CNS), often occurs in multiple sclerosis (MS). ON is an early diagnostic sign in most MS patients caused by damage to the optic nerve leading to visual dysfunction. Various features of both MS and ON can be studied following induction of experimental autoimmune encephalomyelitis (EAE), an animal model of MS, in Lewis rats. Inflammation and cell death in the optic nerve, with subsequent damage to the retinal ganglion cells in the retina, are thought to correlate with visual dysfunction. Thus, characterizing the pathophysiological changes that lead to visual dysfunction in EAE animals may help develop novel targets for therapeutic intervention. We treated EAE animals with and without the calpain inhibitor calpeptin (CP). Our studies demonstrated that the Ca²⁺‐activated neutral protease calpain was upregulated in the optic nerve following induction of EAE at the onset of clinical signs (OCS) of the disease, and these changes were attenuated following treatment with CP. These reductions correlated with decreases in inflammation (cytokines, iNOS, COX‐2, and NF‐κB), and microgliosis (i.e. activated microglia). We observed that calpain inhibition reduced astrogliosis (reactive astroglia) and expression of aquaporin 4 (AQP4). The balance of Th1/Th2 cytokine production and also expression of the Th1‐related CCR5 and CXCR3 chemokine receptors influence many pathological processes and play both causative and protective roles in neuron damage. Our data indicated that CP suppressed cytokine imbalances. Also, Bax:Bcl‐2 ratio, production of tBid, PARP‐1, expression and activities of calpain and caspases, and internucleosomal DNA fragmentation were attenuated after treatment with CP. Our results demonstrated that CP decreased demyelination [loss of myelin basic protein (MBP)] and axonal damage [increase in dephosphorylated neurofilament protein (de‐NFP)], and also promoted intracellular neuroprotective pathways in optic nerve in EAE rats. Thus, these data suggest that calpain is involved in inflammatory as well as in neurodegenerative aspects of the disease and may be a promising target for treating ON in EAE and MS.     

Facts on optic flow

We employ an optimal solution to both the shape from motion problem and the related problem of the estimation of self-movement on a purely optical basis to deduce practical rules of thumb for the limits of the optic flow information content in the presence of perturbation of the motion parallax field. The results are illustrated and verified by means of a computer simulation.The results allow estimates of the accuracy of depth and egomotion estimates as a function of the accuracy of data sampling and the width of field of view, as well as estimates of the interaction between rotational and translational components of the movement.     

Measles-virus-specific IgG in optic neuritis and in multiple sclerosis after optic neuritis.

Measles-virus-specific IgG was measured in the serum of 100 patients who had presented with optic neuritis (ON) during 1960-74. When reviewed 41 of them were found to have developed definite symptoms and signs of multiple sclerosis (MS), their serum containing significantly higher titres of the antibody than sera from either the rest of the patients or a group of normal healthy controls. In a few patients from whom cerebrospinal fluid (CSF) was obtained in the acute phase of ON, titres of measles IgG in the serum was higher in those in whom the antibody was detected in the CSF than the serum of patients without CSF antibody.     

Glaucoma and optic nerve repair

Glaucoma is a leading cause of irreversible blindness worldwide and causes progressive visual impairment attributable to the dysfunction and death of retinal ganglion cells (RGCs). Progression of visual field damage is slow and typically painless. Thus, glaucoma is often diagnosed after a substantial percentage of RGCs has been damaged. To date, clinical interventions are mainly restricted to the reduction of intraocular pressure (IOP), one of the major risk factors for this disease. However, the lowering of IOP is often insufficient to halt or reverse the progress of visual loss, underlining the need for the development of alternative treatment strategies. Several lines of evidence suggest that axonal damage of RGCs occurs primary at the optic nerve head, where axons appear to be most vulnerable. Axonal injury leads to the functional loss of RGCs and subsequently induces the death of the neurons. However, the detailed molecular mechanism(s) underlying IOP-induced optic nerve injury remain poorly understood. Moreover, whether glaucoma pathophysiology is primarily axonal, glial, or vascular remains unclear. Therefore, protective strategies to prevent further axonal and subsequent soma degeneration are of great importance to limit the progression of sight loss. In addition, strategies that stimulate injured RGCs to regenerate and reconnect axons with their central targets are necessary for functional restoration. The present review provides an overview of the context of glaucoma pathogenesis and surveys recent findings regarding potential strategies for axonal regeneration of RGCs and optic nerve repair, focusing on the role of cytokines and their downstream signaling pathways.     

Influence of antioxidant enzymes in reduction of optic disc edema in experimental optic neuritis

Acute experimental allergic optic neuritis was induced in 18 adult strain-13 guinea pigs. The animals were divided into three groups. The first group of six animals received intraperitoneal injections of saline, the second group received superoxide dismutase (SOD), and the third group received catalase, given daily, starting 1 week after encephalogenic myelin sensitization. Morphometric analysis of longitudinal histopathologic sections of the optic nerve head revealed that the animals treated with the antioxidant enzyme catalase had a statistically significant reduction of optic disc edema when compared to the saline-treated group. Although animals treated with SOD had less optic disc swelling than the saline-treated controls, the differences were not statistically significant. These results indicate that detoxification of hydrogen peroxide, released by invading inflammatory cells, can reduce the severity of axonal swelling within the optic nerve head.     

The optic lobes of Diptera

The optic lobes of Diptera have been examined by variants of the Golgi-Colonnier selective staining techniques and by reduced silver procedures. All, bar one, of the elements described by the earlier authors (Vigier 1908; Zawarzin 1913; Cajal & Sanchez 1915) have been seen, in part or in their entirely, in these preparations. Many other forms, hitherto unrecognized, have been found. Their perpendicular topographical relationships have been reconstructed in the optic lobe regions. Some lateral relationships have also been reconstructed between elements in regions whose columnar arrangement is clearly discernible in Golgi preparations; these include the lamina and the medulla. In the Diptera the projection pattern of the retina mosaic into the lamina neuropil involves complex chiasmata between the two regions (Braitenberg 1967); these have been confirmed from these species. The retina-lamina mosaic is, essentially, homotopically preserved in the columnar medulla, via long visual fibres and monopolar cells. The medullary mosaic is preserved through its strata by transmedullary cells and the longest small-field amacrine cells. The mosaic is projected to the two regions of the lobula complex by class I cells (see part I). The organization of the tangential cell processes suggests that some of them may interact with large or whole field aggragates of the relayed retinal mosaic. Others, especially in the lobula, may interact with small oval or narrow strip-field aggragates. Although there are many differences of neural form and number of neurons between species, both the Lepidoptera and Diptera have the same fundamental plan of neuroarchitecture.     

Cell death and optic fiber penetration in the optic stalk of the chick.

The role of dying cells in the optic stalk in relation to retinal fiber migration was investigated in the chick embryo. Cell death was analysed at various stages of development by counting pycnotic nuclei and also by the Gomori acid phosphatase reaction, while nerve fibers were visualised by the Bodian method. A wave of cell death, beginning in the neural retina at stage 18 and advancing with time through the stalk towards the diencephalon, occurred simultaneously or slightly prior to differentiation and migration of ganglion cell axons. Cell death stopped and gliogenesis occurred in the stalk after penetration by retinal fibers. Cell death occurred in the stalk even when fiber penetration was prevented by optic cup ablation. In this case, necrosis ensued until almost complete degeneration of the stalk, usually within three days after the operation, and gliogenesis did not occur. As the stalk degenerated, its cells became heavily pigmented. These observations suggest that the onset of cell death in the optic stalk is determined prior to and independently of retinal fiber penetration. On the other hand, cessation of cell death and subsequent gliogenesis occur only in the presence of ingrowing optic fibers.     

Correlation between conduction velocities in optic nerve and optic radiation fibers in the cat

Responses of relay neurons of the dorsal lateral geniculate body to stimulation of area 17 of the visual cortex and the optic chiasma were studied in curarized cats. A high degree of correlation was found between the latent periods of antidromic responses of these neurons to stimulation of the visual cortex and orthodromic responses of the same neurons to stimulation of the optic chiasma (r=0.895; P=0.01). In 9% of cases antidromic unit responses were recorded to stimulation of the optic chiasma, evidence that the optic nerve contains centrifugal fibers. The functional role of the temporal dispersion of the afferent flow in the visual system is discussed.A. A. Bogomolets Institute of Physiology, Academy of Sciences of the Ukrainian SSR, Kiev. Translated from Neirofiziologiya, Vol. 10, No. 6, pp. 606–612, November–December, 1978.     

Testicular involution following optic enucleation

Summary The testes of adult male Syrian hamsters underwent involution within six weeks after optic enucleation. The diameter of the seminiferous tubules was 39% less than controls. Sertoli cells, spermatogonia, and primary spermatocytes were still present, but all steps of spermatids were completely absent from the involuted testes. Lipid droplets filled the Sertoli cell cytoplasm and often encroached upon the nucleus. Sertoli cells had sparse mitochondria and smooth endoplasmic reticulum, but Golgi cisternae were abundant. Typical SertoliSertoli junctions attached contiguous Sertoli cells. With lanthanum tracers it was demonstrated that these junctions were impenetrable; therefore, the bloodtestis barrier was deemed intact. Irregularly shaped protrusions often arose from the peritubular tissue and extended inward toward the seminiferous epithelium, often displacing the cytoplasm of the Sertoli cells and spermatogonia. The core of these protrusions consisted of irregular extensions of myoid cell cytoplasm surrounded by the myoid cells' basal lamina. External to the myoid cell basal lamina were bundles of collagen filaments with the basal lamina of the seminiferous epithelium forming the outermost layer of these protrusions. The apices of the Sertoli cells gave rise to numerous leaf-like processes that extended into and obliterated the lumen of the tubules. The Sertoli cell basal cytoplasm often contained phagocytized degenerating germ cells that appeared to give rise to the lipid droplets that filled the Sertoli cell cytoplasm. Acid phosphatase rich lysosome-like organelles were seen fusing with the degenerating germ cells and lipid droplets. The degenerating germ cells also were shown to contain acid phosphatase activity.     

少突胶质细胞和视神经损伤

少突胶质细胞在中枢神经系统中具有重要和广泛的生理功能。视神经损伤后,出现髓鞘脱失、少突胶质细胞死亡和髓鞘再生等病理改变,产生的髓鞘碎片能抑制视神经轴索再生。少突胶质细胞的抑制特性由特定的抑制分子介导,目前已鉴定的抑制分子主要有Nogo、髓鞘相关糖蛋白（myelin—associated glycoprotein,MAG）、少突胶质细胞髓鞘糖蛋白（oligodendrocyte myelin glycoprotein,OMgp）等,它们通过同一受体复合体传导抑制信号。阻滞抑制分子及其受体,或调整神经元的内在生长状态以克服抑制分子的抑制作用,可以促进视神经损伤后再生。本文就这方面的进展作一综述。