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Results for “OPTIC PATHWAY”

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PubMed2003

Axonal transport and sorting of herpes simplex virus components in a mature mouse visual system.

The time course for delivery and transport of two major proteins of herpes simplex virus (HSV) has been determined for mature mouse retinal ganglion cell axons in vivo. Twenty-four hours after intravitreal injection of HSV, valacyclovir was introduced into the drinking water of the mice to inhibit subsequent viral replication. Without treatment, viral spread and replication in periaxonal glial cells confound study of axonal transport. At 2 to 5 days after infection, the animals were sacrificed and contiguous segments of the optic pathway were removed. Immunofluorescence microscopy indicated that the number of infected astrocytes was reduced in the proximal optic nerve and eliminated in the optic tract. Western blots of the retina with antibodies for envelope and capsid components, glycoprotein D (gD) and VP5, respectively, revealed that both components were expressed in retinal homogenates by 2 days. Results of reverse transcription-PCR indicated that there was no gD mRNA present in the treated optic tract 5 days after infection. Therefore, we conclude that gD is transcribed from viral mRNA in the retinal ganglion cell bodies. The gD accumulated in the proximal ganglion cell axon by 2 days and reached the most distal segment after 3 days. The VP5 first appeared in the proximal axons at 4 days, about 48 h after the appearance of gD. Thus, gD entered the axon earlier and independent of VP5. These finding confirm the subassembly model of viral transport in neurons and suggest that there is a 4- to 5-day window for initiation of effective antiviral treatment with valacyclovir.

Acyclovir↗

PubMed1988

Axons added to the regenerated visual pathway of goldfish establish a normal fiber topography along the age-axis.

Throughout a goldfish's life, new generations of ganglion cells are added on the retinal margin and their axons extend centrally to occupy predictable positions in the retinotectal pathway, adjacent to their predecessors and subjacent to the pia. The stacking of successive generations of axons defines the age-axis of the pathway. This study examined whether an ordered array of predecessor axons is a prerequisite for the patterned growth of new axons. One optic nerve was crushed intraorbitally and the fish was injected with 3H-thymidine to label the proliferating cells on the retinal margin. The ring of 3H-thymidine-labeled cells separated retina that was present at the time of nerve crush (inside the ring) from new retina added afterward (outside). After a period of 14-16 months postcrush, both tectal lobes received two punctate applications of horseradish peroxidase (HRP), one in the central and the other in peripheral tectum, to retrogradely label contralateral retinal ganglion cell bodies and their axons. The pattern of HRP labeling from the control tectum confirmed earlier work: axons on the central tectum had somata in the central retina, and axons on the peripheral tectum had somata in the peripheral retina. The labeled cells and axons were both in predictable patterns. The somata that were backfilled from applications to the center of the experimental tectum lay inside the radioactive ring and had therefore regenerated their axons. The patterns of their labeled axons in the optic pathway and of their somata in the retina were typical of the regenerated condition as described in earlier studies. The somata backfilled from the periphery of the experimental tectum were outside the radioactive ring and had been added after the optic nerve crush. The patterns of their labeled axons and somata were comparable to the normal pattern. These observations indicate that new axons do not depend on an ordered array of predecessors to reestablish normal order along the age-axis of the pathway.

Aging↗

PubMed1981

Evoked potentials in albinos: efficacy of pattern stimuli in detecting misrouted optic fibers.

Misrouting of retinogeniculostriate projections associated with retinal hypopigmentation has been found to be a general phenomenon in mammals, including humans. Anomalous optic pathway projections of albinos may be detected by recording visually evoked potentials (VEPs). To determine the efficacy of various stimulus conditions for detecting misrouted optic fibers, we compared flash, modulated light, pattern reversal and pattern onset/offset (appearance/disappearance) stimuli. Pattern onset/offset were found superior in detecting anomalies of misrouting of retinogeniculostriate projections. As a group, humans with retinal hypopigmentation have poor evoked potentials to offset and pattern reversal stimuli. Nystagmus seems to be most symptomatic of poor pattern reversal responses. In general onset/offset pattern stimuli are more versatile for detection of abnormalities in the visual system than pattern reversal stimuli.

Adolescent↗

PubMed1999

The spatial tuning of steady state pattern electroretinogram in multiple sclerosis.

In normal subjects, the steady-state electroretinogram in response to contrast reversing gratings (PERG), is spatially band-pass tuned in amplitude, with a maximum at intermediate spatial frequencies and an attenuation at lower and higher ones. The amplitude attenuation at low spatial frequencies is believed to reflect centre-surround antagonistic interactions in the receptive fields of inner retinal neurons. The aim of this study was to evaluate the PERG spatial tuning in multiple sclerosis (MS) patients without a previous optic neuritis history. Steady- state PERGs in response to counterphase-modulated (8 Hz) sinusoidal gratings of variable spatial frequency (0.6, 1.0, 1.4, 2.2 and 4.8 c/deg), were recorded from 18 patients with definite or probable MS and no history of optic neuritis (ON-). Nine of them had no signs of subclinical optic nerve demyelination (asymptomatic) in either eye, while nine had symptoms or signs of optic pathways involvement (symptomatic) in one or both eyes. Results were compared with those obtained from 10 MS patients with a previous history of optic neuritis (ON+) in one or both eyes, as well as from 21 age-matched controls. The amplitudes and phases of the responses' 2nd harmonics were measured. Compared with the controls, asymptomatic ON- patients showed selective losses in mean PERG amplitudes at medium and high (1.0-4.8 c/deg) spatial frequencies. Symptomatic ON- patients and ON+ patients had reductions in mean PERG amplitudes, with respect to controls, involving the whole spatial frequency range, but with greater losses at medium-high (1.0-4.8 c/deg) than at lower spatial frequencies. In all patients' groups, the average PERG spatial tuning function differed significantly from that of the controls, assuming a low-pass instead of the normal band-pass shape. The PERG phase was delayed in ON+ but not in ON- patients, as compared to controls. However, the phase delay was independent of spatial frequency. In both ON- and ON+ patients, losses in PERG amplitude and spatial tuning tended to be associated with corresponding abnormalities in perimetric sensitivity, visual acuity, colour vision and transient visual evoked potential (VEP) latency. The results indicate that abnormalities of the spatial tuning of steady-state PERG can be found in MS patients without either optic neuritis or signs of subclinical optic nerve demyelination. These changes may reflect a retinal dysfunction, developing early in the course of MS, due to a loss of specific subpopulations of inner neurons, changes in lateral interactions of their receptive fields, or both.

Adolescent↗

PubMed2004

[MR imaging study of edema along the optic tract in patient with Rathke's cleft cyst].

We report an 80-year-old woman who was admitted to our hospital with symptoms due to diabetes insipidus. Magnetic resonance (MR) imaging demonstrated a sellar/suprasellar cystic lesion with marginal enhancement and the thick pituitary stalk. The MR imaging depicted edema spreading along the optic tract on fluid-attenuated inversion recovery (FLAIR) images. Upon neurological examination at the time of admission, there were no abnormal findings affecting the field of vision or visual acuity. In endocrinological examination, the basal plasma values of pituitary hormones were within normal range except for that of prolactin, which was 47.9 ng/ml. The preoperative diagnosis was craniopharyngioma, and the intrasellar mass was partially removed by the endoscopic transnasal transsphenoidal approach. Postoperative histopathological examination revealed Rathke's cleft cyst associated with squamous metaplasia. Lymphocytic infiltration was also confirmed in both the anterior and posterior pituitary lobe. The postoperative course was satisfactory. Edema spreading along the optic tract was reported as a characteristic MR imaging finding for diagnosis of craniopharyngiomas or optic nerve glioma. However, it is suggested that edema of the optic pathway seems to be caused not only by craniopharyngioma but also other suprasellar lesions. It was a rare case of secondary lymphocytic hypophysitis caused by Rathke's cleft with edema along the optic tract.

Aged↗

PubMed1989

Slow component B protein kinetics in optic nerve and tract windows.

The transport kinetics of 3 radiolabeled slow component b (SCb) proteins (a 30 kDa protein, clathrin, and actin) were examined in the axons of mouse retinal ganglion cells. To view the transit of these proteins through the entire optic pathway between the eye and the target cells, we used two different windows: (1) a 2 mm segment from the optic nerve located 3-5 mm from the eye, and (2) a 2 mm segment from the optic tract located past the chiasm 6-8 mm from the eye. The radiolabeled proteins from these windows were separated by 1- and 2-dimensional SDS-PAGE, and the individual radiolabeled bands were quantified. Radiolabeled proteins entered and cleared the optic axons between 1 and 119 days post-labeling. All these proteins had broader transport waves in the more distal optic tract window than in the more proximal optic nerve window. The spreading of transport waves as they advance along the axon appears to be produced by a playing out of the natural heterogeneity of axonal transport rates within each population of labeled proteins. Our results confirm the proposals that clathrin and the 30 kDa protein are transported principally with SCb and that actin is transported both with SCb and with SCa. Although these proteins can be generally classified with SCb, their detailed kinetics differed (for example, their median transit times differed) and, in summary, their characteristic rates of movement can be ordered as: clathrin greater than 30 kDa protein greater than actin.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed2000

125I-alpha-conotoxin MII identifies a novel nicotinic acetylcholine receptor population in mouse brain.

alpha-Conotoxin MII (CtxMII), a peptide toxin from the venom of the predatory cone snail Conus magus, displays an unusual nicotinic pharmacology. Specific binding of a radioiodinated derivative ((125)I-alpha-CtxMII) was identified in brain region homogenates and tissue sections. Quantitative autoradiography indicated that (125)I-alpha-CtxMII binding sites have an unique pharmacological profile and distribution in mouse brain, being largely confined to the superficial layers of the superior colliculus, nigrostriatal pathway, optic tract, olivary pretectal, and mediolateral and dorsolateral geniculate nuclei. Expression of alpha-CtxMII binding sites in the nigrostriatal pathway, combined with evidence for alpha-CtxMII-sensitivity of nicotine-induced [(3)H]dopamine release in rodent striatal preparations indicates that (125)I-alpha-CtxMII binding nicotinic acetylcholine receptors are likely to be physiologically important. Unlabeled alpha-CtxMII potently (K(i) < 3 nM) competed for a subset of [(3)H]epibatidine binding sites in mouse brain homogenates, but weakly (IC(50) > 10 microM) interacted with (125)I-alpha-bungarotoxin and (-)-[(3)H]nicotine binding sites, confirming this compound's novel nicotinic pharmacology. Quantitative autoradiography revealed that alpha-CtxMII binds with high affinity at a subset of [(3)H]epibatidine binding sites with relatively low cytisine affinity ("cytisine-resistant" sites), resolving [(3)H]epibatidine binding into three different populations, each probably corresponding to a receptor subtype. The majority population seems to correspond to that which binds nicotine and cytisine with high affinity ("cytisine-sensitive" sites). Comparison of the cytisine-resistant population's distribution with that of alpha3 subunit mRNA expression suggests that the fractions both more and less sensitive to alpha-CtxMII probably contain the alpha3 subunit, perhaps in combination with different beta subunits.

Animals↗

PubMed1985

Neurologic disorders associated with visual loss in childhood.

Acquired visual loss in childhood is often a manifestation of more generalized neurologic dysfunction. This article includes a discussion of lesions of the cornea, lens, retina, anterior visual pathways, optic radiations, and visual cortex that are associated with other neurologic abnormalities in children.

Brain Diseases↗

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↗

PubMedDate not supplied

Electrophysiological tests and CSF examination in patients with optic neuritis.

Electrophysiological tests (visual and somatosensory evoked potentials, flicker fusion test) and electrophoretic examination of cerebrospinal fluid were performed in 17 patients who previously suffered from one or more attacks of optic neuritis. The association of the tests revealed the demyelinating inflammatory pathogenesis in eight cases. In the remaining nine cases the CSF oligoclonal pattern was absent. The evidence that a bilateral delayed VEP, suggesting a subclinical contralateral involvement of optic pathways, could be related to multiple sclerosis, is discussed. A case was finally ascertained as being affected by Leber's optic atrophy.

Adolescent↗

PubMed1980

Mapping the normal and regenerating retinotectal projection of goldfish with autoradiographic methods.

In normal goldfish, lesions of various size were made in nasal or temporal retina immediately prior to retinal labeling with tritiated proline. The resulting gaps in retinal innervation of tectum indicated that the projection is retinotopographically ordered to a precision of about 50 micrometer. Similarly, acute tectal incisions transecting the optic pathways were combined with immediate retinal labeling. The resulting tectal denervation confirmed that most fibers follow highly ordered paths through the stratum opticum of tectum; but a few fibers were found to follow unusual paths to their appropriate tectal positions. In other fish, the optic nerve was crushed. At various times afterwards, retinotopography and pathway order were similarly analyzed by making retinal lesions or tectal incisions just prior to labeling. For up to 40 days after crush, the projection lacked any refined retinotopic order. Only a gross topography could be demonstrated. Over several months, retinotopography gradually improved eventually approaching that of normals. Correlated with this was an initial stereotypic growth through the pathways of the stratum opticum followed by a long period of highly anomalous growth through the innervation layer. Evidently, many regenerated fibers grew in through inappropriate routes to the wrong region of tectum but subsequently arrived at their appropriate locus by circuitous routes within the innervation layer.

Animals↗

PubMed1985

Visual dysfunction with basal skull tumours.

Early detection of visual loss caused by tumours of the base of the skull is accomplished by systematic tests of the pregeniculate optic pathway. Even when central acuity is relatively preserved, a relative afferent pupillary defect and reduced color perception yield evidence of impaired optic nerve conduction. Although confrontation tests of the visual fields are useful screening techniques, unexplained symptoms should be pursued with static and kinetic perimetry. Patterns of optic nerve and chiasmal field loss and atrophy of the dis or retinal nerve fibers are imprecise guides to the location of basal skull tumours. Regardless of the pattern of visual field defect, unexplained progressive loss of vision demands intensive neuroradiologic study of the basal cisterns and skull.

Brain Neoplasms↗

PubMed1995

Microglia in normal and regenerating visual pathways of the tench (Tinca tinca L., 1758; Teleost): a study with tomato lectin.

We have studied the microglial cells in the normal and regenerating visual pathways of Tinca tinca (Cyprinid, Teleost) by using the lectin from Lycopersicum esculentum (tomato), which, in our case, has been demonstrated as a specific marker for teleost microglia. In the normal fish, there are tomato lectin positive microglial cells in the retina, optic nerve, and optic tectum. Following optic nerve crush, we observed a more extensive labeling of the microglia in the crushed optic nerve and in the contralateral optic tectum affecting the stratum opticum and stratum fibrosum et griseum superficiale. In both cases, there was an increase of rounded and less ramified microglial cells, and granular cells. This response of a more extensive labeling of microglial cells increases to a maximum at 2-3 weeks after the crush; the density of labeled microglial cells decreases after 3 months after crushing. However, in the retina no changes were observed after optic nerve crush. These results suggest that the microglial cells could play an important role in regeneration of fish optic pathway, as other neuroglial cells do.

Animals↗

PubMed1985

The application of flash visual evoked potentials during operations on the anterior visual pathways.

Flash visual evoked potentials (F-VEP's) have been recorded in fifteen patients (thirty eyes) with anterior visual pathway compression lesions before, during and after the operation in relation to clinical visual testing. A grading system for the wide variety of abnormal F-VEP's has been established, based on changes in forty patients (eighty eyes). No significant correlation between change in F-VEP and visual acuity or visual field has been demonstrated. Intraoperative F-VEP's have been found to be sensitive to halothane and to surgical manipulation of the optic nerve and/or chiasm during dissection of the tumour. The technique is considered a useful means of identifying the optic pathway during operation and may assist in prevention of optic damage if the transphenoidal approach is used.

Adult↗

PubMed1996

Different rates of horseradish peroxidase transport in the optic nerve of neonatal and adult rats.

In order to evaluate the effects of age upon fast transport kinetics, we studied the velocity of horseradish peroxidase transport along the optic pathway of neonatal and adult rats. Rate of horseradish peroxidase movement was assessed by following the displacement of horseradish peroxidase activity in the optic nerve with time after injection. We estimated a rate about 100 mm/day for bidirectional transport of horseradish peroxidase in the optic nerve of neonatal rats, while a two-fold higher rate was observed for anterograde transport in adult animals. Developmental regulation of fast transport rate may ensure relative constancy of the time required to connect the cell body with axon terminals.

Animals↗

PubMed2004

Mechanisms and time course of neuronal degeneration in experimental autoimmune encephalomyelitis.

Neuronal and axonal damage is considered to be the main cause for long-term disability in multiple sclerosis. We analyzed the mechanism and kinetics of neuronal cell death in experimental autoimmune encephalomyelitis (EAE) induced by myelin oligodendrocyte glycoprotein (MOG) by combining an electrophysiological in vivo assessment of the optic pathway with the investigation of retinal ganglion cell (RGC) counts. In accordance with our previous findings in this animal model, neuritis of the optic nerve (ON) leads to apoptotic RGC death. By further investigating the time course of RGC apoptosis in the present study, we found that neuronal cell death together with decreased visual acuity values occurred before the onset of clinical symptoms. Simultaneously with the time course of RGC apoptosis, we found a down-regulation of phospho-Akt as well as a shift in the relation of 2 proteins of the Bcl-2 family, Bax and Bcl-2, towards a more proapoptotic ratio in these cells. Comparing the kinetics and mechanisms of RGC death during MOG-EAE with those following complete surgical transection of the ON, we found significant agreement. We hypothesize that the main reason for RGC loss in MOG-EAE is the inflammatory attack but RGC death also occurs independently of histopathological ON changes.

Animals↗

PubMed1989

Insights on retina and optic nerve metabolism during rat aging.

Little is known concerning the biochemical response of the various tissue components of the optic pathway to aging. The in vitro incorporation of radioactive precursors into RNA and lipids of whole retina, as well as into glycerophospholipids of optic nerve was tested in male Wistar rats aged 4, 12, and 24 months. The results obtained suggested that RNA metabolism of rat retina (most likely photoreceptor cell layer) was not affected by the age, whereas phospholipid synthesis was on the contrary increased in comparison with that of the optic nerve, for which a serious impairment was observed. The physiological significance of this response, and the mechanism by which retinal tissue is spared from the general age derangement of the nervous system remain to be defined.

Aging↗

PubMed1996

Perturbation of the developing Xenopus retinotectal projection following injections of antibodies against beta1 integrin receptors and N-cadherin.

We have examined the function of beta1 integrin receptors and N-cadherin in the development of the Xenopus retinotectal projection. In vivo perturbation experiments were performed by injecting antibodies directed against beta1 integrin receptors and N-cadherin into the embryonic optic pathway. The antibodies were present during the initial development of the retinal projection, when the axons of the ganglion cells are migrating through the optic tract and terminating within the optic tectum. When injected individually, the antibodies were insufficient to cause obvious pathfinding errors. However, when injected together, the antibodies caused specific abnormalities in the development of the retinotectal projection. Pathfinding errors most commonly observed included ectopically projecting axons within the optic tract region, meandering and splaying of axons in the optic tectum, and the induction of prominent ipsilateral projections. IgGs and Fab' fragments of the antibodies produced pathfinding errors; these defects were not observed in animals injected with control antibodies. These in vivo results show that beta1 integrin receptors and N-cadherin have important roles during the development of the visual projection and provide evidence that a balance between cell-cell and cell-matrix adhesion may be critical for the normal development of the vertebrate visual system.

Animals↗