Optic Tract Lesions Research Articles

Evidence that the relative densities of afferents from both eyes control laminar distribution and binocular segregation of retinotectal projections in rats

In the superior colliculus of normal rodents the crossed retinal projection overlaps the uncrossed projection. The present study describes an abnormal laminar distribution and binocular segregation of the retinotectal afferents induced after the experimental enlargement of the uncrossed retinotectal pathway in pigmented rats. Intraocular injections of anterograde tracers were used to investigate the topographic and laminar organization of retinotectal projections in adult rats given unilateral optic tract lesions at birth. These lesions are known to increase the number of ipsilaterally projecting ganglion cells in the opposite retina. The uncrossed retinal projection to the remaining superior colliculus forms an abnormal band of terminal labeling at the superficial half of the stratum griseum superficiale, markedly different from the laminar distribution of this pathway in unoperated controls. This abnormal uncrossed projection has its maximum density at the rostrolateral quadrant of the tectum. Within this region, the crossed retinotectal projection retracts from the surface of the superior colliculus, leading to partial binocular segregation. The results suggest that both the laminar distribution and the experimental binocular segregation of retinotectal afferents depend on the balance of the densities of the converging pathways from both eyes in the superior colliculus.

Effect of target removal on goldfish optic nerve regeneration: analysis of fast axonally transported proteins

How is axonal transport in regenerating neurons affected by contact with their synaptic target? We investigated whether removing the target (homotopic) lobe of the goldfish optic tectum altered the incorporation of 3H-proline into fast axonally transported proteins in the regenerating optic nerve. Regeneration was induced either by an optic tract lesion (to reveal the changes in the original axon segment that remained connected to the cell body) or by an optic nerve lesion (to reveal the changes in the newly formed axon segment). Of 26 proteins analyzed by 2-dimensional gel electrophoresis and fluorography, all but one showed increased labeling as a result of tectal lobe ablation. By 2 d after the lesion, significantly increased labeling of some proteins was seen with a 6-hr labeling interval, but not with a 24-hr labeling interval. This is probably indicative of an increased velocity of transport, which may have been a nonspecific consequence of the surgery. Otherwise, tectal lobe removal had relatively little effect until 3 weeks, when there was a transitory increase in labeling of transported proteins in the new axon segments of the tectum-ablated animals. Beginning at 5 weeks, tectal lobe ablation caused considerably higher labeling of many of the proteins in the original axon segments. Because this was seen with both 6-hr and 24-hr labeling intervals, it is probably indicative of increased protein synthesis. The increased synthesis lasted until at least 12 weeks, though some proteins were beginning to show a diminished effect at this time. In the late stages of regeneration (8-12 weeks), there was also increased labeling of proteins in the new axon segments as a result of the absence of the target tectal lobe. This included a disproportionately large increase in the relative contribution of cytoskeletal proteins and of protein 4, which is the goldfish equivalent of the growth-associated protein GAP-43 (neuromodulin). We conclude that, after the regenerating axons begin to innervate the tectum, the expression of most of the proteins in fast axonal transport is down-regulated by interaction between the axons and their target. However, the changes in expression may be preceded by a modulation of the turnover and/or deposition of proteins in the newly formed axon segment.

Relative Afferent Pupillary Defect With Normal Visual Function

The afferent arc of the pupillary light reflex is known to coincide with the afferent visual system from the retinal ganglion cell as far as the optic tract. Thus, asymmetric visual field loss resulting from a lesion here is accompanied by a relative afferent pupillary defect. Patients with total optic tract lesions, for example, show complete homonymous hemianopia and a relative afferent pupillary defect, both contralateral to the involved tract. 1 Before axons synapse in the lateral geniculate nucleus, pupillary fibers diverge via the brachium of the superior colliculus to synapse in the pretectal nuclei. These are situated at the level of the posterior commissure just rostral to the superior colliculus. One would expect, therefore, that unilateral damage to the brachium of the superior colliculus would produce a contralateral relative afferent pupillary defect while sparing visual function. We describe a patient with these findings after a thalamic-dorsal midbrain hemorrhage from

Phosphorylation of proteins in normal and regenerating goldfish optic nerve.

Within 6 h after radiolabeled phosphate was injected into the eye of goldfish, labeled acid-soluble and acid-precipitable material began to appear in the optic nerve and subsequently also in the lobe of the optic tectum, to which the optic axons project. From the rate of appearance of the acid-precipitable material, a maximal velocity of axonal transport of 13-21 mm/day could be calculated, consistent with fast axonal transport group II. Examination of individual proteins by two-dimensional gel electrophoresis revealed that approximately 20 proteins were phosphorylated in normal and regenerating nerves. These ranged in molecular weight from approximately 18,000 to 180,000 and in pI from 4.4 to 6.9. Among them were several fast transported proteins, including protein 4, which is the equivalent of the growth-associated protein GAP-43. In addition, there was phosphorylation of some recognizable constituents of slow axonal transport, including alpha-tubulin, a neurofilament constituent (NF), and another intermediate filament protein characteristic of goldfish optic axons (ON2). At least some axonal proteins, therefore, may become phosphorylated as a result of the axonal transport of a phosphate carrier. Some of the proteins labeled by intraocular injection of 32P showed changes in phosphorylation during regeneration of the optic axons. By 3-4 weeks after an optic tract lesion, five proteins, including protein 4, showed a significant increase in labeling in the intact segment of nerve between the eye and the lesion, whereas at least four others (including ON2) showed a significant decrease. When local incorporation of radiolabeled phosphate into the nerve was examined by incubating nerve segments in 32P-containing medium, there was little or no labeling of the proteins that showed changes in phosphorylation during regeneration. Segments of either normal or regenerating nerves showed strong labeling of several other proteins, particularly a group ranging in molecular weight from 46,000 to 58,000 and in pI from 4.9 to 6.4. These proteins were presumably primarily of nonneuronal origin. Nevertheless, if degeneration of the axons had been caused by removal of the eye 1 week earlier, most of the labeling of these proteins was abolished. This suggests that phosphorylation of these proteins depends on the integrity of the optic axons.

Internal hydrocephalus, optic nerve aplasia, and microphthalmia in CPB-WE (Wezob) and Cpb:WU (Wistar) rats.

Wistar rats of the inbred CPB-WE and the random bred Cpb:WU strains have been used in neuroanatomical studies. In both groups of rats a high incidence of hydrocephalus was observed. In the CPB-WE rats the ventricular dilatation was accompanied by optic tract lesions and microphthalmia. The present report describes the gross and microscopic findings in these rats and discusses the possible aetiology.

Evidence for differential effects of terminal and dendritic competition upon developmental neuronal death in the retina

Retinal ganglion cells with ipsilaterally projecting axons were labelled with horseradish peroxidase injected unilaterally along the optic pathway in adult rats. Unoperated controls were compared with three groups of animals operated at birth, given (a) contralateral enucleation, (b) contralateral lesion to the optic tract or (c) both lesions simultaneously. The numbers of ipsilaterally projecting cells were increased in all three operated groups, presumably because of a reduction in natural neuronal death following diminished terminal and dendritic competition. The pattern of increase of labelled cell density varied with the type of lesion: enucleation led to a major increase within lower temporal retina; optic tract lesion caused its major increase in upper temporal retina, centred at the location of the area centralis; and the double lesion combined both effects above. The distribution of cell-body sizes was differentially affected by the lesions: enucleation led to a shift in the distribution towards the small cell side of the spectrum, when compared with the controls; optic tract lesion shifted the distribution towards the large cell side of the spectrum, but only outside the temporal crescent; and the double lesion led to a shift towards small cells within the temporal crescent and towards large cells outside the crescent, again combining the effects of the single lesions. Large alpha-like neurones with ipsilateral axons were common in the nasal retina of both groups given optic tract lesions but they were rare in the nasal retina of unoperated and, especially, of enucleated rats. The limits of the temporal crescent were unchanged, notwithstanding the large numbers of cells outside the crescent in operated rats. It is suggested that postnatal competitive interactions at the level of terminals and of dendrites control natural neuronal death in the rat retina with different requirements regarding retinal topography and ganglion cell types. The postnatal regulation of neuronal numbers is not responsible for the generation of the nasotemporal division but may be involved in the development of differential distributions of specific ganglion cell types across the retina.

RNA content of normal and axotomized retinal ganglion cells of rat and goldfish

The responses of rat and goldfish retinal ganglion cells to axotomy were examined by a quantitative cytochemical method for RNA and by morphometric measurement 1-60 (rat) and 3-90 (goldfish) days after interruption of one optic nerve or tract intracranially. Unoperated control animals were studied also. The RNA content of axotomized neurons of rat fell 7-60 days postoperatively. Additionally, atrophy of the axotomized somas occurred. Over time, neuronal atrophy approximately paralleled the loss of RNA, and mean cell area and RNA content were reduced by about 25% 60 days after axotomy. Incorporation of 3H-uridine by axotomized neurons declined also. Axotomized retinal ganglion cells of goldfish behaved differently from those of the rat and showed increases in RNA content, most conspicuously 14-60 days postoperatively. Enlargement of axotomized fish neurons occurred but was less proportionately than concomitant increases in RNA content. The nonaxotomized ganglion cells of goldfish displayed statistically significant increases in size and RNA content 14-49 days after unilateral optic nerve or tract lesions. In contrast, alterations in rat retinal ganglion cells contralateral to interruption of one optic nerve were of limited and questionable significance. The contrasting reactions to axotomy by the retinal ganglion cells of these two vertebrates, one of which regenerates optic axons and one of which does not, may support the proposition that the somal response to axon injury has an important bearing upon the success or failure of CNS regeneration.(ABSTRACT TRUNCATED AT 250 WORDS)

Modification of visual callosal projections in rats.

The effects of a variety of developmental manipulations on the distribution of the callosal pathway to visual cortex were examined by using the Fink Heimer technique in adult rats. First, the callosal projections in albino and pigmented rats were compared and found to be similar. The callosal pathway was limited in area 17 to a region adjoining its lateral border with area 18a. Second, dark-reared rats were found to have normal callosal projections. Third, rats bilaterally enucleated at birth and expanded callosal inputs within area 17. Fourth, monocular enucleation at birth produced an expanded callosal pathway to area 17 contralateral to the enucleation and normal callosal projections to the opposite hemisphere. The expanded callosal inputs after enucleation showed a patchy distribution and usually avoided the most medial part of area 17. Fifth, a reduction in the callosal projections to the area 17/18a border was found after neonatal unilateral optic tract lesions. Sixth, expanded callosal inputs to area 17 were found following unilateral thalamic lesions at birth. The abnormal projection occupied mainly layers IV and III. The results of the different experiments indicate that the detailed distribution of the visual callosal projection within area 17 depends heavily on the organization of the retinogeniculocortical pathways to each hemisphere.

Central visual pathways and the distribution of sleep in 24-hr and 1-hr light-dark cycles

The role of the central visual pathways in determining the distribution of sleep in light-dark (LD) cycles in the circadian and ultradian range was examined. EEG, EMG, and brain temperature were recorded under 24-hr (LD 12:12 or LD 10:14) and 1-hr (LD 0.5:0.5) cycles in rats which received either (1) no lesion, (2) primary optic tract lesions, (3) lesions of dorsal and lateral terminal nuclei of the accessory optic system, (4) lesions of medial terminal nucleus of the accessory optic system, or (5) retinohypothalamic tract-suprachiasmatic nucleus lesions. Under 24-hr cycles, about 40% of sleep occurred in the dark in intact rats. Retinohypothalamic tract-suprachiasmatic nucleus lesions abolished this entrainment of sleep to the LD cycle. Under 1-hr cycles, 90% of REM sleep occurred in the dark periods in intact rats. While primary optic tract lesions attenuated this response, it was not completely abolished by any of the visual system lesions. The characteristic LD distributions of sleep in circadian and ultradian cycles may therefore be under separate neural control by the central visual system.

The Marcus Gunn Pupil in Experimental Tract Lessons

Isolated surgical lesions were made in three Macaca mulatta monkeys. Two had right optic tract section. One control underwent section of the right half of the chiasm. Preoperative evaluation revealed no fundus, pupil, or VER abnormalities. Postoperatively, a classic Marcus Gunn pupil was found contralateral to the isolated optic tract lesions. The control had normal pupils. The nature of the lesions was documented histopathologically, the pupillary findings, photographically. Possible explanations are explored. Contrary to traditional teaching, lesions occurring posterior to the chiasm may indeed produce the Marcus Gunn pupillary phenomenon.

Experimentally induced enlargement of the uncrossed retinotectal pathway in rats

The present experiments investigate the effects of neonatal lesions upon projection patterns of the uncrossed retinotectal pathway in albino rats. The results indicate that enlargement of the terminal field from one eye can be induced either by a contralateral optic tract lesion or by removal of the opposite eye at birth. The extent of the enlargement is more prominent in the latter case. If an optic tract lesion is accompanied by eye enucleation on the side ipsilateral to the tract lesion, the uncrossed retinotectal projection from the remaining eye will undergo further enlargement. However, optic fiber counts show that such an enlargement of the terminal field is not due to a significant increase in the number of uncrossed optic axons which contribute to the enlarged projection, but rather to an increased terminal arbor of individual axons (as shown by results from fiber counts). While a severe ganglion cell loss was observed in the retina contralateral to a tract lesion, a substantial population of cells persists in the ganglion cell layer and the number of cells appears much higher than the number of uncrossed optic axons arising from the same eye. The implications of these findings are discussed in relation to results reported in previous studies.

Relative Afferent Pupillary Defect in Optic Tract Hemianopias

We saw four patients with optic tract lesions and complete homonymous hemianopia. In each patient, the visual acuity was good in both eyes. All four patients had a relative afferent pupillary defect in the eye with the temporal field loss. This pupillary sign is to be expected in all such cases and may serve to differentiate acute optic tract lesions from acute geniculostriate lesions when the characteristic midnasal pallor of the nerve head has not had time to develop.

Analysis of sleep-wakefulness rhythms in male rats after suprachiasmatic nucleus lesions and ocular enucleation

To determine quantitatively characteristics of sleep-wakefulness rhythms in male albino rats, computer analysis of long term polygraphic records (24 h/day) of cortical EEG activity, neck EMG and EOG taken from 23 rats under 12:12 light-dark schedule was performed. After bilateral suprachiasmatic nucleus (SCN) lesions, the circadian rhythm in sleep-wakefulness was completely eliminated, although no attenuation or even slight enhancement of the ultradian rhythms with 2–4 h periodicity was observed. After enucleation of both eyes, the circadian rhythm was free-runing with a phase shift in the range from −12 to +22 min/day in 6 rats. A gradual decrease of the spectral value of the circadian rhythm and inverse enhancement of the ultradian rhythms with 4–7 periodicity (predominantly 6 h in 4 out of 6 rats) were also shown. In the spectral diagram, the appearance of paradoxical sleep (PS) paralleled slow-wave sleep (SWS), in the cases of the circadian rhythm and ultradian rhythms with 4–7 h periodicity. Behaviorally blind rats with bilateral primary optic tract (POT) lesions maintained the circadian rhythm in sleep-wakefulness entrained to the environmental light-dark cycle. Power spectral analysis showed no characteristic difference from normal rats. Based on these data, the role of the SCN as a pacemaker of endogenous circadian rhythm in sleep-wakefulness is discussed.

Cortical blindness after overlapping retinal-striate lesions: A limit to plasticity in the central visual system

Lesions in cats, rats, and monkeys that spare more than 2% of the optic tract or visual cortex cause trivial deficits on most measures of vision. Overlap in the topography of the visual system may allow the spared remnant to ‘see’ a wider field of vision than the physiological map predicts. We tested whether monkeys left with only the lower retinal-field portion of their striate map could see with information coming from the upper half of the retina. In 6 rhesus monkeys the ganglion fibers exiting from the lower half of both retinae were cut with a photocoagulator. Later, the portion of area 17 which, according to the electrophysiological map, controls upper retinal vision, was ablated bilaterally. The combined retinal and striate lesions overlapped to include the entire visual field. Together they produced cortical blindness. The monkeys' performance of two pattern and object tasks remained at chance throughout the survival period. A previous study has described considerable sparing of vision after combined optic tract and visual cortex lesions in cats. Differences in the lesion methods and in the anatomy of the cat and monkey visual system may explain the disagreement.

The midbrain tectum in visual relay

Commissures other than the corpus callosum receive very little attention as to their possible role in interhemispheric visual communication. Lyubimov's anatomical and electrophysiological study in a carnivore (dog) suggested the possibility that primary afferent optic fibers could pass through the commissure of the superior colliculus to terminate in the other superior colliculus and that visual information could be relayed via the superior colliculus by means of multisynaptic pathways from the retina to the striate cortex. Nauta preparations of 25 experimental cat brains with optic nerve sections, optic tract lesions with different surgical approaches, or superior collicular lesions were used in the present experiments to study the degrees of degeneration of the commissure. After comparing the differential results of these experiments it is concluded that primary afferent optic fibers do not pass across the commissure. Evidence from the literature does not establish the existence of pathways from the superior colliculus to the striate cortex in the manner proposed by Lyubimov. Thus it is concluded that the concept of a midbrain tectal relay of visual information from the retina to the striate cortex and of interhemispheric visual communication via the commissure of the superior colliculus does not have an adequate anatomical basis from experiments on another carnivore with a very similar general nervous organization. Some other visual relay routes are suggested in which the midbrain tectum may play a role.

Temporal course of synaptic degeneration in the lateral geniculate nucleus: Its dependence on axonal stump length

The temporal course of the ultrastructural and functional changes taking place in degenerating optic terminals were studied under three conditions: (a) after bilateral eye enucleation; (b) electrolytic optic tract lesion; and (c) surgical section of the optic chiasm. The ultrastructural study revealed, in (a), the sequence of two typical degenerative patterns: neurofibrillar hypertrophy (72–96 hr) and dark degeneration (120 hr). Synaptic transmission in the LGN ceased at 72–96 hr. The same sequence of ultrastructural patterns was observed in (b), but each stage was completed at an earlier time. Neurofibrillar hypertrophy was total at 48 hr while dark degeneration appeared at 72 hr. Cessation of transmission occurred at 48–54 hr. In (c) the changes were similar in pattern, sequence, and time course to those found in (b). The differential temporal course of the ultrastructural and electrophysiological alterations in conditions (a) and (b) is related to the length of the axon stump (a = 35 mm; b = 7 mm).

Behavioral and neuroendocrine responses to light mediated by separate visual pathways in the rat

Vision plays an important role in the behavioral adaptation of animals and in the control of neuroendocrine responses to light such as that of the pineal melatonin-forming enzyme, hydroxyindole-O-methyltransferase (HIOMT). Previous experiments have suggested that there is a separation of function between primary and accessory components of the visual pathways in the mediation of behavioral responses and the pineal HIOMT response to light. The present experiments were performed to test this further. Rats were trained to make a simple visual discrimination (light-on vs. light-off). Lesions were placed which either: (1) transected the inferior accessory optic tracts bilaterally sparing one primary optic tract or (2) transected both primary optic tracts sparing the inferior accessory optic tracts. Following accessory optic tract lesions, the pineal HIOMT response to light was lost but the visual discrimination habit was retained. In contrast to this primary optic tract lesions resulted in loss of the visual discrimination but preservation of the pineal HIOMT response. These data support the view that there is a separation of function among the central visual pathways.

Visual evoked responses in cats with optic tract lesions

Some electrophysiological consequences of lesions destroying 80% or more of the optic tract were studied in nine cats with chronically implanted electrodes, the visual capacities of which have previously been described. Lesions sparing as little as 5–10% of the optic tract left the photically-elicited averaged response recorded from central visual projection sites unaffected or only minimally attenuated, as compared to prelesion response. Larger subtotal lesions greatly attenuated and distorted the potentials, and total transection of the optic tract abolished them entirely Recordings from sites distal to the lesion showed that the input from the retina was not affected by the lesions. Responses elicited by electrical stimulation of the optic tract distal to the lesion were somewhat more affected than the photic responses. Barbiturate anesthesia had no differential effect on the electrophysiological consequences of the lesions.

Optic tract lesions destroying pattern vision in cats

The visual capacities of six cats were studied after bilateral stereotaxic lesions which destroyed more than 99 per cent of their optic tracts. Three animals with total lesions were blind. Three others with no more than 1 per cent intact appeared blind in gross behavioral tests but were able to perform a flux discrimination when tested approximately 35 days after the lesion. Despite extensive training they were, however, unable to relearn a pattern discrimination, indicating that the optic tract remaining was insufficient to support pattern vision.

Effect of cortical lesions and elimination of retinal impulses on labyrinthine nystagmus.

ABLATION of one cerebral hemisphere in rabbits facilitates nystagmus in the direction toward the side of the operation and diminishes nystagmus to the normal hemisphere. This reaction has been observed in postrotational nystagmus (Bauer and Leidler1), as well as on calorization of the labyrinth (Dusser de Barenne and de Kleyn2). It seemed of interest to ascertain whether circumscribed parts of the cerebral cortex are responsible for this phenomenon, particularly in view of the observation of Fitzgerald and Hallpike3that tumors of the temporal lobe may be associated with such a directional preponderance of caloric nystagmus to the diseased hemisphere. Spiegel and Scala4found a similar prevalence of the nystagmus to the side operated on following section of the optic tract or electrolytic lesion of the external geniculate ganglion. Thus, the further problem arose as to whether afferent retinal impulses may play a role in the mechanism