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Biomedical subjects

J Wallman

Publications and source records attributed to J Wallman.

At least 19 recordsLinked to original sources
PubMed1995

Choroidal and scleral mechanisms of compensation for spectacle lenses in chicks.

It is known that when hyperopic or myopic defocus is imposed on chick eyes by spectacle lenses, they rapidly compensate, becoming myopic or hyperopic respectively, by altering the depth of their vitreous chamber. Changes in two components--ocular length and choroidal thickness--underlie this rapid compensation. With monocular lens treatment, hyperopic defocus imposed by negative lenses resulted in substantially increased ocular elongation and a slight thinning of the choroid, both changes resulting in myopia; myopic defocus imposed by positive lenses resulted a dramatic increase in choroidal thickness, which pushed the retina forward toward the image plane, and a slight decrease in ocular elongation, both changes resulting in hyperopia. The refractive error after 5 days of lens wear correlated well with vitreous chamber depth, which reflected the changes in both choroidal thickness and ocular length. The degree of compensation for lenses was not affected by whether the fellow eye was covered or open. Both form-deprivation myopia and lens-induced myopia declined with age in parallel, but wearing a -15 D lens produced more myopia than did form deprivation. The spectacle lenses affected the refractive error not only of the lens-wearing eye, but also, to a much lesser degree, of the untreated fellow eye. At lens removal refractive errors were opposite in sign to the lense worn, and the subsequent changes in choroidal thickness and ocular length were also opposite to those that occurred when the lenses were in place. In this situation as well, effects of the spectacle lenses on the fellow eyes were observed. Eyes with no functional afferent connection to the brain because of either prior optic nerve section or intraocular tetrodotoxin injections showed compensatory changes to imposed defocus, but these were limited to compensation for imposed myopic defocus, at least for the eyes with optic nerve section. In addition, optic nerve section, but not tetrodotoxin treatment, moved the set-point of the visual compensatory mechanism toward hyperopia. Optic nerve section prevents myopia in response to negative lenses but not to diffusers, suggesting that compensation for hyperopia requires the central nervous system.

Animals↗
PubMed1995

Does experimentally-induced amblyopia cause hyperopia in monkeys?

We assessed refractive errors in 19 monkeys (Macaca nemestrina) raised with experimentally produced strabismus or unilateral defocus. These procedures resulted in hyperopic anisometropia in 10 monkeys. All 10 of the hyperopic animals were amblyopic; the amblyopic eye was always the more hyperopic eye. The degree of anisometropia was correlated with the degree of amblyopia. Hyperopic anisometropia did not develop in non-amblyopic animals. There was an association between early onset of visual abnormality and later development of hyperopic anisometropia. Since the refractive changes were correlated with changes in axial length and vitreous chamber depth, we suggest that amblyopia may cause alterations in eye growth and late-onset hyperopia.

Amblyopia↗
PubMed1995

Moving the retina: choroidal modulation of refractive state.

The chick eye is able to change its refractive state by as much as 7 D by pushing the retina forward or pulling it back; this is effected by changes in the thickness of the choroid, the vascular tissue behind the retina and pigment epithelium. Chick eyes first made myopic by wearing diffusers and then permitted unrestricted vision developed choroids several times thicker than normal within days, thereby speeding recovery from deprivation myopia. Choroidal expansion does not occur when visual cues are reduced by dim illumination during the period of unrestricted vision. Furthermore, in chick eyes presented with myopic or hyperopic defocus by means of spectacle lenses, the choroid expands or thins, respectively, in compensation for the specific defocus imposed. Consequently, when the lenses are removed, the eye finds its refractive error suddenly of opposite sign, and the choroidal thickness again compensates by changing in the opposite direction. If a local region of the eye is made myopic by a partial diffuser and then given unrestricted vision, the choroid expands only in the myopic region. Although the mechanism of choroidal expansion is unknown, it might involve either a increased routing of aqueous humor into the uveoscleral outflow or osmotically generated water movement into the choroid. The latter is compatible with the increased choroidal proteoglycan synthesis either when eyes wear positive lenses or after diffuser removal.

Accommodation, Ocular↗
PubMed1994

A putative suprachiasmatic nucleus of birds responds to visual motion.

In mammals, the suprachiasmatic nucleus (SCN) is a pacemaker regulating daily rhythms. In birds, two retinorecipient nuclei have been called the avian SCN, one in the lateral hypothalamus and the other more medial and rostral. We asked whether the proto-oncogene c-fos is expressed in either nucleus after light exposure during subjective night, but not during subjective day, as is the case in the SCN of mammals. Chicks raised with one eye covered by a diffuser were exposed to vertically moving surroundings, after the diffuser had been switched to the other eye. Surprisingly, we saw strong Fos label only in the lateral nucleus contralateral to the eye newly exposed to visual motion, but not in the ipsilateral nucleus nor in either medial SCN. No label was seen in animals kept in darkness or if the diffuser was not switched. Fos labeling did not differ between subjective day and night. The sensitivity to "novel" motion is also seen in motion-processing nuclei of the accessory optic system and pretectum; this suggests either that the lateral SCN is not the SCN, but part of the motion pathway, or that the avian SCN may by motion-sensitive during both day and night.

Animals↗
PubMed1993

Synchrotron X-ray diffraction and histochemical studies of normal and myopic chick eyes.

Synchrotron X-ray diffraction patterns were obtained from the cornea and posterior sclera of control and myopic chicks. No significant differences was found in the interfibrillar or in the intermolecular spacing of the collagen fibrils from the corneas of control and myopic chicks. The intermolecular spacing of myopic sclera was shown to be significantly (p < 0.01) higher than in controls. Sclera and cornea from normal and myopic chicks were stained for proteoglycans using the 'critical electrolyte' method of Scott and Orford (1981). In the sclera, two morphologically distinct types of proteoglycans could be distinguished; one small and usually elongated (approximately 20 nm), the other larger and irregularly shaped. The small proteoglycans were seen binding preferentially to the 'd' and 'e' bands of the collagen fibrils. Small proteoglycans were also present within the fibrils, these were usually approximately 10 nm in diameter although sizes up to 30 nm were observed. Longitudinal sections of fibrils revealed that these intrafibrillar proteoglycans were chiefly orientated parallel to the axis of the collagen fibrils, and preferentially located along the gap region of the fibrils. No difference was observed in the binding sites of the proteoglycans between normal and myopic sclera. The larger proteoglycans were also seen aggregated into clumps, which were usually associated with spaces between collagen bundles. The differences between control and myopic sclera appear to be quantitative rather than qualitative suggesting that the scleral expansion in myopia is an enhanced form of normal scleral growth.

Animals↗
PubMed1991

The regulation of eye growth and refractive state: an experimental study of emmetropization.

During growth the vertebrate eye achieves a close match between the power of its optics and its axial length with the result that images are focused on the retina without accommodative effort (emmetropia). The possibility that vision is required for the regulation of eye growth was studied experimentally in chicks made myopic or hyperopic by different visual manipulations. After discontinuing these visual manipulations, the eyes returned quickly to emmetropia mainly by adjusting the growth of their vitreous chambers; growth stopped in eyes recovering from myopia and continued in eyes recovering from hyperopia. Because both hyperopic and myopic eyes were already larger than normal controls, the difference in growth indicates that refractive error, rather than eye size per se, guides the eye toward emmetropia. Evidence is also presented for nonvisual shape-related control of eye growth, but this is slow-acting and cannot explain the emmetropization from induced refractive errors. Both the visually guided and shape-related mechanisms work even in eyes with the optic nerve cut, indicating that the two mechanisms are local to the eye. Although the optic-nerve-sectioned eye can sense the sign of a refractive error and initially adjust growth accordingly, it eventually overshoots emmetropia and reverses the sign of the initial refractive error. Whether this is due to loss of feedback from the central nervous system or retinal ganglion cells is unclear.

Aging↗
PubMed1991

Evidence that increased scleral growth underlies visual deprivation myopia in chicks.

The authors evaluated three measures of scleral growth in chicks that were visually deprived with the use of translucent occluders. The authors sought to determine whether the ocular elongation and myopia that results from this deprivation is associated with increased growth of the sclera. The authors found that the dry weight of the sclera of deprived eyes increased 65% faster than that of nondeprived eyes. Furthermore, the uptake of labeled methionine and thymidine was significantly increased by visual deprivation, whether expressed as incorporation per sclera, per milligram of sclera, per milligram of protein, or per milligram of DNA. In addition, the amount of DNA and soluble protein was significantly greater in the scleras of deprived eyes than in those of nondeprived eyes. Finally, the degree of hydration of the scleras from deprived eyes was greater relative to their weight than that of the scleras from nondeprived eyes. These results suggest that visual deprivation causes increased cellular proliferation and increased protein synthesis in the sclera of chicks.

Animals↗
PubMed1990

Retinal influences on sclera underlie visual deprivation myopia.

Visual deprivation of chicks rapidly induces an increased growth of the vitreous chamber which results in axial myopia, even after a day or so. This experimental myopia provides an opportunity to trace the causal path from altered visual experience to altered eye growth. With respect to the visual factors involved, the gross activity of the retinal neurons seems an important variable. The eyes of animals raised wearing translucent occluders do not become myopic or elongated if stroboscopic illumination is present. Conversely, the eyes do become myopic and elongated if deprived of all form vision, if reared in a featureless environment or if deprived in only part of the visual field. The deprivation must, however, be continuous if myopia is to result; even as little as two hours of normal vision per day almost completely eliminates the effect of 12 hours of deprivation. The control of eye growth by vision seems to take place in local regions of the eye. Deprivation of various parts of the visual field produces myopia and elongation in only the deprived part, even in animals in which the optic nerve has been cut. It seems that at the level of the sclera ocular elongation (and thus myopia) results from local growth, because we find increases in synthesis of DNA and protein as well as more new cells. The protein synthesis increase is also local, in the sense that the posterior sclera grows much more than other parts, explaining why deprivation causes ocular elongation and myopia, rather than simply larger eyes. These results suggest that some factor in part of the retina can influence the growth of the subjacent sclera.

Animals↗
PubMed1990

Saccade-related responses of centrifugal neurons projecting to the chicken retina.

Centrifugal projections to several sensory systems modulate the afferent activity during active behaviors. To see whether such modulation occurred in the visual system, we recorded the activity of isthmo-optic neurons in awake chickens during eye movements. We find that the discharge of all isthmo-optic neurons tends to stop during saccades, although every neuron does not pause for every saccade. The pause begins at approximately the same time as the saccade, and pause duration is correlated with saccade duration. Pausing during saccades occurs in both dark and light suggesting that it is motoric rather that visual in origin. In addition, we find that the spontaneous activity of isthmo-optic neurons increases in darkness. We discuss the significance of the saccadic modulation of isthmo-optic activity in terms of possible functions of the centrifugal projection in modulation of ganglion cell activity.

Animals↗
PubMed1990

Local ocular compensation for imposed local refractive error.

Chicks were raised in a low-ceiling environment to find out if their eye growth could compensate for locally imposed hyperopic refractive errors. These chicks became selectively more myopic in the upper visual field than chicks raised in a high-ceiling environment. The vitreous chamber in the low-ceiling birds showed a selective elongation in the ventral region that was not seen in the eyes of the high-ceiling birds. This morphological difference was small, but probably adequate to account for the additional myopia in the low-ceiling birds. These results are consistent with the idea of a visually mediated growth mechanism regulating the local refractive state across the entire visual field so that it matches the customary viewing conditions. Such a mechanism might account for the finding of Fitzke, Hayes, Hodos, Holden and Low (Journal of Physiology, London, 369, 33-44, 1985) that the refractive errors in the lower field are exactly appropriate for focusing the image of the ground on the retina.

Animals↗
PubMed1990

Developing eyes that lack accommodation grow to compensate for imposed defocus.

The eyes of growing chicks adjust to correct for myopia (eye relatively long for the focal length of its optics) or hyperopia (eye relatively short for the focal length of its optics). Eyes made functionally hyperopic with negative spectacle lenses become myopic and long, whereas eyes made functionally myopic with positive spectacle lenses become hyperopic and short. We report here that these compensatory growth adjustments occur not only in normal eyes but also in eyes unable to accommodate (focus) because of lesions to the Edinger-Westphal nuclei. Thus, at least in chicks, accommodation is not necessary for growth that reduces refractive errors during development, and may not be necessary for the normal control of eye growth.

Accommodation, Ocular↗
PubMed1990

Fourier analysis of saccades in monkeys and humans.

1. By recording eye movements with the search coil technique and subjecting them to an accurate infinite Fourier transform algorithm, we describe the Fourier spectra of human and monkey saccades. In both species we find heretofore undescribed features consisting of a regular pattern of local minima in the power plot, which cannot be attributed to noise. The frequency of these minima is well correlated with saccade duration. 2. Computer simulation shows that if the pulse component of the saccade is considered to be rectangular, then the first of these minima (called M1) occurs at a frequency that is the reciprocal of the duration of the pulse. 3. Comparing the position of this component during individual monkey saccades with electrophysiological recordings of motoneurons during the same saccades leads to the conclusion that these minima are related to the burst components in ocular motoneuron discharges. Specifically, the reciprocals of the frequencies of these minima are correlated with the duration of the burst component in the motoneuron discharge. 4. In the Fourier spectra of human saccades, the relationship of the frequency of M1 to saccadic duration is a function similar to that in the monkey. This adds to the evidence that the human saccade also is driven by a pulse-step signal. 5. In both monkeys and humans, T1, the reciprocal of the frequency of M1, is shorter than both the saccade duration and the burst duration of individual motoneurons, even though neurophysiological studies in monkeys generally report the saccadic burst duration to be equal to the saccade duration. This probably arises because the saccadic pulse is not rectangular, with the extremes contributing very little energy to the Fourier spectrum. By further computer modeling we show these shape effects explicitly: as the rise- and falltime increase, making the pulse less rectangular, T1 becomes shorter; in addition, as the asymmetry of rise and fall increases, the depth of the minima is reduced. We conclude that T1 measures the "effective pulse" duration of the motoneuron. 6. There is a difference in the relationship of effective pulse duration to the saccade duration between short and long saccades. For saccades shorter than approximately 40 ms in the human and 50 ms in the monkey, the pulse width as measured by this technique varies little with saccade duration. For longer saccades, effective pulse width increases linearly with duration. We agree with others that for short saccades the pulse is both height- and width-modulated; but for longer saccades, height modulation saturates and only width modulation remains.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1990

Clinical value of an integrated ELISA system for the detection of 6 autoantibodies (ssDNA, dsDNA, Sm, RNP/Sm, SSA, and SSB).

An ELISA panel assay (ANA/6) which simultaneously detects IgG autoantibodies against 6 antigens (ssDNA, dsDNA, Sm, RNP/Sm, SSA, and SSB) was evaluated with sera from 98 patients with systemic lupus erythematosus (SLE) and related conditions, 68 disease controls, who were positive or negative by fluorescent ANA (FANA), and 100 healthy controls. The antigen panel specifically identified the particular autoantibodies present and had a high level of sensitivity which was reflected by the frequency of detection of autoantibodies in different patient groups. All active patients with SLE were positive for at least one autoantibody and 80% of these patients had 3 or more autoantibodies compared to only 20% of inactive patients. A large heterogeneity in antibody profiles was also noted. About 90% of patients with positive FANA, but no detectable autoimmune rheumatic disorder, i.e., false positive, were negative by the panel. A new method of standardization was designed to use the ANA/6 quantitatively. Very large differences in the level of all 6 autoantibodies were observed between sera from patients with active and inactive SLE, suggesting a potential usefulness of ANA/6 for patient management.

Antibody Specificity↗