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Cortical binocularity is disrupted by strabismus more slowly than by monocular deprivation
De velopmental Brain Research, 3 (1982) 311-316 Elsevier Biomedical Press
31 1
Cortical binocularity is disrupted by strabismus more slowly than by monocular deprivation
R. D. FREEMAN, G. SCLAR and 1. OHZAWA School of Optometry, University of California, Berkeley, CA 94720 (U.S.A.)
(Accepted September 3rd, 1981) Key words: kitten -- cortex - - monocular deprivation -- experimental strabismus
Two groups of normally reared kittens were exposed on postnatal day 28 to brief periods of monocular deprivation or experimental strabismus caused by optical prisms. Single-unit analysis was then carried out in striate cortex and ocular dominance distributions were determined. Both procedures were found to disrupt binocular connections, but effects from monocular deprivation occurred more rapidly and were more extensive. We conclude that in the short term, monocular deprivation is a more potent procedure and it is possible that, at least initially, it may involve different mechanisms. There are several apparent similarities between the effects o f experimentally imposed m o n o c u l a r deprivation and those from induced binocular misalignment (strabismus). In each case, the major physiological consequence is that, unlike the normal condition, most cortical cells cannot be activated binocularly. Morphological changes in the L G N have been observed both for monocular occlusion and for eyes surgically deviated to cause strabismus11,15. Behavioral deficits have also been reported in both cases4, ~0. Finally, to a first approximation, the periods o f susceptibility to the consequences o f monocular deprivation and strabismus appear to coincidc 9,1n. Because of these similarities, it has been assumed generally that similar or identical mechanisms underlie these two types o f visual deprivation. However, there is a fundamental difference in that monocular occlusion interferes with binocular vision by blocking all or most spatial input to one eye. In strabismus, on the other hand, each eye receives spatial input, although some restriction may occur because o f mobility problems or partial blockage of the visual field o f the deviated eye. It is possible, however, to create a misalignment without the potential restrictions caused by surgical intervention by use o f optical prisms. And, as in the case o f surgical strabismus, cortical binocularity is disrupted when catsS,13,14 or monkeys 3 are reared with optically produced ocular misalignment. This result suggests that visual misalignment, per se, is the major cause o f binocular breakdown in strabismus. Binocular alignment is also prevented in the case of m o n o c u l a r deprivation which causes a functional reduction o f binocular cells prior to loss o f input from the deprived eye6,12. A reasonable supposition is that, as in the case 0165-3806/82/0000-0000/$02.75 © Elsevier Biomedical Press
312 of strabismus, this disrupted binocular alignment during monocular dcpr~vation i,~, initially, the critical factor. One may expect, therefore, that the time-cotlJ,:c of binocular disconnection after unilateral occlusion should be similar to that of qrabismus. It has been shown that, under the appropriate conditions, a reduction (~cctir,~ in the number of cortical cells that can be activated through both eyes aftcr only hours of monocular deprivation 6. We have extended this result to the case of optically induccd strabismus by showing that ocular misalignment induces changes signiticantly more slowly than monocular occlusion. Four groups of normally reared 4-week-old kittens were studied. Ihc lirst (4 animals) was occluded monocularly w'ith an opaque contact lens for a perit~d of 24 h. G r o u p 2 (3 kittens) was also monocularly deprived, but for only 8 h. The third (3 kittens) and fourth (3 kittens) groups were reared for similar periods as lhc ~thers (8 or 24 h) using a procedure that caused binocular misalignment. Spcciall~ designed goggles 7 were fitted with optical prisms 8 ensurc that goggles remained clean and in placc. Immediately following the rearing procedures, kittens were prepared Ior the study of single units in visual cortex. Aftcr administration of atropine and accpromazine, anesthesia was induced with halothane. Venous and tracheal cannulas were placed and anesthesia was maintained with sodium methohexital while !!LG screw electrodes were positioned and skull bone and dura were removcd over area 17 ncar the midline and slightly antelior to lamlzda suture. Tungsten-in-glass micrcelectrodcs were used and standard electronic devices allowed audio and visual displays (;t" amplified spikes from individual neurons. During recording sessions temperature was maintained at 37.5'~C, and EEG, ECG, heart rate. and expired CO._, levels were monitored. Animals were paralyzed with a continuous infusion of gallaminc triethiodide (10 mg.kg i.h 1), and artificially ventilated using a mixture or N:OiO._, (70 °,~/30 7~,,). Cells that were isolated but could not be reliably activated with visual stimuli were classified as unresponsive (U). Receptive fields of neurons thai were rcsponsi~c were plotted to note borders, orientation limits, and ccll type according t~ standard classification s . Using optimal stimuli, absolute response strengths were subjectively judged on a scale of 1 (weak) to 5 (vigorous). In addition, relative response strengths
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Fig. I. Summary ocular dominance histograms, which give mean percentages, are shown for 4 groups of kittens, who had been reared normally for 4 weeks. Those in a and b were then occluded monocularly for 24 or 8 h, respectively. Similarly, the data in c and d are from kittens ocularly misaligned with optical prisms for 24 or 8 h, respectively. The histogram in a was obtained from the recording of 36, 41, 30 and 31 cells, respectively, in 4 kittens. Other histograms represent data from 3 kittens each with the following cell totals: (b) 33, 32, and 32; (c) 39, 31, and 31; (d) 32, 31,33. Of these totals, small percentages were visually unresponsive (U), as indicated. Groups I and 7 refer to monocular cells responsive through the contralateral or ipsilateral eyes, respectively, in relation to the hemisphere containing the electrode. Other groups are binocular in varying degrees with 2 and 3 contralateral-dominant, and 5 and 6 ipsilateral-dominant. Vertical bars represent I S.E. of the mean values. Above each histogram bar is given the mean absolute response strength for the group, and vertical bars depict .:_ 1 S.E. of the mean.
314 between the eyes were judged and ocular dominance was categorized ~nt,, 7 groups" Most cells in the visual cortex of normal 4-week-old kittens ca~ he driven through either eye, but previous work has shown that binocular disconnection can occur very quickly 6.~. In the present case, the ocular dominance distributions from all 4 kittens, occluded monocularly for 24 h were markedly abnormah Relatively few binocular cells (groups 2-6) were found and there was a clear preponderance of cells activated through the nondeprived (ipsilateral) eye. The results from thi~ group me summarized in Fig. la. A similar but slightl) lc.ss extensive abnormalit\ in ocular dominance distributions was found when only 8 h oJ monoct, lar occlusion wa.~ u.-:ed. For this condition. 34 i?,,,of the cells were binocular, compared to 12.7 'I. in the former case. Once again, the monocular cell population was substantially biased tmvard Ihc nondeprived (ipsilateral) eye. These results are summarized in Fig. lb. l)ata comprising both these histograms, as well as the other two discussed below, were quite homogeneous as indicated by the S.E. bars. As noted above, in addition to ocular dominance classifications, cells were judged subjectively in terms of absolute strength of the most responsb, e eye. Mean values are shown above each histogram bar of Fig. I. Cells that were recorded from cats that had been occluded for 24 or 8 h (Fig. la and b, respectively) tended to bc more responsive if they were binocular. This suggests that cells with vigorou.,, response characteristics may be less vulnerable to the effects of monocular occlusion, but. ot" course, the sample size here is too limited to draw a tirm conclusion. Absolute response strengths are more uniformb distributed anaong binocular and monocular cells for the groups of kittens which had undergone ocular misalignment. Ocular dominance distributions for these animals are summarized in Fig. lc and d. In the case of 24 h of misalignment, (Fig. Ic). the histogram is clearly abnormal, but the proportion of binocular cells, 59.7";,, is higher than that for the monocularly occluded group shown in i-ig, la (12.7 '!,,). 1his difference is highly significant (7.'-' : 52, P .: 0.01). The misalignment procedure was bilaterally symmetrical so that neither eye would be at a visual advantage, although this does not necessarily mean that visual experience was identical. In any case. the monocular population wa,~ c,mtralatcraldominant. Previous work has shown that there is relatively more p,-ominent representation of contralateral cells in normal cats '4 and it is possible that a~, the binocula, population is functionally reduced in ocularly misaligned kittens, a similar bias occurs. Another possible asymmetry could result from the prism rearing procedure because image dissociation was vertical rather than lateral and cells with orientation preferences around vertical could be less affected than those near horizontal. Analysis of the data, however, revealed no differences based on preferred cell orientation which suggests that there was complete optical dissociation between the retinal images of both eyes. The most striking difference between the monocularly occluded and optically misaligned kittens is seen by comparing the histograms of Fig. Ib and d. Although the proportion of group I cells in Fig. Id may be slightly high. the overall ocular dominance distribution is clearly within a normal range. The proportion of binocular cells (79.3 o,) compares well with that from normal 4-week-old kittens recorded in this laboratory (mean of 78.5 o,/from two animals).
315 We conclude, then, that during the initial stages, the process of functional binocular disconnection occurs more rapidly as a result of monocular occlusion, compared to ocular misalignment alone. Blockage of vision through one eye is therefore a more potent procedure for disruption of functional binocular vision under the conditions we have tested. It is possible, of course, that binocular disruption from strabismus may occur more quickly if a surgical procedure is used to cause misalignment, but we specifically avoided this method because of the potential complication of eye motility. The difference we have found appears applicable only during the earliest process of binocular disconnection, for other studies have shown that in both cases, monocular deprivation 12 or surgical strabismus 14, two days of deprivation in 4-week-old kittens results in a nearly total breakdown of binocularity. It is not clear why there should be short-term differences between squint and monocular occlusion, except that in the latter case, disruption of binocular vision is more severe and might therefore produce a quicker effect. This implies that the same process, in different stages, underlies both conditions. On the other hand, correlated discharge between the two afferent pathways is prevented in both cases, if this is the critical factor, and the amount and type of asychrony is relatively unimportant, then it is possible that these short-term differences reflect separate mechanisms. Extensive binocular interaction within visual cortex is well established1,2, 8 and the maintenance of binocularity in young kittens may depend upon intracortical connections. During the initial stages of monocular deprivation, binocularity is lost first, perhaps, because intracortical pathways to binocular cells are fragile and cannot remain intact with reduced input activity. On the other hand, direct afferent input to monocular cells from the LGN, which generally has high spontaneous activity, may be relatively unaffected initially by lack of stimulation. However, nonspecific activity from the LGN does not sustain these cells for long and eventually, the deprived eye is functionally disconnected.
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Fig. 2. A schematic representation is shown of what might occur during an initial stage of monocular deprivation (left) or optically caused ocular misalignment(right). Left: the first effect is a breakdown of intracortical binocular connections and the second change is disconnection of direct afferent input to monocular cells from the covered eye. Right: normal intracortieal pathways are disrupted, but alternate connections permit binocularity to remain for an additional period.
316 Now, in the case of optically produced squint, direct affercnt mptn i,, ~,,ailtd~lc through either eye. Perhaps initially, the misalignment causes activation ~)t ~thernativc pathways to cortical cells which allow m a i n t e n a n c e of some intracortical t o n n e c t i o n s . These pathways are i n a d e q u a t e to sustain the appropriate intracortical t't~nnections and eventually, binocularity breaks down. A schematic representatk~n ol'¢his notion is shown in Fig, 2. i n summary, we have shown that the effects of m o n o c u l a r depriw~tion proceed more quickly than those of optically caused strabismus. ] h i s difference in timc-coursc suggests that, initially, the mechanisms underlying binocular dysfunction may he dissimilar for these conditions, or if they are similar, they occur in dit]Z'rcnl ~,tagcs. The work was supported by G r a n t EY01 175 and Research Career I)cvelopmenl A w a r d EY00092 from the National Eye Institute to R.D.F.
I Barlow, H. B., Blakemore, C. and Pettigrew, J. D., The neural mechanism of binocular depth discrimination, J. Physiol. (Lond.), 193 (1967) 327-342. 2 Bishop, P. O., Henry, G. H. and Smith, C. J., Binocular interaction tields of single umts in the c~lt striate cortex, J. PhysivL (Lond.), 216 (1971) 39-68. 3 Crawford, M. L. J. and yon Noorden, G. K., Optically induced concomitant strabismus in monkeys, htvest. Ophthal. Vis. Sci., 19 (1980) 1105-1109. 4 Dews, P. B. and Wiesel, T. N., Consequences of monocular deprivation on visual t~haviour in kittens, J. Physiol. (Lond.), 206 (1970) 437 455. 5 Freeman, R. D., Some neural and non-neural factors in visual development of the kitten, Arch. ital. Biol., 116 (1978) 338--351. 6 Freeman. R. D. and Olson, ('. R., Is there a 'consolidation' effect for monocular deprivation?, Nature (Lond.), 282 (1979) 404-406. 7 Freeman, R. D. and Pettigrew, J., Alteration of visual cortex from environmental asymmetries, Nature (Lond.), 246 (1973) 359-360. 8 Hubel, D. H. and Wiesel, T. N., Receptive fields, binocular interaction, and functional architecture in the cat's visual cortex, J. Physh)l. cLond.J, 160 (1962) 106 154. 9 Hubel, D. H. and Wiesel, T. N., The period of susceptibility to the physiological cffccls c~l"unilateral eye closure in kittens, J. Physiol. (Lond.), 206 (1970) 419-436. 10 lkeda, H. and Jacobson, S. G., Nasal field loss in cats reared with convergent squinl: hcha~,ioural studies, J. Physhd. (Lond.), 270 (1977) 367 381. II Ikeda, H., Plant, G. T. and Tremain, K, E., Nasal field loss in kittens reared with convergenl squint: neurophysiological and morphological studies of the lateral geniculate nucleu,,. ,/. Physhd. {Lond.), 270 (1977) 345 366. 12 Olson, C. R. and Freeman, R. D., Progressive changes in kitten striate cortex during monocular ~,ision, J. Neurophyshd., 38 (1975) 26- 32. 13 Smith, E. L., Bennett, M. J., Harwerth, R. S. and Crawford, M. I_,.J., Binocularity in kittens reared with optically induced squint, Science, 204 (1979) 875. 14 Van Sluyters, R. C. and Leavitt, R. B.. Experimental strabismus in the kitten, J. ,Veur,Jphy.~hd., 43 (1980) 686-699. 15 Wiesel, T. N. and Hubcl, D. H., Effects of visual deprivation on morphology and physi(~logyof cells in the cat's lateral geniculate body, J. Neurophysiol., 26 (1963) 978-993. 16 Yinon, U., Age dependence of the effect of squint on cells in kittens" visual cortex, l-xp. Brain Res., 26 (1976) 151 157.
31 1
Cortical binocularity is disrupted by strabismus more slowly than by monocular deprivation
R. D. FREEMAN, G. SCLAR and 1. OHZAWA School of Optometry, University of California, Berkeley, CA 94720 (U.S.A.)
(Accepted September 3rd, 1981) Key words: kitten -- cortex - - monocular deprivation -- experimental strabismus
Two groups of normally reared kittens were exposed on postnatal day 28 to brief periods of monocular deprivation or experimental strabismus caused by optical prisms. Single-unit analysis was then carried out in striate cortex and ocular dominance distributions were determined. Both procedures were found to disrupt binocular connections, but effects from monocular deprivation occurred more rapidly and were more extensive. We conclude that in the short term, monocular deprivation is a more potent procedure and it is possible that, at least initially, it may involve different mechanisms. There are several apparent similarities between the effects o f experimentally imposed m o n o c u l a r deprivation and those from induced binocular misalignment (strabismus). In each case, the major physiological consequence is that, unlike the normal condition, most cortical cells cannot be activated binocularly. Morphological changes in the L G N have been observed both for monocular occlusion and for eyes surgically deviated to cause strabismus11,15. Behavioral deficits have also been reported in both cases4, ~0. Finally, to a first approximation, the periods o f susceptibility to the consequences o f monocular deprivation and strabismus appear to coincidc 9,1n. Because of these similarities, it has been assumed generally that similar or identical mechanisms underlie these two types o f visual deprivation. However, there is a fundamental difference in that monocular occlusion interferes with binocular vision by blocking all or most spatial input to one eye. In strabismus, on the other hand, each eye receives spatial input, although some restriction may occur because o f mobility problems or partial blockage of the visual field o f the deviated eye. It is possible, however, to create a misalignment without the potential restrictions caused by surgical intervention by use o f optical prisms. And, as in the case o f surgical strabismus, cortical binocularity is disrupted when catsS,13,14 or monkeys 3 are reared with optically produced ocular misalignment. This result suggests that visual misalignment, per se, is the major cause o f binocular breakdown in strabismus. Binocular alignment is also prevented in the case of m o n o c u l a r deprivation which causes a functional reduction o f binocular cells prior to loss o f input from the deprived eye6,12. A reasonable supposition is that, as in the case 0165-3806/82/0000-0000/$02.75 © Elsevier Biomedical Press
312 of strabismus, this disrupted binocular alignment during monocular dcpr~vation i,~, initially, the critical factor. One may expect, therefore, that the time-cotlJ,:c of binocular disconnection after unilateral occlusion should be similar to that of qrabismus. It has been shown that, under the appropriate conditions, a reduction (~cctir,~ in the number of cortical cells that can be activated through both eyes aftcr only hours of monocular deprivation 6. We have extended this result to the case of optically induccd strabismus by showing that ocular misalignment induces changes signiticantly more slowly than monocular occlusion. Four groups of normally reared 4-week-old kittens were studied. Ihc lirst (4 animals) was occluded monocularly w'ith an opaque contact lens for a perit~d of 24 h. G r o u p 2 (3 kittens) was also monocularly deprived, but for only 8 h. The third (3 kittens) and fourth (3 kittens) groups were reared for similar periods as lhc ~thers (8 or 24 h) using a procedure that caused binocular misalignment. Spcciall~ designed goggles 7 were fitted with optical prisms 8
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Fig. I. Summary ocular dominance histograms, which give mean percentages, are shown for 4 groups of kittens, who had been reared normally for 4 weeks. Those in a and b were then occluded monocularly for 24 or 8 h, respectively. Similarly, the data in c and d are from kittens ocularly misaligned with optical prisms for 24 or 8 h, respectively. The histogram in a was obtained from the recording of 36, 41, 30 and 31 cells, respectively, in 4 kittens. Other histograms represent data from 3 kittens each with the following cell totals: (b) 33, 32, and 32; (c) 39, 31, and 31; (d) 32, 31,33. Of these totals, small percentages were visually unresponsive (U), as indicated. Groups I and 7 refer to monocular cells responsive through the contralateral or ipsilateral eyes, respectively, in relation to the hemisphere containing the electrode. Other groups are binocular in varying degrees with 2 and 3 contralateral-dominant, and 5 and 6 ipsilateral-dominant. Vertical bars represent I S.E. of the mean values. Above each histogram bar is given the mean absolute response strength for the group, and vertical bars depict .:_ 1 S.E. of the mean.
314 between the eyes were judged and ocular dominance was categorized ~nt,, 7 groups" Most cells in the visual cortex of normal 4-week-old kittens ca~ he driven through either eye, but previous work has shown that binocular disconnection can occur very quickly 6.~. In the present case, the ocular dominance distributions from all 4 kittens, occluded monocularly for 24 h were markedly abnormah Relatively few binocular cells (groups 2-6) were found and there was a clear preponderance of cells activated through the nondeprived (ipsilateral) eye. The results from thi~ group me summarized in Fig. la. A similar but slightl) lc.ss extensive abnormalit\ in ocular dominance distributions was found when only 8 h oJ monoct, lar occlusion wa.~ u.-:ed. For this condition. 34 i?,,,of the cells were binocular, compared to 12.7 'I. in the former case. Once again, the monocular cell population was substantially biased tmvard Ihc nondeprived (ipsilateral) eye. These results are summarized in Fig. lb. l)ata comprising both these histograms, as well as the other two discussed below, were quite homogeneous as indicated by the S.E. bars. As noted above, in addition to ocular dominance classifications, cells were judged subjectively in terms of absolute strength of the most responsb, e eye. Mean values are shown above each histogram bar of Fig. I. Cells that were recorded from cats that had been occluded for 24 or 8 h (Fig. la and b, respectively) tended to bc more responsive if they were binocular. This suggests that cells with vigorou.,, response characteristics may be less vulnerable to the effects of monocular occlusion, but. ot" course, the sample size here is too limited to draw a tirm conclusion. Absolute response strengths are more uniformb distributed anaong binocular and monocular cells for the groups of kittens which had undergone ocular misalignment. Ocular dominance distributions for these animals are summarized in Fig. lc and d. In the case of 24 h of misalignment, (Fig. Ic). the histogram is clearly abnormal, but the proportion of binocular cells, 59.7";,, is higher than that for the monocularly occluded group shown in i-ig, la (12.7 '!,,). 1his difference is highly significant (7.'-' : 52, P .: 0.01). The misalignment procedure was bilaterally symmetrical so that neither eye would be at a visual advantage, although this does not necessarily mean that visual experience was identical. In any case. the monocular population wa,~ c,mtralatcraldominant. Previous work has shown that there is relatively more p,-ominent representation of contralateral cells in normal cats '4 and it is possible that a~, the binocula, population is functionally reduced in ocularly misaligned kittens, a similar bias occurs. Another possible asymmetry could result from the prism rearing procedure because image dissociation was vertical rather than lateral and cells with orientation preferences around vertical could be less affected than those near horizontal. Analysis of the data, however, revealed no differences based on preferred cell orientation which suggests that there was complete optical dissociation between the retinal images of both eyes. The most striking difference between the monocularly occluded and optically misaligned kittens is seen by comparing the histograms of Fig. Ib and d. Although the proportion of group I cells in Fig. Id may be slightly high. the overall ocular dominance distribution is clearly within a normal range. The proportion of binocular cells (79.3 o,) compares well with that from normal 4-week-old kittens recorded in this laboratory (mean of 78.5 o,/from two animals).
315 We conclude, then, that during the initial stages, the process of functional binocular disconnection occurs more rapidly as a result of monocular occlusion, compared to ocular misalignment alone. Blockage of vision through one eye is therefore a more potent procedure for disruption of functional binocular vision under the conditions we have tested. It is possible, of course, that binocular disruption from strabismus may occur more quickly if a surgical procedure is used to cause misalignment, but we specifically avoided this method because of the potential complication of eye motility. The difference we have found appears applicable only during the earliest process of binocular disconnection, for other studies have shown that in both cases, monocular deprivation 12 or surgical strabismus 14, two days of deprivation in 4-week-old kittens results in a nearly total breakdown of binocularity. It is not clear why there should be short-term differences between squint and monocular occlusion, except that in the latter case, disruption of binocular vision is more severe and might therefore produce a quicker effect. This implies that the same process, in different stages, underlies both conditions. On the other hand, correlated discharge between the two afferent pathways is prevented in both cases, if this is the critical factor, and the amount and type of asychrony is relatively unimportant, then it is possible that these short-term differences reflect separate mechanisms. Extensive binocular interaction within visual cortex is well established1,2, 8 and the maintenance of binocularity in young kittens may depend upon intracortical connections. During the initial stages of monocular deprivation, binocularity is lost first, perhaps, because intracortical pathways to binocular cells are fragile and cannot remain intact with reduced input activity. On the other hand, direct afferent input to monocular cells from the LGN, which generally has high spontaneous activity, may be relatively unaffected initially by lack of stimulation. However, nonspecific activity from the LGN does not sustain these cells for long and eventually, the deprived eye is functionally disconnected.
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Fig. 2. A schematic representation is shown of what might occur during an initial stage of monocular deprivation (left) or optically caused ocular misalignment(right). Left: the first effect is a breakdown of intracortical binocular connections and the second change is disconnection of direct afferent input to monocular cells from the covered eye. Right: normal intracortieal pathways are disrupted, but alternate connections permit binocularity to remain for an additional period.
316 Now, in the case of optically produced squint, direct affercnt mptn i,, ~,,ailtd~lc through either eye. Perhaps initially, the misalignment causes activation ~)t ~thernativc pathways to cortical cells which allow m a i n t e n a n c e of some intracortical t o n n e c t i o n s . These pathways are i n a d e q u a t e to sustain the appropriate intracortical t't~nnections and eventually, binocularity breaks down. A schematic representatk~n ol'¢his notion is shown in Fig, 2. i n summary, we have shown that the effects of m o n o c u l a r depriw~tion proceed more quickly than those of optically caused strabismus. ] h i s difference in timc-coursc suggests that, initially, the mechanisms underlying binocular dysfunction may he dissimilar for these conditions, or if they are similar, they occur in dit]Z'rcnl ~,tagcs. The work was supported by G r a n t EY01 175 and Research Career I)cvelopmenl A w a r d EY00092 from the National Eye Institute to R.D.F.
I Barlow, H. B., Blakemore, C. and Pettigrew, J. D., The neural mechanism of binocular depth discrimination, J. Physiol. (Lond.), 193 (1967) 327-342. 2 Bishop, P. O., Henry, G. H. and Smith, C. J., Binocular interaction tields of single umts in the c~lt striate cortex, J. PhysivL (Lond.), 216 (1971) 39-68. 3 Crawford, M. L. J. and yon Noorden, G. K., Optically induced concomitant strabismus in monkeys, htvest. Ophthal. Vis. Sci., 19 (1980) 1105-1109. 4 Dews, P. B. and Wiesel, T. N., Consequences of monocular deprivation on visual t~haviour in kittens, J. Physiol. (Lond.), 206 (1970) 437 455. 5 Freeman, R. D., Some neural and non-neural factors in visual development of the kitten, Arch. ital. Biol., 116 (1978) 338--351. 6 Freeman. R. D. and Olson, ('. R., Is there a 'consolidation' effect for monocular deprivation?, Nature (Lond.), 282 (1979) 404-406. 7 Freeman, R. D. and Pettigrew, J., Alteration of visual cortex from environmental asymmetries, Nature (Lond.), 246 (1973) 359-360. 8 Hubel, D. H. and Wiesel, T. N., Receptive fields, binocular interaction, and functional architecture in the cat's visual cortex, J. Physh)l. cLond.J, 160 (1962) 106 154. 9 Hubel, D. H. and Wiesel, T. N., The period of susceptibility to the physiological cffccls c~l"unilateral eye closure in kittens, J. Physiol. (Lond.), 206 (1970) 419-436. 10 lkeda, H. and Jacobson, S. G., Nasal field loss in cats reared with convergent squinl: hcha~,ioural studies, J. Physhd. (Lond.), 270 (1977) 367 381. II Ikeda, H., Plant, G. T. and Tremain, K, E., Nasal field loss in kittens reared with convergenl squint: neurophysiological and morphological studies of the lateral geniculate nucleu,,. ,/. Physhd. {Lond.), 270 (1977) 345 366. 12 Olson, C. R. and Freeman, R. D., Progressive changes in kitten striate cortex during monocular ~,ision, J. Neurophyshd., 38 (1975) 26- 32. 13 Smith, E. L., Bennett, M. J., Harwerth, R. S. and Crawford, M. I_,.J., Binocularity in kittens reared with optically induced squint, Science, 204 (1979) 875. 14 Van Sluyters, R. C. and Leavitt, R. B.. Experimental strabismus in the kitten, J. ,Veur,Jphy.~hd., 43 (1980) 686-699. 15 Wiesel, T. N. and Hubcl, D. H., Effects of visual deprivation on morphology and physi(~logyof cells in the cat's lateral geniculate body, J. Neurophysiol., 26 (1963) 978-993. 16 Yinon, U., Age dependence of the effect of squint on cells in kittens" visual cortex, l-xp. Brain Res., 26 (1976) 151 157.