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Reverse occlusion leads to a precise restoration of orientation preference maps in visual cortex.

In the visual system of young kittens, the layout of the cortical maps for ocular dominance and orientation preference converges to an equilibrium state within the first few weeks of life and normally remains largely unchanged. If during the critical period, however, patterned visual experience is restricted to only one eye for a few days, cortical neurons lose their ability to respond to stimulation of the deprived eye. We used the 'reverse occlusion' protocol together with chronical optical imaging to investigate how the profound anatomical changes accompanying monocular deprivation affect the spatial pattern of the cortical orientation preference map. We report here that after 1 week of monocular deprivation, cortical orientation maps for the deprived eye had vanished. But we also discovered that after subsequent reverse occlusion the restored orientation maps were very similar to the original maps. This demonstrates that in spite of functional disconnection of one eye after monocular deprivation, the layout of cortical orientation maps, when re-established for this eye, is not formed from scratch but is strongly influenced by previous experience.

Animals↗

Rapid visual learning in neurones of the primate temporal visual cortex.

The human visual system can learn to recognize visual stimuli rapidly. For example, humans can accurately reconstruct meaningful objects out of fragmentary evidence, once they have seen the same object in its unambiguous form. The anterior temporal cortical areas of macaques contain some neurones with invariant visual responses which appear to provide a representation of complex patterns and objects, such as faces. Remarkably, these neurones show an enhancement of response after brief (e.g. 5 s) exposure to the unambiguous stimulus, an effect that appears to reflect the neural basis of the rapid perceptual learning seen in humans.

Animals↗

Excitatory-inhibitory network in the visual cortex: psychophysical evidence.

At early stages in visual processing cells respond to local stimuli with specific features such as orientation and spatial frequency. Although the receptive fields of these cells have been thought to be local and independent, recent physiological and psychophysical evidence has accumulated, indicating that the cells participate in a rich network of local connections. Thus, these local processing units can integrate information over much larger parts of the visual field; the pattern of their response to a stimulus apparently depends on the context presented. To explore the pattern of lateral interactions in human visual cortex under different context conditions we used a novel chain lateral masking detection paradigm, in which human observers performed a detection task in the presence of different length chains of high-contrast-flanked Gabor signals. The results indicated a nonmonotonic relation of the detection threshold with the number of flankers. Remote flankers had a stronger effect on target detection when the space between them was filled with other flankers, indicating that the detection threshold is caused by dynamics of large neuronal populations in the neocortex, with a major interplay between excitation and inhibition. We considered a model of the primary visual cortex as a network consisting of excitatory and inhibitory cell populations, with both short- and long-range interactions. The model exhibited a behavior similar to the experimental results throughout a range of parameters. Experimental and modeling results indicated that long-range connections play an important role in visual perception, possibly mediating the effects of context.

Feedback↗

Identification of Munc13-3 as a candidate gene for critical-period neuroplasticity in visual cortex.

The first several months of life are a critical period for neuronal plasticity in the visual cortex during which anatomic and physiological development depends on visual experience. In cats, electrophysiologically assessed neuronal plasticity is minimal until approximately 3 weeks, peaks at 5 weeks, gradually declines to low levels at 20 weeks, and disappears at approximately 1 year of age (Daw, 1994). Rearing in darkness slows the entire time course of this critical period, such that at 5 weeks of age, normal cats are more plastic than dark-reared cats, whereas at 20 weeks, dark-reared cats are more plastic (Mower, 1991; Beaver et al., 2001). Thus, a stringent criterion is that genes that are important for plasticity in visual cortex will show differences in expression between normal rearing and dark rearing that are of opposite direction in young versus older animals. The present study reports the identification by differential display PCR of Munc13-3, a mammalian homolog of the Caenorhabditis elegans "uncoordinated" gene (unc-13), as a candidate gene for critical-period neuronal plasticity, the expression of which is regulated according to this criterion specifically in visual cortex and not in frontal cortex. Other members of the Munc13 family (Munc13-1 and Munc13-2) do not meet this criterion in visual cortex, indicating that Munc13-3 is the only family member that is regulated by age and dark rearing in the same manner as physiological plasticity during the visual cortical critical period.

Animals↗

Control of cell number in the developing visual system. III. Effects of visual cortex ablation.

The effect of unilateral deletion of the visual cortex on early cell death and eventual cell number in various structures of the visual system was examined. At minimum, this manipulation potentially provides excess retinal afference to the superior colliculi, partially denervates the superior colliculi, reduces normal retinal terminal area and opens up potential target space for the retina and superior colliculus in those areas where they share terminal space with the visual cortex. All layers of the superior colliculus, bilaterally, showed an initial decrease in the rate of cell death relative to normal followed by an increase in cell death rates. No change in the number or distribution of cells in the retinal ganglion cell layer resulted despite a substantial loss of retinal terminal area, and a substantial alteration of the pattern of retinal central termination. These results are interpreted as evidence for two stages in normally occurring cell death, a first in which axons compete to colonize any available terminal space, and a second in which axon-to-target specificity must be matched. These results also provide evidence that the amount of target required for neuron survival is clearly variable.

Animals↗

Laminar and regional distribution of galanin binding sites in cat and monkey visual cortex determined by in vitro receptor autoradiography.

The distribution of galanin (GAL) binding sites in the visual cortex of cat and monkey was determined by autoradiographic visualization of [125I]-GAL binding to tissue sections. Binding conditions were optimized and, as a result, the binding was saturable and specific. In cat visual cortex, GAL binding sites were concentrated in layers I, IVc, V, and VI. Areas 17, 18, and 19 exhibited a similar distribution pattern. In monkey primary visual cortex, the highest density of GAL binding sites was observed in layers II/III, lower IVc, and upper V. Layers IVA and VI contained moderate numbers of GAL binding sites, while layer I and the remaining parts of layer IV displayed the lowest density. In monkey secondary visual cortex, GAL binding sites were mainly concentrated in layers V-VI. Layer IV exhibited a moderate density, while the supragranular layers contained the lowest proportion of GAL binding sites. In both cat and monkey, we found little difference between regions subserving central and those subserving peripheral vision. Similarities in the distribution of GAL and acetylcholine binding sites are discussed.

Animals↗

Cytochrome oxidase and neurofilament reactivity in monocularly deprived human primary visual cortex.

Previous studies of human primary visual cortex (V1) have demonstrated a significant eye-specific decrease in cytochrome oxidase (CO) staining following monocular enucleation. We have extended these results by examining CO staining and neurofilament labeling in V1 from a patient with long-standing monocular blindness. A pattern of reduced neurofilament reactivity was found to align with pale CO-stained ocular dominance columns. Neurons located within deprived ocular dominance columns were significantly smaller compared with those in nondeprived columns. A spatial analysis of the relationship between CO blobs and ocular dominance columns revealed that both deprived and nondeprived blobs tended to align with the centers of ocular dominance columns.

Aged, 80 and over↗

Receptive field properties of near neighbor orientation selective neurons in the visual cortex: a modeling study.

The primary visual cortex is organized into clusters of cells having similar receptive fields (RFs). A purely feedforward model has been shown to produce realistic simple cell receptive fields. The modeled cells capture a wide range of receptive field properties of orientation selective cortical cells. We have analyzed the responses of 78 nearby cell pairs to study which RF properties are clustered. Orientation preference shows strongest clustering. Orientation tuning width (hwhh) and tuning height (spikes/sec) at the preferred orientation are not as tightly clustered. Spatial frequency is also not as tightly clustered and RF phase has the least clustering. Clustering property of orientation preference, orientation tuning height and width depend on the location of cells in the orientation map. No such location dependence is observed for spatial frequency and RF phase. Our results agree well with experimental data.

Animals↗

Local cortical lesions abolish lateral inhibition at direction selective cells in cat visual cortex.

Many cells in the cat visual cortex display a strong selectivity for the direction of motion of an optimally oriented stimulus. Postsynaptic inhibition has been suggested to generate this direction selectivity in simple cells, but the intracortical pathways involved have not been identified. While continuously recording from simple cells in layers 4 and 6, we have inactivated the superficial cortical layers in small regions 0.4-2.5 mm from the cortical column under study by using heat lesions, localized cooling or gamma-aminobutyric acid (GABA) microiontophoresis. When inactivation affected cortical regions retinotopically representing motion in the non-preferred direction towards the receptive field, the responses to movement in this direction increased, and the recorded cells lost direction selectivity due to loss of inhibition. Our results indicate that direction selectivity of simple cells involves asymmetric inhibition of predictable cortical topography.

Animals↗

Coding of natural scenes in primary visual cortex.

Natural scene coding in ferret visual cortex was investigated using a new technique for multi-site recording of neuronal activity from the cortical surface. Surface recordings accurately reflected radially aligned layer 2/3 activity. At individual sites, evoked activity to natural scenes was weakly correlated with the local image contrast structure falling within the cells' classical receptive field. However, a population code, derived from activity integrated across cortical sites having retinotopically overlapping receptive fields, correlated strongly with the local image contrast structure. Cell responses demonstrated high lifetime sparseness, population sparseness, and high dispersal values, implying efficient neural coding in terms of information processing. These results indicate that while cells at an individual cortical site do not provide a reliable estimate of the local contrast structure in natural scenes, cell activity integrated across distributed cortical sites is closely related to this structure in the form of a sparse and dispersed code.

Action Potentials↗

Experience-dependent changes in NMDAR1 expression in the visual cortex of an animal model for amblyopia.

When normal binocular visual experience is disrupted during postnatal development, it affects the maturation of cortical circuits and often results in the development of poor visual acuity known as amblyopia. Two main factors contribute to the development of amblyopia: visual deprivation and reduced binocular competition. We investigated the affect of these two amblyogenic factors on the expression of the NMDAR1 subunit in the visual cortex because activation of the NMDA receptor is a key mechanism of developmental neural plasticity. We found that disruption of binocular correlations by monocular deprivation promoted a topographic loss of NMDAR1 expression within the cortical representations of the central visual field and the vertical and horizontal meridians. In contrast, binocular deprivation, which primarily affects visual deprivation, promoted an increase in NMDAR1 expression throughout the visual cortex. These different changes in NMDAR1 expression can be described as topographic and homeostatic plasticity of NMDA expression, respectively. In addition, the changes in NMDA expression in the visual cortex provide a greater understanding of the neural mechanisms that underlie the development of amblyopia and the potential for visual recovery.

Amblyopia↗

Development of neuronal activity and activity-dependent expression of brain-derived neurotrophic factor mRNA in organotypic cultures of rat visual cortex.

We have analyzed in organotypic rat visual cortex cultures the way in which expression of brain-derived neurotrophic factor (BDNF) mRNA depends on synaptically generated spontaneous bioelectric activity (SBA) as monitored by recordings of pyramidal cells. SBA was initially low, but from the fourth week onwards 83% of the neurons fired action potentials at 0.2-1.2 impulses/s in a well-balanced state of excitation and inhibition. BDNF mRNA expression increased during the second week to a level surprisingly similar to the adult visual cortex in vivo, despite the fact that activity rates in vitro were approximately 10-fold lower than rates reported in vivo. Thus, SBA generated by a cortical neuronal network in the absence of sensory input is sufficient to elicit and maintain BDNF expression. The transient BDNF peak occurring after eye opening in vivo did not occur in vitro. A blockade of SBA seems not to alter the expression of neurotrophin (NT)-3 and -4/5, and tyrosine kinase receptor C and B mRNA. However, BDNF expression remained extremely low. A recovery of SBA after a period of blockade concurred with a transient hyperexcitability. BDNF immediately increased, driven by calcium influx through voltage-gated channels in synergy with NMDA receptors. Expression transiently reached high levels in neurons of supragranular layers. Infragranular neurons, although firing action potentials, recovered BDNF expression much slower. After 5 days in vitro recovery, the network had de novo established a balanced state of excitation and inhibition. Distribution and expression level of BDNF mRNA had returned to control. Even in 'adult' cultures an acute blockade of SBA downregulated BDNF, and a subsequent recovery of SBA restored BDNF expression. We conclude that BDNF mRNA expression depends on and responds with a fast kinetic to changes of the SBA. Steady-state levels do not depend on the absolute levels of activity, but more likely on the balance between excitation and inhibition, suggesting a role for BDNF in activity homeostasis.

Action Potentials↗

The effects of ablation of visual cortex in neonatal rabbits on the organization of retinothalamic and retinopretectal projections.

Primary visual cortex was ablated unilaterally in neonatal rabbits. Following a survival of 2-4 months, retrograde degeneration of the dorsal lateral geniculate nucleus (LGd) was assessed, and reorganization of retinofugal pathways was studied using methods of anretrograde transport of [3H]proline or of horseradish peroxidase. A complete lesion of primary visual cortex resulted in complete retrograde degeneration of the LGd with no sparing of any class of neurons. The terminations of retinofugal axons in the pretectum and thalamus were compared with those observed in normal animals. No major reorganization of ipsilateral retinofugal projections was observed in either the thalamus and pretectum ipsilateral to the ablated cortex, or in the thalamus and pretectum contralateral to the ablated cortex. However, contralateral retinofugal projections to the thalamus and to the pretectum ipsilateral to the ablated cortex were significantly different from normal. In the thalamus, the projections to the lateral posterior nucleus were expanded in area and increased in density. In the pretectum, the projections to the rostral pretectal areas were greatly increased in area, especially in the region of the olivary pretectal nucleus and posterior pretectal nucleus. However, the density of these projections was not increased relative to normal. Consideration of these results in relation to other published data on the anatomical consequences of neonatal visual cortex lesions, both in mammals which show behavioral sparing following neonatal visual cortex lesions and in mammals which, like the rabbit, show no behavioral sparing, suggests that: (1) behavioral sparing may correlate with patterns of survival or death of neurons in the thalamus and retina; and (2) reorganization of retinofugal pathways is not necessarily associated with behavioral sparing.

Animals↗

Responses of human visual cortex to uniform surfaces.

Surface perception is fundamental to human vision, yet most studies of visual cortex have focused on the processing of borders. We therefore investigated the responses of human visual cortex to parametric changes in the luminance of uniform surfaces by using functional MRI. Early visual areas V1 and V2/V3 showed strong and reliable increases in signal for both increments and decrements in surface luminance. Responses were significantly larger for decrements than for increments, which was fully accounted for by differences in retinal illumination arising from asymmetric pupil dynamics. Responses to both sustained and transient changes of illumination were transient. Signals in early visual cortex scaled linearly with the magnitude of change in retinal illumination, as did subjects' subjective ratings of the perceived brightness of the stimuli. Our findings show that early visual cortex responds strongly to surfaces and that perception of surface brightness is compatible with brain responses at the earliest cortical stages of processing.

Humans↗

Coding of border ownership in monkey visual cortex.

Areas V1 and V2 of the visual cortex have traditionally been conceived as stages of local feature representations. We investigated whether neural responses carry information about how local features belong to objects. Single-cell activity was recorded in areas V1, V2, and V4 of awake behaving monkeys. Displays were used in which the same local feature (contrast edge or line) could be presented as part of different figures. For example, the same light-dark edge could be the left side of a dark square or the right side of a light square. Each display was also presented with reversed contrast. We found significant modulation of responses as a function of the side of the figure in >50% of neurons of V2 and V4 and in 18% of neurons of the top layers of V1. Thus, besides the local contrast border information, neurons were found to encode the side to which the border belongs ("border ownership coding"). A majority of these neurons coded border ownership and the local polarity of luminance-chromaticity contrast. The others were insensitive to contrast polarity. Another 20% of the neurons of V2 and V4, and 48% of top layer V1, coded local contrast polarity, but not border ownership. The border ownership-related response differences emerged soon (<25 msec) after the response onset. In V2 and V4, the differences were found to be nearly independent of figure size up to the limit set by the size of our display (21 degrees ). Displays that differed only far outside the conventional receptive field could produce markedly different responses. When tested with more complex displays in which figure-ground cues were varied, some neurons produced invariant border ownership signals, others failed to signal border ownership for some of the displays, but neurons that reversed signals were rare. The influence of visual stimulation far from the receptive field center indicates mechanisms of global context integration. The short latencies and incomplete cue invariance suggest that the border-ownership effect is generated within the visual cortex rather than projected down from higher levels.

Animals↗

Synaptic reorganization in the dorsal lateral geniculate nucleus following damage to visual cortex in newborn or adult cats.

We have studied the effects of making large lesions of visual cortex on the synaptic organization of the dorsal lateral geniculate nucleus (LGN) in the cat. Visual cortex was removed at birth in one group of cats and during adulthood in a second group. Following survival periods of 6 months to 2 years, the organization of synapses made by afferents from the retina in the LGN was investigated quantitatively with the electron microscope. In single thin sections we determined the percentage of retinal axon terminals that made synapses in the LGN, the average number of synapses made by each retinal axon terminal, and the identity of each postsynaptic process. These measurements were made separately for retinogeniculate connections in the A and C laminae of the LGN. For comparison, similar sets of measurements were made in adult cats that had been reared normally. When single thin sections from the A or C laminae of the LGN in normal cats are examined, about 60% of the axon terminals from the retina are seen to make at least one synaptic contact. These contacts can be with dendrites or F profiles or both. On average, each retinogeniculate terminal makes approximately 1.4 synapses in the plane of a single section and contacts dendrites three times as often as F profiles. In the A laminae of the LGN in cats that received a visual cortex lesion at birth or in adulthood, the percentage of retinal terminals that make synapses is the same as in normal cats. Similarly, the average number of synaptic contacts made by each retinogeniculate terminal is not changed by a lesion of visual cortex. In contrast, the number of contacts made with dendrites is reduced markedly, by about 29% after a lesion at birth and 53% after a lesion as an adult. However, these reductions are offset by compensatory increases in the number of contacts made with F profiles, and thus the mean number of contacts made by each retinogeniculate terminal is stabilized at a normal value. In the C laminae of the LGN, retinogeniculate terminals also reapportion their synaptic contacts. In cats with a lesion during adulthood, the redistribution of synapses is compensatory, as in the A laminae. When a lesion is made at birth, however, the number of new retinal contacts made with F profiles exceeds the number of dendritic contacts that are lost. As a result, each retinogeniculate terminal makes about 26% more synapses, in total, than normal.(ABSTRACT TRUNCATED AT 400 WORDS)

Age Factors↗

Differential properties of cells in the feline primary visual cortex providing the corticofugal feedback to the lateral geniculate nucleus and visual claustrum.

We have examined the responses of 141 layer VI cells in the feline visual cortex. Within this group we compared the responses of a subpopulation of cells checked for connectivity by electrical stimulation in the dLGN and the visual claustrum. The antidromically identified corticogeniculate projecting cells had relatively short receptive fields, as judged from length response curves, measured quantitatively, and were located at the "short" end of the receptive field length spectrum seen in the general population. Of the 17 corticogeniculate projecting cells, 71% were S type cells, which were typically monocular and directionally selective, with relatively long latencies following electrical stimulation. The remaining 29% were C type cells, also directionally selective, but with a wider spread of ocular dominance preferences and shorter latencies following electrical stimulation. S and C type subpopulations did not differ in their receptive field lengths. The mean receptive field length for this subpopulation was 2.2 degrees +/- 0.27, the shortest field being 1 degrees and the longest 5 degrees. The five layer VI cells activated by electrical stimulation from electrodes within the dorsocaudal (visual) claustrum all had much longer receptive field lengths than the corticogeniculate population, often 10 degrees or longer and were monocular and directionally selective S type cells. These data indicate that the information carried in the corticogeniculate stream (and that from layer VI directly to layer IV carried by axon collaterals) is relatively tightly focused in spatial terms whilst the less spatially focused, long receptive field output from layer VI projects to the claustrum.

Animals↗

Spatial contrast and flicker sensitivity following medial thalamic or visual cortex lesions in hooded rats.

In rats, lesions of the medial thalamus that involve the intralaminar nuclei produce a number of visual impairments similar to those obtained with visual cortex ablation, suggesting that the former functionally disrupt visual cortex. This was tested by a direct comparison between the two lesions on spatial contrast and flicker sensitivity, using behavioural techniques. Both lesions depressed spatial contrast sensitivity, visual cortex damage more than thalamic lesions. Only medial thalamic lesions produced statistically significant changes in flicker sensitivity. This dissociation suggests that medial thalamic and visual cortex lesions are disrupting different mechanisms. Alternative explanations of the thalamic deficit are discussed.

Animals↗