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Eric L. Schwartz - One of the best experts on this subject based on the ideXlab platform.
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Cortical hyperColumn size determines stereo fusion limits.
Biological Cybernetics, 1999Co-Authors: Yehezkel Yeshurun, Eric L. SchwartzAbstract:The size of a pair of cortical Ocular Dominance Columns determines a basic anatomical module of V-1 which Hubel and Wiesel have termed the hyperColumn. Does this correspond to a basic functional, or psychophysically measurable, module as well? This is the basic question addressed in the present paper. Since the Ocular Dominance Column architecture is presumed to be related to stereo vision, it is natural to assume that hyperColumn size should provide a modular basis for basic phenomena of stereopsis. In previous work, we have suggested that local nonlinear filtering via the cepstral transform, operating on a local window of cortical tissue scaled by hyperColumn size, provides such a modular model of stereopsis. In the present paper, we review this model and then discuss a number of issues related to the biological plausibility and implementation of this algorithm. Then, we present the main result of this paper: we have analyzed a number of experiments related to stereo fusion limits (Panum's area) and to disparity gradient and disparity scaling, and demonstrate that there is a simple unifying explanation for these phenomena in terms of a constant cortical module whose size is determined by a pair of Ocular Dominance Columns. As a corollary, Panum's area must increase according to (inverse) cortical magnification factor. We show that this is supported by all existing experimental data.
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Cortical HyperColumn Size Determines Stereo Fusion Limits
1999Co-Authors: Yehezkel Yeshurun, Eric L. SchwartzAbstract:The size of a pair of cortical Ocular Dominance Columns determines a basic anatomical module of V-1 which Hubel and Wiesel have termed the hyperColumn. Does this correspond to a basic functional, or psychophysically measurable, module as well? This is the basic question addressed in the present paper. Since the Ocular Dominance Column architecture is presumed to be related to stereo vision, it is natural to assume that hyperColumn size should provide a modular basis for basic phenomena of stereopsis
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Topographic shear and the relation of Ocular Dominance Columns to orientation Columns in primate and cat visual cortex
Neural Networks, 1999Co-Authors: Richard J. Wood, Eric L. SchwartzAbstract:Abstract Shear has been known to exist for many years in the topographic structure of the primary visual cortex, but has received little attention in the modeling literature. Although the topographic map of V1 is largely conformal (i.e. zero shear), several groups have observed topographic shear in the region of the V1/V2 border. Furthermore, shear has also been revealed by anisotropy of cortical magnification factor within a single Ocular Dominance Column. In the present paper, we make a functional hypothesis: the major axis of the topographic shear tensor provides cortical neurons with a preferred direction of orientation tuning. We demonstrate that isotropic neuronal summation of a sheared topographic map, in the presence of additional random shear, can provide the major features of cortical functional architecture with the Ocular Dominance Column system acting as the principal source of the shear tensor. The major principal axis of the shear tensor determines the direction and its eigenvalues the relative strength of cortical orientation preference. This hypothesis is then shown to be qualitatively consistent with a variety of experimental results on cat and monkey orientation Column properties obtained from optical recording and from other anatomical and physiological techniques. In addition, we show that a recent result of Das and Gilbert (Das, A., & Gilbert, C. D., 1997. Distortions of visuotopic map match orientation singularities in primary visual cortex. Nature, 387, 594–598) is consistent with an infinite set of parameterized solutions for the cortical map. We exploit this freedom to choose a particular instance of the Das–Gilbert solution set which is consistent with the full range of local spatial structure in V1. These results suggest that further relationships between Ocular Dominance Columns, orientation Columns, and local topography may be revealed by experimental testing.
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Topographic Shear and the Relation of Ocular Dominance Columns to Orientation Columns in Primate and Cat Visual Cortex
1998Co-Authors: Richard J. Wood, Eric L. SchwartzAbstract:Shear has been known to exist for many years in the topographic structure of primary visual cortex, but has received little attention in the modeling literature. Although the topographic map of V1 is largely conformal (i.e. zero shear), several groups have observed topographic shear in the region of the V1/V2 border. Furthermore, shear has also been revealed by anisotropy of cortical magnification factor within a single Ocular Dominance Column. In the present paper, we make a functional hypothesis: the major axis of the topographic shear tensor provides cortical neurons with a preferred direction of orientation tuning
Carla J Shatz - One of the best experts on this subject based on the ideXlab platform.
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Rapid Regulation of Brain-Derived Neurotrophic Factor mRNA within Eye-Specific Circuits during Ocular Dominance Column Formation
2013Co-Authors: Edward S. Lein, Carla J ShatzAbstract:The neurotrophin brain-derived neurotrophic factor (BDNF) has emerged as a candidate retrograde signaling molecule for geniculocortical axons during the formation of Ocular Dominance Columns. Here we examined whether neuronal activity can regulate BDNF mRNA in eye-specific circuits in the developing cat visual system. Dark-rearing throughout the critical period for Ocular Dominance Column formation decreases levels of BDNF mRNA within primary visual cortex, whereas shortterm (2 d) binOcular blockade of retinal activity with tetrodotoxin (TTX) downregulates BDNF mRNA within the lateral geniculate nucleus (LGN) and visual cortical areas. Brief (6 hr to 2 d) monOcular TTX blockade during the critical period and also in adulthood causes downregulation in appropriate eye-specific laminae in the LGN and Ocular Dominance Columns within primary visual cortex. MonOcular TTX blockade at postnata
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Dynamic regulation of BDNF and NT-3 expression during visual system development.
The Journal of Comparative Neurology, 2000Co-Authors: Edward S. Lein, Andreas Hohn, Carla J ShatzAbstract:Recent studies have proposed roles for neurotrophins in the formation and plasticity of Ocular Dominance Columns as well as in the regulation of dendritic arborization in visual cortex of higher mammals. To assess potential roles for neurotrophins in these processes, we have examined the developmental expression of BDNF and NT-3 mRNA in the cat's visual system using in situ hybridization. BDNF and NT-3 mRNAs are dynamically regulated in many CNS structures during embryonic and postnatal development, and both mRNAs undergo striking developmental changes in laminar specificity and levels of expression within primary visual cortex during the critical period for Ocular Dominance Column formation. Within visual cortex, BDNF mRNA is found in neurons in deep cortical layers (5 and 6) prior to eye opening, and in both deep and superficial layers (2 and 3) shortly afterwards. Within layer 4, the target of thalamocortical axons, BDNF mRNA is low initially and rises to high levels by the end of the critical period for Ocular Dominance Column formation. NT-3 mRNA is first detectable in small stellate neurons at the base of layer 4 (4c) after eye opening, and levels decrease near the end of the critical period. BDNF and NT-3 mRNAs can be detected in the lateral geniculate nucleus at birth, and levels peak during the critical period. In both structures, BDNF mRNA expression is maintained into adulthood, while NT-3 is undetectable in the adult. The presence and dynamic regulation of these neurotrophins in visual structures is consistent with suggested roles for both of these neurotrophins in axonal and dendritic remodeling known to accompany the formation of Ocular Dominance Columns.
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Rapid Regulation of Brain-Derived Neurotrophic Factor mRNA within Eye-Specific Circuits during Ocular Dominance Column Formation
The Journal of Neuroscience, 2000Co-Authors: Edward S. Lein, Carla J ShatzAbstract:The neurotrophin brain-derived neurotrophic factor (BDNF) has emerged as a candidate retrograde signaling molecule for geniculocortical axons during the formation of Ocular Dominance Columns. Here we examined whether neuronal activity can regulate BDNF mRNA in eye-specific circuits in the developing cat visual system. Dark-rearing throughout the critical period for Ocular Dominance Column formation decreases levels of BDNF mRNA within primary visual cortex, whereas short-term (2 d) binOcular blockade of retinal activity with tetrodotoxin (TTX) downregulates BDNF mRNA within the lateral geniculate nucleus (LGN) and visual cortical areas. Brief (6 hr to 2 d) monOcular TTX blockade during the critical period and also in adulthood causes downregulation in appropriate eye-specific laminae in the LGN and Ocular Dominance Columns within primary visual cortex. MonOcular TTX blockade at postnatal day 23 also downregulates BDNF mRNA in a periodic fashion, consistent with recent observations that Ocular Dominance Columns can be detected at these early ages by physiological methods. In contrast, 10 d monOcular TTX during the critical period does not cause a lasting decrease in BDNF mRNA expression in Columns pertaining to the treated eye, consistent with the nearly complete shift in physiological response properties of cortical neurons in favor of the unmanipulated eye known to result from long-term monOcular deprivation. These observations demonstrate that BDNF mRNA levels can provide an accurate “molecular readout” of the activity levels of cortical neurons and are consistent with a highly local action of BDNF in strengthening and maintaining active synapses during Ocular Dominance Column formation.
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Subplate neuron ablation alters neurotrophin expression and Ocular Dominance Column formation
Proceedings of the National Academy of Sciences, 1999Co-Authors: Edward S. Lein, E. M. Finney, Patrick S. Mcquillen, Carla J ShatzAbstract:Ocular Dominance Column formation in visual cortex depends on both the presence of subplate neurons and the endogenous expression of neurotrophins. Here we show that deletion of subplate neurons, which supply glutamatergic inputs to visual cortex, leads to a paradoxical increase in brain-derived neurotrophic factor mRNA in the same region of visual cortex in which Ocular Dominance Columns are absent. Subplate neuron ablation also increases glutamic acid decarboxylase-67 levels, indicating an alteration in cortical inhibition. These observations imply a role for this special class of neurons in modulating activity-dependent competition by regulating levels of neurotrophins and excitability within a developing cortical circuit.
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Brain Waves and Brain Wiring: The Role of Endogenous and Sensory-Driven Neural Activity in Development
Pediatric Research, 1999Co-Authors: Anna A Penn, Carla J ShatzAbstract:Neural activity is critical for sculpting the intricate circuits of the nervous system from initially imprecise neuronal connections. Disrupting the formation of these precise circuits may underlie many common neurodevelopmental disorders, ranging from subtle learning disorders to pervasive developmental delay. The necessity for sensory-driven activity has been widely recognized as crucial for infant brain development. Recent experiments in neurobiology now point to a similar requirement for endogenous neural activity generated by the nervous system itself before sensory input is available. Here we use the formation of precise neural circuits in the visual system to illustrate the principles of activity-dependent development. Competition between the projections from lateral geniculate nucleus neurons that receive sensory input from the two eyes shapes eye-specific connections from an initially diffuse projection into Ocular Dominance Columns. When the competition is altered during a critical period for these changes, by depriving one eye of vision, the normal Ocular Dominance Column pattern is disrupted. Before Ocular Dominance Column formation, the highly ordered projection from retina to lateral geniculate nucleus develops. These connections form before the retina can respond to light, but at a time when retinal ganglion cells spontaneously generate highly correlated bursts of action potentials. Blockade of this endogenous activity, or biasing the competition in favor of one eye, results in a severe disruption of the pattern of retinogeniculate connections. Similar spontaneous, correlated activity has been identified in many locations in the developing central nervous system and is likely to be used during the formation of precise connections in many other neural systems. Understanding the processes of activity-dependent development could revolutionize our ability to identify, prevent, and treat developmental disorders resulting from disruptions of neural activity that interfere with the formation of precise neural circuits.
Siegrid Löwel - One of the best experts on this subject based on the ideXlab platform.
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The pattern of Ocular Dominance Columns in cat primary visual cortex: Intra- and interindividual variability of Column spacing and its dependence on genetic background
European Journal of Neuroscience, 2003Co-Authors: Matthias Kaschube, Theo Geisel, Fred Wolf, Mathias Puhlmann, Stefan Rathjen, Karl-friedrich Schmidt, Siegrid LöwelAbstract:We present a comprehensive analysis of the intrinsic variability of the periodicity of Ocular Dominance Columns in cat primary visual cortex (area 17) and its relationship to genetic background and visual experience. We characterized the intra-areal and interindividual variability of Column spacing in a large set (n = 49) of Ocular Dominance patterns adapting a recently developed technique for the two-dimensional analysis of orientation Column patterns. Patterns were obtained from three different cat colonies (termed F, M and D), the cats having either normal visual experience or experimentally induced strabismus. Two-dimensional maps of local Column spacing were calculated for every pattern. In individual cortices, local Column spacings varied by > 50% with the majority of Column spacings ranging between 0.6 and 1.5 mm in different animals. In animals from colonies F and M (n = 29), the mean Column spacing ranged between 1.03 and 1.27 mm and exhibited no significant differences, either between the two breeds or between strabismic and normal animals. The mean spacing was moderately clustered in the left and right brain hemisphere of individual animals but not in littermates. In animals from colony D (n = 2), average Column spacing ranged between 0.73 and 0.95 mm, and was thus significantly different from the distribution of spacings in animals from breeds F and M, suggesting an influence of genetic factors on the layout of Ocular Dominance Columns. Local Column spacing exhibited a considerable systematic intra-areal variation, with largest spacings along the representation of the horizontal meridian and smallest spacings along the peripheral representation of the vertical meridian. The total variability of Ocular Dominance Column spacing comprised 24% systematic intra-areal variation, 18% interindividual differences of mean Column spacing and 58% nonsystematic intra-areal variability.
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Theory meets experiment: correlated neural activity helps determine Ocular Dominance Column periodicity
Trends in Neurosciences, 1995Co-Authors: Geoffrey J. Goodhill, Siegrid LöwelAbstract:The development of Ocular Dominance Columns in primary visual cortex has attracted much interest from both experimentalists and theoreticians. One key parameter of these Columns is their periodicity - it is thus important to understand how this is determined. Novel experimental work demonstrates that the periodicity is influenced by the temporal patterning of afferent activity, as predicted by recent theoretical work.
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Ocular Dominance Column development strabismus changes the spacing of adjacent Columns in cat visual cortex
The Journal of Neuroscience, 1994Co-Authors: Siegrid LöwelAbstract:To investigate the role of visual experience for the gross layout of Ocular Dominance (OD) Columns in the visual cortex, I compared the respective patterns in normally raised and strabismic cats. OD domains were visualized by (1) transneuronal labeling of the afferents from the left or right eye with intraOcular 3H-proline injections or (2) 14C-2- deoxyglucose autoradiography after monOcular visual stimulation in awake animals. To obtain the complete pattern of OD Columns, flat-mount sections were prepared from the unfolded cortical hemispheres. Eliminating correlated activity between the two eyes by making the animals strabismic influenced the gross layout of the OD domains. In area 17, OD domains become more sharply delineated than in normal animals and spaced more widely. Spatial frequency analyses revealed a mean spacing of adjacent Columns of 1100–1300 microns in strabismic and of 800–1000 microns in normal cats. In area 18, the spacing of the Ocular Dominance domains is larger than in area 17 for both normal and strabismic cats (1500–1650 microns), but little influenced by strabismus. These results indicate that in area 17 decreased correlation of activity between the eyes alters the periodicity of OD Columns. In addition, these observations suggest that not only the segregation of afferents into distinct Columns but also the final expression of the Columnar grid is influenced by visual experience, and in particular by the temporal patterning of neural activity. This is further evidence for the hypothesis that the development of OD Columns is governed by activity-dependent self-organizing principles.
Jonathan C. Horton - One of the best experts on this subject based on the ideXlab platform.
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MonOcular cells without Ocular Dominance Columns.
Journal of Neurophysiology, 2006Co-Authors: Daniel L. Adams, Jonathan C. HortonAbstract:In many regions of the mammalian cerebral cortex, cells that share a common receptive field property are grouped into Columns. Despite intensive study, the function of the cortical Column remains unknown. In the squirrel monkey, the expression of Ocular Dominance Columns is variable, with Columns present in some animals and not in others. By searching for differences between animals with and without Columns, it should be possible to infer how Columns contribute to visual processing. Single-cell recordings outside layer 4C were made in nine squirrel monkeys, followed by labeling of Ocular Dominance Columns in layer 4C. In the squirrel monkey, compared with the macaque, cells outside layer 4C were more likely to respond to stimulation of either eye whether Ocular Dominance Columns were present or not. In three animals lacking Ocular Dominance Columns, single cells were recorded from layer 4C. Remarkably, 20% of cells in layer 4C were monOcular despite the absence of Columns. This observation means that Ocular Dominance Columns are not necessary for monOcular cells to occur in striate cortex. In macaques each row of cytochrome oxidase (CO) patches is aligned with an Ocular Dominance Column and receives koniocellular input serving one eye only. In squirrel monkeys this was not true: CO patches and Ocular Dominance Columns had no spatial correlation and the koniocellular input to CO patches was binOcular. Thus even when Ocular Dominance Columns occur in the squirrel monkey, they do not transform the functional architecture to resemble that of the macaque.
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A precise retinotopic map of primate striate cortex generated from the representation of angioscotomas
2003Co-Authors: Daniel L. Adams, Jonathan C. HortonAbstract:Shadows cast by retinal blood vessels are represented in striate cortex of the squirrel monkey. Their pattern was exploited to generate a true retinotopic map of V1. For calibration, retinal landmarks were projected onto a tangent screen to measure their visual field location. Next, the retina was warped onto striate cortex, distorting it as necessary to match each retinal vessel to its cortical representation. Maps from four hemispheres of two normal adult squirrel monkeys were created and used to derive expressions for cortical magnification factor (M). A mean map was produced by averaging the individual maps. To address the controversial issue of whether the ratio of retinal ganglion cell (RGC) density to M is constant at all eccentricities, we stained a retinal whole mount from one of the two monkeys for Nissl substance. A ganglion cell density map was compiled by sampling the concentration of cells at 171 retinal points. Allowance was made for displaced amacrine cells and for the centripetal displacement of RGCs from central photoreceptors. After these corrections the V1 surface area and RGC density were compared at each eccentricity. The cortical representation of the macula was found to be amplified, even beyond the magnification expected from its high density of RGCs. For example, the central 4 ° of visual field were allotted 27 % of the surface area of V1 but were supplied by only 12 % of RGCs. We conclude that, in monkey striate cortex, more tissue is allocated per ganglion cell for the analysis of information emanating from the macula as compared with the peripheral retina. Key words: blind spot; monOcular crescent; retina; blood vessel; flat-mount; Ocular Dominance Column; cytochrome oxidase; magnification factor; anisotropy; displaced amacrine cell; GABA; retinal ganglion cell; cone; macula; Henle fiber laye
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An albino-like decussation error in the optic chiasm revealed by anomalous Ocular Dominance Columns.
Visual Neuroscience, 2002Co-Authors: Lawrence C. Sincich, Jonathan C. HortonAbstract:We report a unique anomaly in the Ocular Dominance Column pattern of a single, normally pigmented macaque monkey. The Column pattern contained large monOcular areas inserted between the normal Columns and the dorsal V1 border. These monOcular regions received transneuronal input from the contralateral eye, indicating that a small population of temporal ganglion cells erroneously decussated at the optic chiasm. Projection of the Column pattern back onto the visual field showed that the monOcular wedges represented a approximately 5-deg sector of ipsilateral field. This corresponded to the extent of naso-temporal overlap of ganglion cells in the normal retina, suggesting an error in axon guidance affecting cells close to the vertical midline of the retina. The consequences of the crossing error in this animal were threefold: it produced an anomalous monOcular zone near the V1 border, the vertical meridian was not represented at the V1 border, and points near the vertical meridian were represented twice in the brain, once in each hemisphere.
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Emergence of Ocular Dominance Columns in cat visual cortex by 2 weeks of age.
The Journal of Comparative Neurology, 2000Co-Authors: Michael C. Crair, Jonathan C. Horton, Antonella Antonini, Michael P. StrykerAbstract:Previous anatomic studies of the geniculocortical projection showed that Ocular Dominance Columns emerge by 3 weeks of age in cat visual cortex, but recent optical imaging experiments have revealed a pattern of physiologic eye Dominance by the end of the second week of life. We used two methods to search for an anatomic correlate of this early functional Ocular Dominance pattern. First, retrograde labeling of lateral geniculate nucleus (LGN) inputs to areas of cortex preferentially activated by one eye showed that the geniculocortical projection was already partially segregated by eye at postnatal day 14 (P14). Second, transneuronal label of geniculocortical afferents in flattened sections of cortex after a tracer injection into one eye showed a periodic pattern at P14 but not at P7. In the classic model for the development of Ocular Dominance Columns, initially overlapping geniculocortical afferents segregate by means of an activity-dependent competitive process. Our data are consistent with this model but suggest that Ocular Dominance Column formation begins between P7 and P14, approximately a week earlier than previously believed. The functional and anatomic data also reveal an early developmental bias toward contralateral eye afferents. This initial developmental bias is not consistent with a strictly Hebbian model for geniculocortical afferent segregation. The emergence of Ocular Dominance Columns before the onset of the critical period for visual deprivation also suggests that the mechanisms for Ocular Dominance Column formation may be partially distinct from those mediating plasticity later in life. J.
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Intrinsic Variability of Ocular Dominance Column Periodicity in Normal Macaque Monkeys
The Journal of Neuroscience, 1996Co-Authors: Jonathan C. Horton, Davina R. HockingAbstract:Little is known about intrinsic variation from animal to animal in the periodicity of Columnar systems within various regions of the mammalian cerebral cortex. To address this issue, complete mosaics of the Ocular Dominance Columns were reconstructed from flat-mounts of the left and right striate cortex (V1) in six normal adult macaques ( Macaca fascicularis ). To identify the Columns, we enucleated the right eye and subsequently processed striate cortex for cytochrome oxidase (CO) activity. Average Column areas for the intact eye and the missing eye were nearly equal, confirming that monOcular enucleation in adult macaques produces negligible Column shrinkage. The contralateral eye’s Columns occupied more territory than the ipsilateral eye’s Columns, even in the central visual field representation (0° to 8°), where they predominated by 52 to 48%. The Column mosaics showed remarkable variation in periodicity. The number of Column pairs along the V1/V2 border ranged from 101 sets in one monkey to 154 sets in another. Average Column width along the V1/V2 border ranged between 670 and 395 μm, a nearly twofold difference. The widest Columns were found in the foveal representation. This high degree of innate variability should be taken into account when considering the effects of various sensory manipulations (e.g., strabismus, anisometropia), which have been reported to alter the periodicity of Ocular Dominance Columns. We found pronounced intrinsic variation in the width and number of Ocular Dominance Columns in a sample of six M . fascicularis , indicating that the number of hyperColumns within a given cortical area can range widely among normal members of the same species.
Steven L. Small - One of the best experts on this subject based on the ideXlab platform.
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A model of Ocular Dominance Column development by competition for trophic factor: effects of excess trophic factor with monOcular deprivation and effects of antagonist of trophic factor.
Journal of Computational Neuroscience, 2000Co-Authors: Anthony E. Harris, G. Bard Ermentrout, Steven L. SmallAbstract:Recent experimental evidence has implicated neurotrophic factors (NTs) in the competitive process believed to drive the development of Ocular Dominance (OD) Columns. Application of excess amounts of particular NTs can prevent the segregation process, suggesting that they could be the substance for which geniculocortical afferents compete during development. We have previously presented a model that accounts for normal OD development as well as the prevention of that development with excess NT. The model uses a Hebbian learning rule in combination with competition for a limiting supply of cortical trophic factor to drive OD segregation, without any weight normalization procedures.
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A Model of Ocular Dominance Column Development by Competition for Trophic Factor: Effects of Excess Trophic Factor with MonOcular Deprivation and Effects of Antagonist of Trophic Factor
Journal of Computational Neuroscience, 2000Co-Authors: Anthony E. Harris, G. Bard Ermentrout, Steven L. SmallAbstract:Recent experimental evidence has implicated neurotrophic factors (NTs) in the competitive process believed to drive the development of Ocular Dominance (OD) Columns. Application of excess amounts of particular NTs can prevent the segregation process, suggesting that they could be the substance for which geniculocortical afferents compete during development. We have previously presented a model that accounts for normal OD development as well as the prevention of that development with excess NT. The model uses a Hebbian learning rule in combination with competition for a limiting supply of cortical trophic factor to drive OD segregation, without any weight normalization procedures. Subsequent experimental evidence has further suggested that NTs may be causally involved in the competitive process. Application of NT antagonist can prevent OD Columns by causing inputs from both eyes to be eliminated, suggesting that NTs may be the substance for which geniculocortical afferents compete. Also, excess NT can mitigate the shift to the open eye normally caused by monOcular deprivation (MD). In this article, we show that the current model can account for these subsequent experiments. We show that deprivation of NT causes inputs from both eyes to decay and that excess NT can mitigate the shift to the open eye normally seen with MD. We then present predictions of the model concerning the effects of NT on the length of the critical period during which MD is effective. The model presents a novel mechanism for competition between neural populations inspired by particular biological evidence. It accounts for three specific experimental results, and provides several testable predictions.
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A MODEL OF Ocular Dominance Column DEVELOPMENT BY COMPETITION FOR TROPHIC FACTOR
Proceedings of the National Academy of Sciences of the United States of America, 1997Co-Authors: Anthony E. Harris, Ermentrout Gb, Steven L. SmallAbstract:Recent experimental evidence has shown that application of certain neurotrophic factors (NTs) to the developing primary visual cortex prevents the development of Ocular Dominance (OD) Columns. One interpretation of this result is that afferents from the lateral geniculate nucleus compete for postsynaptic trophic factor in an activity-dependent manner. Application of excess trophic factor eliminates this competition, thereby preventing OD Column formation. We present a model of OD Column development, incorporating Hebbian synaptic modification and activity-driven competition for NT, which accounts for both normal OD Column development as well as the prevention of that development when competition is removed. In the “control” situation, when available NT is below a critical amount, OD Columns form normally. These Columns form without weight normalization procedures and in the presence of positive inter-eye correlations. In the “experimental” case, OD Column development is prevented in a local neighborhood in which excess NT has been added. Our model proposes a biologically plausible mechanism for competition between neural populations that is motivated by several pieces of experimental data, thereby accounting for both normal and experimentally perturbed conditions.
