Formation Of Ocular Dominance Columns Research Articles

Generalized neural field theory of cortical plasticity illustrated by an application to the linear phase of ocular dominance column formation in primary visual cortex.

Physiologically based neural field theory (NFT) is extended to encompass cortical plasticity dynamics. An illustrative application is provided which treats the evolution of the connectivity of left- and right-eye visual stimuli to neuronal populations in the primary visual cortex (V1), and the initial, linear phase of formation of approximately one-dimensional (1D) ocular dominance columns (ODCs) that sets their transverse spatial scale. This links V1 activity, structure, and physiology within a single theory that already accounts for a range of other brain activity and connectivity phenomena, thereby enabling ODC formation and many other phenomena to be interrelated and cortical parameters to be constrained across multiple domains. The results accord with experimental ODC widths for realistic cortical parameters and are based directly on a unified description of the neuronal populations involved, their connection strengths, and the neuronal activity they support. Other key results include simple analytic approximations for ODC widths and the parameters of maximum growth rate, constraints on cortical excitatory and inhibitory gains, elucidation of the roles of specific poles of the V1 response function, and the fact that ODCs are not formed when input stimuli are fully correlated between eyes. This work provides a basis for further generalization of NFT to model other plasticity phenomena, thereby linking them to the range multiscale phenomena accounted for by NFT.

Theory for the alignment of cortical feature maps during development

We present a developmental model of ocular dominance column formation that takes into account the existence of an array of intrinsically specified cytochrome oxidase blobs. We assume that there is some molecular substrate for the blobs early in development, which generates a spatially periodic modulation of experience-dependent plasticity. We determine the effects of such a modulation on a competitive Hebbian mechanism for the modification of the feedforward afferents from the left and right eyes. We show how alternating left and right eye dominated columns can develop, in which the blobs are aligned with the centers of the ocular dominance columns and receive a greater density of feedforward connections, thus becoming defined extrinsically. More generally, our results suggest that the presence of periodically distributed anatomical markers early in development could provide a mechanism for the alignment of cortical feature maps.

The Subplate and Early Cortical Circuits

The developing mammalian cerebral cortex contains a distinct class of cells, subplate neurons (SPns), that play an important role during early development. SPns are the first neurons to be generated in the cerebral cortex, they reside in the cortical white matter, and they are the first to mature physiologically. SPns receive thalamic and neuromodulatory inputs and project into the developing cortical plate, mostly to layer 4. Thus SPns form one of the first functional cortical circuits and are required to relay early oscillatory activity into the developing cortical plate. Pathophysiological impairment or removal of SPns profoundly affects functional cortical development. SPn removal in visual cortex prevents the maturation of thalamocortical synapses, the maturation of inhibition in layer 4, the development of orientation selective responses and the formation of ocular dominance columns. SPn removal also alters ocular dominance plasticity during the critical period. Therefore, SPns are a key regulator of cortical development and plasticity. SPns are vulnerable to injury during prenatal stages and might provide a crucial link between brain injury in development and later cognitive malfunction.

Subplate neurons: crucial regulators of cortical development and plasticity.

The developing cerebral cortex contains a distinct class of cells, subplate neurons, which form one of the first functional cortical circuits. Subplate neurons reside in the cortical white matter, receive thalamic inputs and project into the developing cortical plate, mostly to layer 4. Subplate neurons are present at key time points during development. Removal of subplate neurons profoundly affects cortical development. Subplate removal in visual cortex prevents the maturation of thalamocortical synapse, the maturation of inhibition in layer 4, the development of orientation selective responses in individual cortical neurons, and the formation of ocular dominance columns. In addition, monocular deprivation during development reveals that ocular dominance plasticity is paradoxical in the absence of subplate neurons. Because subplate neurons projecting to layer 4 are glutamatergic, these diverse deficits following subplate removal were hypothesized to be due to lack of feed-forward thalamic driven cortical excitation. A computational model of the developing thalamocortical pathway incorporating feed-forward excitatory subplate projections replicates both normal development and plasticity of ocular dominance as well as the effects of subplate removal. Therefore, we postulate that feed-forward excitatory projections from subplate neurons into the developing cortical plate enhance correlated activity between thalamus and layer 4 and, in concert with Hebbian learning rules in layer 4, allow maturational and plastic processes in layer 4 to commence. Thus subplate neurons are a crucial regulator of cortical development and plasticity, and damage to these neurons might play a role in the pathology of many neurodevelopmental disorders.

The model of ocular dominance pattern formation in the presence of gradients of chemical labels.

Event Abstract Back to Event The model of ocular dominance pattern formation in the presence of gradients of chemical labels. Dmitry Tsigankov1, 2* and Alexei Koulakov3 1 Bernstein Center for Computational Neuroscience, Germany 2 Max Planck Institute for Dynamics and Self-organization, Germany 3 Cold Spring Harbor Laboratory, United States The formation of ocular dominance (OD) columns in the mammalian visual cortex is thought to be driven by electrical activity of the projecting neurons. Indeed, theoretical modeling have shown that lateral cortical activity-dependent interactions are capable of producing such a periodic pattern of regions dominated by inputs from left or right eye. This scenario for OD pattern formation based on self-organization of inputs due to excitatory and inhibitory lateral interactions of Mexican-hat shape was recently confronted by several lines of experimental observations. First, the anatomical data on primary visual cortex indicate that the inhibition can have a shorter range than excitation, the regime in which the classical model fails to produce OD structure. Second, the measurements of the width of OD regions following the manipulations with the strength of the inhibitory connections are inconsistent with the predictions of the model. When the strength of inhibitory connections is increased the OD width is found to increase and when inhibition is decreased the OD width also decreases. This behavior is opposite to one predicted by the classical model. Finally, the sole role of activity-dependent self-organization in the formation of OD structure was questioned as it was observed that OD patterns can be formed in optic tectum in the presence of other factors such as gradients of interacting chemical labels.Here we present theoretical analysis of the possible interplay between genetically encoded labeling and experience-driven reorganization of the projections in the formation of OD patterns. We show that in the presence of single gradient of chemical marker the projections from two eyes are segregated into OD columns for a wide class of lateral interaction profiles. We obtain that depending on the range and strength of inhibitory and excitatory lateral connections the projecting neurons may prefer to form segregated or mixed inputs. We find the regimes when OD structure emerges for short-range inhibition and long-range excitation. We also investigate the role of lateral inhibition and excitation for different interaction profiles to find a novel regime when increase in the inhibition strength increases the width of OD columns in agreement with the experiment. Conference: Bernstein Conference on Computational Neuroscience, Frankfurt am Main, Germany, 30 Sep - 2 Oct, 2009. Presentation Type: Poster Presentation Topic: Learning and plasticity Citation: Tsigankov D and Koulakov A (2009). The model of ocular dominance pattern formation in the presence of gradients of chemical labels.. Front. Comput. Neurosci. Conference Abstract: Bernstein Conference on Computational Neuroscience. doi: 10.3389/conf.neuro.10.2009.14.146 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 28 Aug 2009; Published Online: 28 Aug 2009. * Correspondence: Dmitry Tsigankov, Bernstein Center for Computational Neuroscience, Göttingen, Germany, dmitry@nld.ds.mpg.de Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers Dmitry Tsigankov Alexei Koulakov Google Dmitry Tsigankov Alexei Koulakov Google Scholar Dmitry Tsigankov Alexei Koulakov PubMed Dmitry Tsigankov Alexei Koulakov Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.

Human white matter pathway development: connections to cognition

Event Abstract Back to Event Human white matter pathway development: connections to cognition Brian Wandell1* 1 Stanford University, Department of Psychology, United States Brain development depends significantly on circumstances. One of the best known examples is the experience-dependent plasticity that influences ocular dominance column formation in V1. In this example the long-range white matter projections are intact and developmental plasticity is mediated by competition for synaptic space within the dendritic and axonal arbors. There are also more extreme circumstances, in which entire sets of long-range projections are missing or abnormal. To compensate for such profound white matter abnormalities, the brain may use other strategies. Several types of white matter conditions related to development will be reviewed. First, I will describe two severe disturbances of the white matter projections: (a) achiasmic subjects, and (b) subjects born with only one hemisphere. In some of these extreme cases, development plasticity can compensate and produce surprisingly good behavioral outcomes. Second, I will describe two examples in which variations of white matter microstructure correlates with cognition. In one example the white matter microstructure is associated with reading development; in a second example white matter microstructure is associated with numerical processing. By understanding the relationship between white matter development and behavioral outcome, we may broaden our understanding of the mechanisms available to developmental plasticity. Studies of the development of white matter projections and microstructure may help to identify key cognitive systems and understand the basis for behavioral disorders. Conference: Conference on Neurocognitive Development, Berkeley, CA, United States, 12 Jul - 14 Jul, 2009. Presentation Type: Oral Presentation Topic: Language Citation: Wandell B (2009). Human white matter pathway development: connections to cognition. Conference Abstract: Conference on Neurocognitive Development. doi: 10.3389/conf.neuro.09.2009.10.006 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 06 Jul 2009; Published Online: 06 Jul 2009. * Correspondence: Brian Wandell, Stanford University, Department of Psychology, Stanford, CA, United States, wandell@stanford.edu Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers Brian Wandell Google Brian Wandell Google Scholar Brian Wandell PubMed Brian Wandell Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.

Properties of Persistent Postnatal Cortical Subplate Neurons

Subplate (SP) neurons are important for the proper development of thalamocortical innervation. They are necessary for formation of ocular dominance and orientation columns in visual cortex. During the perinatal period, many SP neurons die. The surviving cohort forms interstitial cells in the white matter (WM) and a band of horizontally oriented cells below layer VI (layer VIb, layer VII, or subplate cells). Although the function of embryonic SP neurons has been well established, the functional roles of WM and postnatal SP cells are not known. We used a combination of anatomical, immunohistochemical, and electrophysiological techniques to explore the dendritic morphology, neurotransmitter phenotype, intrinsic electrophysiological, and synaptic input properties of these surviving cells in the rat visual cortex. The density of SP and WM cells significantly decreases during the first month of life. Both populations express neuronal markers and have extensive dendritic arborizations within the SP, WM, and to the overlying visual cortex. Some intrinsic electrophysiological properties of SP and WM cells are similar: each generates high-frequency slowly adapting trains of action potentials in response to a sustained depolarization. However, SP cells exhibit greater frequency-dependent action potential broadening than WM neurons. Both cell types receive predominantly AMPA/kainate receptor-mediated excitatory synaptic input that undergoes paired-pulse facilitation as well as NMDA receptor and GABAergic input. Synaptic inputs to these cells can also undergo long-term synaptic plasticity. Thus, surviving SP and WM cells are functional electrogenic neurons integrated within the postnatal visual cortical circuit.

Spontaneous Retinal Activity Mediates Development of Ocular Dominance Columns and Binocular Receptive Fields in V1

The mechanisms that give rise to ocular dominance columns (ODCs) during development are controversial. Early experiments indicated a key role for retinal activity in ODC formation. However, later studies showed that in those early experiments, the retinal activity perturbation was initiated after ODCs had already formed. Moreover, recent studies concluded that early eye removals do not impact ODC segregation. Here we blocked spontaneous retinal activity during the very early stages of ODC development. This permanently disrupted the anatomical organization of ODCs and led to a dramatic increase in receptive field size for binocular cells in primary visual cortex. Our data suggest that early spontaneous retinal activity conveys crucial information about whether thalamocortical axons represent one or the other eye and that this activity mediates binocular competition important for shaping receptive fields in primary visual cortex.

Early Retinal Activity and Visual Circuit Development

Does spontaneous retinal activity prior to vision play a role in the establishment of visual maps? In this issue of Neuron, two separate papers by Huberman et al. and Hooks and Chen demonstrate a role for early spontaneous retinal activity in the establishment of ocular dominance columns and synaptic refinement at retinogeniculate synapses.

Ocular dominance columns in strabismus

During development, the projection from the lateral geniculate nucleus to striate cortex becomes segregated into monocular regions called ocular dominance columns. Prior studies in cats have suggested that experimental strabismus or alternating monocular occlusion increases the width and segregation of columns. In the squirrel monkey, strabismus has been reported to induce the formation of ocular dominance columns. However, these studies are difficult to interpret because no animal can serve as its own control and the degree of inter-individual variability among normal subjects is considerable. We have re-examined the effect of strabismus on ocular dominance columns in a large group of strabismic and normal squirrel monkeys. Five animals rendered strabismic at age one week had well-developed, widely spaced columns. Among 16 control animals, a wide spectrum of column morphology was encountered. Some control animals lacked ocular dominance columns, whereas others had columns similar to those observed in strabismic animals. Natural variation in column expression in normal squirrel monkeys, and potential uncontrolled genetic influences, made it impossible to determine if strabismus affects ocular dominance columns. It was evident however, that strabismus does not affect the binocular projection from the lateral geniculate nucleus to each CO patch in the upper layers. In strabismic monkeys, just as in normal animals, each patch received input from geniculate afferents serving both the left eye and the right eye. In addition, in strabismic monkeys, as in normal animals, patches were not aligned with ocular dominance columns.

Subplate Neurons Regulate Maturation of Cortical Inhibition and Outcome of Ocular Dominance Plasticity

Synaptic plasticity during critical periods of development requires intact inhibitory circuitry. We report that subplate neurons are needed both for maturation of inhibition and for the proper sign of ocular dominance (OD) plasticity. Removal of subplate neurons prevents the developmental upregulation of genes involved in mature, fast GABAergic transmission in cortical layer 4, including GABA receptor subunits and KCC2, and thus prevents the switch to a hyperpolarizing effect of GABA. To understand the implications of these changes, a realistic circuit model was formulated. Simulations predicted that without subplate neurons, monocular deprivation (MD) paradoxically favors LGN axons representing the deprived (less active) eye, exactly what was then observed experimentally. Simulations also account for published results showing that OD plasticity requires mature inhibition. Thus, subplate neurons regulate molecular machinery required to establish an adult balance of excitation and inhibition in layer 4, and thereby influence the outcome of OD plasticity.

Subplate Neurons Foster Inhibition

Previous work demonstrates an essential role of subplate neurons during ocular dominance (OD) column formation in the developing visual cortex. While inhibitory circuitry has also been shown to play an essential role in OD plasticity, the relationship between subplate neurons and the development of inhibitory circuits has been unclear. In this issue of Neuron, Kanold and Shatz provide evidence that maturation of inhibitory circuitry requires subplate neurons in the developing cortex.

Brain‐derived neurotrophic factor enhances expression of superior cervical ganglia clone 10 in lateral geniculate nucleus and visual cortex of developing kittens

Neuronal growth-associated proteins, including superior cervical ganglia clone 10 (SCG10) family molecules, play roles in neurite outgrowth and network formation as well as structural and functional plasticity. The present ontogenetic study revealed that the expression of neuronal growth-associated proteins in the visual cortex (VC) exhibited a sharp peak in the early postnatal period when growing lateral geniculate nucleus (LGN) axon terminals segregate into the ocular dominance columns depending on retinal activity. We then hypothesized that SCG10 family molecules, known for catastrophic factors of microtubules, play important roles in the formation of ocular dominance columns. To test this hypothesis, we studied whether: (i) monocular blockade of retinal activity changed the SCG10 expression in LGN and VC and (ii) brain-derived neurotrophic factor (BDNF) cortical infusion modified the expression of SCG10 family molecules and the number of excitatory/inhibitory cortical synapses. Using northern blot and in situ hybridization, we revealed that: (i) silencing retinal activity with tetrodotoxin eye injections dynamically reduced the expression of SCG10 mRNA and (ii) it was enhanced by BDNF in VC and LGN of kittens but not adult cats. These findings suggest that cortical infusion of BDNF and retinal activity up-regulate the expression of SCG10 in the LGN and VC and that up-regulated SCG10 in turn initiates marked reorganization of the microtuble network, eventually resulting in increase in synapse formation in the VC.

A Developmental Model of Ocular Dominance Column Formation on a Growing Cortex

We derive an activity-based developmental model of ocular dominance column formation in primary visual cortex that takes into account cortical growth. The resulting evolution equation for the densities of feedforward afferents from the two eyes exhibits a sequence of pattern forming instabilities as the size of the cortex increases. We use linear stability analysis to investigate the nature of the transitions between successive patterns in the sequence. We show that these transitions involve the splitting of existing ocular dominance (OD) columns, such that the mean width of an OD column is approximately preserved during the course of development. This is consistent with recent experimental observations of postnatal growth in cat.

Laminar distribution of NMDA receptor subunit (NR1, NR2A, NR2B) expression during the critical period in cat visual cortex

Changes in NMDA subunit composition may be part of the molecular basis for critical period plasticity. The present study used immunohistochemistry to determine developmental changes in the laminar distribution of the three major cortical NMDA subunits (NR2A, NR2B, NR1) during the critical period in cat visual cortex. For all three subunits, at 1 week staining was concentrated in two bands: an upper band consisting of layer I, the compact zone and the upper half of the cortical plate; a lower band consisting of layers V and VI. In the lower part of the cortical plate (immature layer IV) staining was very low. For NR2A and NR2B, immunoreactivity in layer IV remained low until 10 weeks of age. At 20 weeks and adult, layer IV filled in and NR2A and NR2B label was rather uniform across all layers. NR1 showed a developmental pattern of expression different from NR2A and NR2B after 1 week. At 5 and 10 weeks, label was prominent in layer IV and superficial layers, but low in layers V and VI. The main change after 10 weeks was a progressive decrease in staining, such that in older animals label was markedly densest in superficial layers. Thus, during the rise of the critical period, NR1 is the dominant subtype in layer IV and could play a role in anatomical ocular dominance column formation and plasticity. At the same time, NR2A and NR2B subunits are concentrated outside layer IV, and could be related to physiological plasticity in extragranular layers, which precedes and outlasts plasticity in layer IV. For all three NMDA receptor subunits, the laminar distribution was similar in normal and dark reared visual cortex at 20 weeks, indicating that the developmental changes in laminar pattern of expression are independent of visual input.

Role of Cajal-Retzius and subplate neurons in cerebral cortical development

A synaptic network is already formed in the marginal zone of the early telencephalon before the arrival of the first wave of radial migration of neuroblasts from the subventricular zone to form the cortical plate. Cells and fibers forming the marginal zone are mainly the Cajal-Retzius (C-R) neurons and their processes. The origin of these cells is not yet proved but is likely either the median ganglionic eminence or the mesencephalic neuromere. The bipolar or multipolar C-R neurons populate the molecular layer of the fetal cortical plate and are sparse in the adult. Their thick axon emits collaterals for synaptic contact with pyramidal neurons initially in layer 6 and later with in all layers. C-R neurons produce GABA, possibly ACh, several calcium-binding proteins (eg, calmodulin, parvalbumin, calretinin) and several neuropeptides; they are rich in ribosomes. Subplate neurons, beneath the cortical plate, emit pioneer axons in the incipient formation of the internal capsule and also commissural fibers of the early hippocampus. C-R cells express products of the genes RELN, LIS1, and DS-CAM, which mediate radial neuroblast migration and lamination of the cortical plate and important in the pathogenesis of lissencephaly. A subpopulation of C-R neurons also expresses a p53 product implicated in cell survival and apoptosis. In addition to forming the first intrinsic synaptic circuits of the cortical plate and its first afferent and efferent connections with subcortical structures, they may play additional roles in the formation of ocular dominance columns, in regulating neuronogenesis, and in cortical repair. They do not disappear by apoptosis at the completion of cell migration, as was previously thought, but their functional role in the mature brain remains unknown.

SCG10-related neuronal growth-associated proteins in neural development, plasticity, degeneration, and aging.

Neuronal growth-associated proteins (nGAPs) are in general neuron-specific gene products whose expression correlates tightly with neuronal process outgrowth and/or regeneration, and are mostly good downstream targets of neurotrophin stimulation. Expression of genes encoding nGAPs such as GAP-43, SCG10, and stathmin is upregulated following lesioning of cortical and hippocampal regions of the adult rat brain. In the brains of aged animals, however, the magnitude of the response is reduced, whereas the time course of the response is mostly unchanged when compared with that for brains of young ones. Expression of GAP-43 and stathmin is reduced by aging, and is also changed in age-related neurodegenerative conditions such as Alzheimer's disease in humans. Certain nGAPs are induced during long-term potentiation (LTP) and also during critical periods of song-learning and ocular dominance column formation in birds and cats, respectively. Recent evidence further supports the idea that functional synaptic modulation is often associated with remodeling of synaptic structures. These results suggest that neurotrophin-responsive nGAPs serve as molecular markers of neuronal plasticity during development and aging, and that the neuronal plasticity decreases, at least in certain neuronal circuits, in the aged brain and neurodegenerative diseases. Recent findings on the roles of stathmin and SCG10-related proteins in microtubule destabilization and its functional block by phosphorylation further support the importance of the SCG10 family proteins in neuronal cytoskeletal regulation, particularly as to microtubule dynamics. We summarize here a decade of research on SCG10 and its related molecules with special interests to brain aging and disease.

Infusion of nerve growth factor (NGF) into kitten visual cortex increases immunoreactivity for NGF, NGF receptors, and choline acetyltransferase in basal forebrain without affecting ocular dominance plasticity or column development

Intracerebroventricular or intracortical administration of nerve growth factor (NGF) has been shown to block or attenuate visual cortical plasticity in the rat. In cats and ferrets, the effects of exogenous NGF on development and plasticity of visual cortex have been reported to be small or nonexistent. To determine whether locally delivered NGF affects ocular dominance column formation or the plasticity produced by monocular deprivation in cats at the height of the critical period, we infused recombinant human NGF into the primary visual cortex of kittens using an implanted cannula minipump. NGF had no effect on the normal developmental segregation of geniculocortical afferents into ocular dominance columns as determined both physiologically and anatomically. The plasticity of binocular visual cortical responses induced by monocular deprivation was also normal in regions of immunohistochemically detectable NGF infusion, as measured using intrinsic signal optical imaging and single-unit electrophysiology. Immunohistochemical analysis of the basal forebrain regions of the same animals demonstrated that the NGF infused into cortex was biologically active, producing an increase in the number of NGF-, TrkA-, p75 NTR-, and choline acetyltransferase-positive neurons in basal forebrain nuclei in the hemisphere ipsilateral to the NGF minipump compared to the contralateral basal forebrain neurons. We conclude that NGF delivered locally to axon terminals of cholinergic basal forebrain neurons resulted in increases in protein expression at the cell body through retrograde signaling.

Early development of ocular dominance columns. Crowly JC, Katz LC. Science 2000;290:1321–1324.

The segregation of lateral geniculate nucleus (LGN) axons into ocular dominance columns is believed to involve a prolonged, activity-dependent sorting process. However, visualization of early postnatal ferret LGN axons by direct LGN tracer injections revealed segregated ocular dominance columns less than seven days after innervation of layer four. These early columns were unaffected by experimentally induced imbalances in retinal activity, implying that different mechanisms govern initial column formation and their modification during the subsequent critical period. Instead of activity-dependent plasticity, the authors propose that ocular dominance column formation relies on the targeting of distinct axonal populations to defined locales in cortical layer four. This study shows that ocular dominance columns in ferrets appear long before the columns can be modified by visual experience. The data presented suggests that neural activity from the eyes has little influence over the formation of the columns, questioning the earlier work of Hubel and Wiesel.—Hans E. Grossniklaus

Competition in the development of nerve connections: a review of models

The establishment and refinement of neural circuits involve both the formation of new connections and the elimination of already existing connections. Elimination of connections occurs, for example, in the development of mononeural innervation of muscle fibres and in the formation of ocular dominance columns in the visual cortex. The process that leads to the elimination of connections is often referred to as axonal or synaptic competition. Although the notion of competition is commonly used, the process is not well understood - with respect to, for example, the type of competition, what axons and synapses are competing for, and the role of electrical activity. This article reviews the types of competition that have been distinguished and the models of competition that have been proposed. Models of both the neuromuscular system and the visual system are described. For each of these models, the assumptions on which it is based, its mathematical structure, and the extent to which it is supported by the experimental data are evaluated. Special attention is given to the different modelling approaches and the role of electrical activity in competition.