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• We tested activation-inhibition hypothesis of distribution of attention in space. • Lateralised cue-target pairs presented to same or opposite visual field. • Handedness affected word processing in left hemisphere due to contralateral cueing. • Eye dominance associated with interhemispheric communication. • Interacting control systems contribute to information transfer between hemispheres. Dominance of the left hemisphere for language processing is a prominent feature of brain organisation. Whereas structural models clarify the functional asymmetry due to direct access to local language circuits, dynamic models propose functional states of intrahemispheric activation and interhemispheric inhibition that are coupled with attentional processes. Real word settings often require modulations of lateralised neural processing and further express individual heterogeneity. In this research, we tested left- and right-handers, and used a behavioural paradigm with presentation of lateralised cue-target pairs to the same or opposite visual field. We observed that handedness distinctly affected word processing in the left hemisphere following contralateral cueing. Moreover, left-hemispheric dominance strengthened for right-handers vs abolished for left-handers, influencing behavioural efficiency. In combination with eye dominance recordings, these data suggest that attentional biases guided the processing strategies of both groups and in turn their achievements. Therefore, hand and eye dominance are both essential factors with a functional role in directing the communication of visual information between both hemispheres. Overall, the findings underline the importance of interacting hand-eye control systems in contributing to interhemispheric patterns in the context of language processing. [ABSTRACT FROM AUTHOR]

• Activity dependent mechanisms that organize sensory projections are reviewed. • Optic flow-induced sequential activity exemplifies a spatiotemporal (ST) code. • Temporospatial (TS) transformations decode temporal codes into spatial maps. • STS transformations maintain topography by counteracting distorting effects. Sensory information in the brain is organized into spatial representations, including retinotopic, somatotopic, and tonotopic maps, as well as ocular dominance columns. The spatial representation of sensory inputs is thought to be a fundamental organizational principle that is important for information processing. Topographic maps are plastic throughout an animal's life, reflecting changes in development and aging of brain circuitry, changes in the periphery and sensory input, and changes in circuitry, for instance in response to experience and learning. Here, we review mechanisms underlying the role of activity in the development, stability and plasticity of topographic maps, focusing on recent work suggesting that the spatial information in the visual field, and the resulting spatiotemporal patterns of activity, provide instructive cues that organize visual projections. [ABSTRACT FROM AUTHOR]

• Neural maps convert complex environments into neural space in the brain. • Maps form by molecular guidance, competition, and activity-dependent plasticity. • Maps exhibit a nested structure that allows multiplexing of information. • Fine-scale heterogeneity enhances the computational capacity of the neural circuit. Neural maps are found ubiquitously in the brain, where they encode a wide range of behaviourally relevant features into neural space. Developmental studies have shown that animals devote a great deal of resources to establish consistently patterned organization in neural circuits throughout the nervous system, but what purposes maps serve beneath their often intricate appearance and composition is a topic of active debate and exploration. In this article, we review the general mechanisms of map formation, with a focus on the visual system, and then survey notable organizational properties of neural maps: the multiplexing of feature representations through a nested architecture, the interspersing of fine-scale heterogeneity within a globally smooth organization, and the complex integration at the microcircuit level that enables a high dimensionality of information encoding. Finally, we discuss the roles of maps in cortical functions, including input segregation, feature extraction and routing of circuit outputs for higher order processing, as well as the evolutionary basis for the properties we observe in neural maps. [ABSTRACT FROM AUTHOR]

The paper presents an adaptive WTA circuit where the firing of a neuron depends on input stimuli and the circuit self-adapts which in turn allow the loosing neuron to win. The CMOS based design have been simulated at 45 nm CMOS process which occupies less chip area (of about 12 × 25 μm2) and consume low power (about 124 nW). The design is stable as temperature coefficient is about 11.5 μV/°C and noise figure is about 11.6 nV/Hz. The self-adaption feature depends on the value of capacitor ratio which is equal to 50 fF. A visual brain feature called Binocular Rivalry (BR) has been demonstrated and explained using simulated results of proposed circuit. Three features of visual brain; superimposition of images obtained from two eyes; binocular rivalry when different images are presented to eyes: suppression and dominance of images, and neural adaption, have been explained using circuit simulation. The real time images processed using image processing illustrating BR features has also been implemented to circuit for real time operations. The time taken for neural adaption which causes switching of images in human brain when distinguish images are provided to eyes is about 0.2s, as demonstrated in circuit simulations using BR images. The proposed design can be implanted in machines (humanly robots) with which it can see, learn and self-adapt like a human visual brain. The circuit and the concept can also be implemented in devices used in assistive technology for helping visually disabled or less able persons. The Papers proposes a novel idea of CMOS based hardware for implementing BR features in machines. • Binocular Rivalry and its functionality. • Visualization and its effect with the help of image processing. • Relationship between CMOS circuits and images to get better understanding. • Emulate features of suppression and dominance and also neural adaptation. • The neural adaption leads to the concept of perceptual awareness. [ABSTRACT FROM AUTHOR]

• Why do we sometimes choose the right eye or the left eye randomly in studies?. • Are we making mistakes?. • Is there a difference due to retinal blood supply?. • Should we conduct studies on selected eyes instead of choosing randomly?. • We aimed to examine whether there is a difference in retinal blood supply. To determine the existence of differences in the retinal microcirculation of dominant and non-dominant eyes, as well as of interocular differences in macular microcirculation, using swept-source optical coherence tomography angiography (OCTA). In total, 122 eyes of 61 individuals were enrolled in this cross-sectional study. Measurements were taken using the swept-source optical coherence tomography Triton device (Topcon Corp, Tokyo, Japan) coupled with non-invasive OCTA technology. Macular perfusion parameters were assessed, including superficial vascular complex, vascular density of the deep vascular complex, vascular density of the choriocapillaris vascular complex, superficial foveal avascular zone and deep foveal avascular zone. Ocular dominance was determined among individuals with healthy eyes using the hole-in-the-card test. Ocular dominance was found in 68.9 % of right eyes and 31.1 % of left eyes. The mean age of the subjects was 34.45 ± 16.48 years (range: 18–73 years). We found that 16 (30.76 %) males and 22 (31.42 %) females had left-eye dominance (p > 0.05). None of the OCTA parameters differed between the eyes based on dominance (p > 0.05). Central macular thickness and sub-foveal choroidal thickness did not show significant differences (p > 0.05). When comparing interocular parameters, a significant difference was observed only in the inferior sector of the superficial vascular complex (p = 0.04). There was no significant difference in OCTA parameters between dominant and non-dominant eyes. There was no predominant interocular difference in the measurements. [ABSTRACT FROM AUTHOR]

Short-term monocular deprivation in normally sighted adult humans produces a transient shift of ocular dominance, boosting the deprived eye. This effect has been documented with both perceptual tests and through physiological recordings, but no previous study simultaneously measured physiological responses and the perceptual effects of deprivation. Here we propose an integrated experimental paradigm that combines binocular rivalry with pupillometry, to introduce an objective physiological index of ocular dominance plasticity, acquired concurrently with perceptual testing. Ten participants reported the perceptual dynamics of binocular rivalry, while we measured pupil diameter. Stimuli were a white and a black disk, each presented monocularly. Rivalry dynamics and pupil-size traces were compared before and after 2 h of monocular deprivation, achieved by applying a translucent patch over the dominant eye. Consistent with prior research, we observed that monocular deprivation boosts the deprived-eye signal and consequently increases ocular dominance. In line with previous studies, we also observed subtle but systematic modulations of pupil size that tracked alternations between exclusive dominance phases of the black or white disk. Following monocular deprivation, the amplitude of these pupil-size modulations increased, which is consistent with the post-deprivation boost of the deprived eye and the increase of ocular dominance. This provides evidence that deprivation impacts the effective strength of monocular visual stimuli, coherently affecting perceptual reports and the automatic and unconscious regulation of pupil diameter. Our results show that a combined paradigm of binocular rivalry and pupillometry gives new insights into the physiological mechanisms underlying deprivation effects. [ABSTRACT FROM AUTHOR]

[Display omitted] Brain-specific loss of a microtubule-binding protein collapsin response mediator protein-2 (CRMP2) in the mouse recapitulates many schizophrenia-like behaviors of human patients, possibly resulting from associated developmental deficits in neuronal differentiation, path-finding, and synapse formation. However, it is still unclear how the Crmp2 loss affects neuronal circuit function and plasticity. By conducting in vivo and ex vivo electrophysiological recording in the mouse primary visual cortex (V1), we reveal that CRMP2 exerts a key regulation on the timing of postnatal critical period (CP) for experience-dependent circuit plasticity of sensory cortex. In the developing V1, the Crmp2 deficiency induces not only a delayed maturation of visual tuning functions but also a precocious CP for visual input-induced ocular dominance plasticity and its induction activity – coincident binocular inputs right after eye-opening. Mechanistically, the Crmp2 deficiency accelerates the maturation process of cortical inhibitory transmission and subsequently promotes an early emergence of balanced excitatory-inhibitory cortical circuits during the postnatal development. Moreover, the precocious CP plasticity results in deteriorated binocular depth perception in adulthood. Thus, these findings suggest that the Crmp2 deficiency dysregulates the timing of CP for experience-dependent refinement of circuit connections and further leads to impaired sensory perception in later life. [ABSTRACT FROM AUTHOR]

Brief periods of monocular deprivation significantly modify binocular visual processing. For example, patching one eye for a few hours alters the inter-ocular balance, with the previously patched eye becoming dominant once the patch is removed. However, the contribution of higher-level visual processing to this phenomenon is still unclear. Here, we compared changes in sensory eye dominance produced by three types of monocular manipulations in adult participants with normal binocular vision. One eye was covered for 150 min using either an opaque patch, a diffusing lens, or a prism that inverted the image. All three manipulations altered dominance duration and predominance during binocular rivalry (BR) in favour of the treated eye and the time courses of the changes were similar. These results indicate that modifications of luminance or contrast are not strictly necessary to drive shifts in eye dominance, as both were unaltered in the prism condition. Next, we found that shifts in eye dominance were dependent on attentional demands during the monocular treatment period, providing support for the role of attentional eye selection in modulating eye dominance. Finally, we found relatively rapid build-up of the ocular dominance shift after the onset of monocular treatment. Taken together, our results suggest that modifications to monocular input alter inter-ocular balance via selective attentional mechanisms that bias output towards the deprived eye. Eye-based attention may play an important role in conditions where normal input to one eye is disrupted, such as childhood amblyopia. [ABSTRACT FROM AUTHOR]

Short term monocular deprivation modulates ocular dominance, such that the previously deprived eye's contribution to the binocular percept increases, supposedly as a result of changes in contrast-gain. Therefore, the processing time of the previously patched eye would be expected to speed up as a result of an increase in contrast gain. In order to test this hypothesis, this study examines the effects of short-term monocular deprivation on interocular synchronicity. The present study uses a paradigm based on the Pulfrich phenomenon. The stimulus used for testing consists of elements defining a cylinder rotating in depth, that allows measurement of any interocular delay. The interocular delay was measured at baseline before patching and at outcome, after one hour of monocular deprivation with an opaque or translucent patch. Contrary to expectations, short-term monocular deprivation induces an interocular delay, albeit not always significant, in the previously patched eye. The amplitude of this effect is larger with opaque patching compared to translucent patching. These results are the first report of a non-beneficial effect - i.e. a slowing down in the processing time of the previously patched-eye. They indicate that the plasticity effects of monocular deprivation are not exclusively mediated by contrast gain mechanisms and that light adaptation mechanisms might also be involved in the plasticity resulting from short-term monocular deprivation. [ABSTRACT FROM AUTHOR]

Defocus blur and spatial attention both act on our ability to see clearly over time. However, it is currently unknown how these two factors interact because studies on spatial resolution only focused on the separate effects of attention and defocus blurs. In this study, eleven participants performed a resolution acuity task along the diagonal 135˚/315˚ with horizontal, at 8˚ eccentricity for clear and blurred Landolt C images under various manipulations of covert endogenous attention. All the conditions were interleaved and viewed binocularly on a visual display. We observed that attention not just improves the resolution of clear stimuli, but also modulates the resolution of defocused stimuli for compensating the loss of resolution caused by retinal blur. Our results show, however, that as the degree of attention decreases, the differences between clear and blurred images largely diminish, thus limiting the benefit of an image quality enhancement. It also appeared that attention tends to enhance the resolution of clear targets more than blurred targets, suggesting potential variations in the gain of vision correction with the level of attention. This demonstrates that the interaction between spatial attention and defocus blur can play a role in the way we see things. In view of these findings, the development of adaptive interventions, which adjust the eye's defocus to attention, may hold promise. [ABSTRACT FROM AUTHOR]

How do V1 cells respond to, adapt to, and combine signals from the two eyes? We tested a simple functional model that has monocular and binocular stages of divisive contrast gain control (CGC) that sit before, and after, binocular summation respectively. Interocular suppression (IOS) was another potential influence on contrast gain. Howarth, Vorobyov & Sengpiel (2009, Cerebral Cortex, 19, 1835-1843) studied contrast adaptation and interocular transfer in cat V1 cells. In our re-analysis we found that ocular dominance (OD) and contrast adaptation at a fixed test contrast were well described by a re-scaling of the unadapted orientation tuning curve - a simple change in response gain. We compared six variants of the basic model, and one model fitted the gain data notably better than the others did. When the dominant eye was tested, adaptation reduced cell response gain more when that eye was adapted than when the other eye was adapted. But when the non-dominant eye was tested, adapting either eye gave about the same reduction in overall gain, and there was an interaction between OD and adapting eye that was well described by the best-fitting model. Two key features of this model are that signals driving IOS arise 'early', before attenuation due to OD, while suppressive CGC signals are 'late' and so affected by OD. We show that late CGC confers a functional advantage: it yields partial compensation for OD, which should reduce ocular imbalance at the input to binocular summation, and improve the cell's sensitivity to variation in stereo disparity. [ABSTRACT FROM AUTHOR]

• Kv3.1 potassium channels regulate cortical fast-spiking behavior postnatally. • Visual cortical receptive field properties develop normally in the absence of Kv3.1. • Sensory plasticity is slowed but critical period timing is normal without Kv3.1. • Rate of plasticity reflects Kv3.1 gene dosage controlling prolonged spiking. • Diazepam effectively rescues Kv3.1 deficiency of relevance to mental disorders. Experience-dependent plasticity within visual cortex is controlled by postnatal maturation of inhibitory circuits, which are both morphologically diverse and precisely connected. Gene-targeted disruption of the voltage-dependent potassium channel K v 3.1 broadens action potentials and reduces net inhibitory function of parvalbumin (PV)-positive GABA subtypes within the neocortex. In mice lacking K v 3.1, the rate of input loss from an eye deprived of vision was slowed two-fold, despite otherwise normal critical period timecourse and receptive field properties. Rapid ocular dominance plasticity was restored by local or systemic enhancement of GABAergic transmission with acute benzodiazepine infusion. Diazepam instead exacerbated a global suppression of slow-wave oscillations during sleep described previously in these mutant mice, which therefore did not account for the rescued plasticity. Rapid ocular dominance shifts closely reflected K v 3.1 gene dosage that prevented prolonged spike discharge of their target pyramidal cells in vivo or the spike amplitude decrement of fast-spiking cells during bouts of high-frequency firing in vitro. Late postnatal expression of this unique channel in fast-spiking interneurons thus subtly regulates the speed of critical period plasticity with implications for mental illnesses. [ABSTRACT FROM AUTHOR]

• Using natural-scene-based steady-state visual evoked potential (SSVEP) technique we measured the ocular-specific signals. • Two hours of monocular deprivation (MD) boosted the neural gain for the deprived eye. • Neural gain for the deprived eye increased progressively during the MD. • The effects of short-term MD can manifest when viewing natural scenes. • Our method is powerful in tracking neural responses to natural adapting environment. Ocular dominance plasticity beyond the critical period has been demonstrated in adult humans in recent investigations of short-term monocular deprivation (MD). To our knowledge, all previous research adopted non-natural synthetic stimuli in testing perceptual ocular dominance before and after the MD. However, it is recognized that complex natural stimuli may engage cortical mechanisms substantially different from simple synthetic stimuli. Therefore, it remains largely unknown whether reshaping of ocular dominance following MD could be observed during perception of natural scene stimuli without conspicuous interocular competition. Here we used the steady-state visual evoked potential (SSVEP) technique to measure the ocular-specific neural effects of MD with natural scene stimuli where the two eyes' images were tagged with different frequencies. Two hours of MD boosted the neural gain for the deprived eye. During the course of MD, the SSVEP amplitude ratio for the deprived eye compared to the non-deprived eye increased significantly over time, indicating a progressive increase of neural gain for the deprived eye. These findings demonstrate that the effects of short-term MD can manifest when viewing natural scenes, providing a natural case in support of the homeostatic compensation theory of MD. Our work also indicates that the technique of natural-scene-based SSVEP could be particularly useful for future work exploring the neural dynamics during adaptation to natural stimuli. [ABSTRACT FROM AUTHOR]

We propose a model for synaptic plasticity based on a calcium signaling cascade. The model simplifies the full signaling pathways from a calcium influx to the phosphorylation (potentiation) and dephosphorylation (depression) of glutamate receptors that are gated by fictive C 1 and C 2 catalysts, respectively. This model is based on tangible chemical reactions, including fictive catalysts, for long-term plasticity rather than the conceptual theories commonplace in various models, such as preset thresholds of calcium concentration. Our simplified model successfully reproduced the experimental synaptic plasticity induced by different protocols such as (i) a synchronous pairing protocol and (ii) correlated presynaptic and postsynaptic action potentials (APs). Further, the ocular dominance plasticity (or the experimental verification of the celebrated Bienenstock—Cooper—Munro theory) was reproduced by two model synapses that compete by means of back-propagating APs (bAPs). The key to this competition is synapse-specific bAPs with reference to bAP-boosting on the physiological grounds. [ABSTRACT FROM AUTHOR]

• Combine binocular adding and subtracting channels with binocularity theory. • Dynamic weight is used for binocular fusion with the energy map. • Natural scene statistics feature is extracted to describe stereo image quality. • Achieve the balance between accuracy and timeliness. • The proposed algorithm has high performance on public datasets. Stereoscopic image quality evaluation is extremely significance as a performance evaluator of modern 3D display technology. Due to the complexity of human visual system (HVS) and the incomprehensive study of stereoscopic perception of human eyes, stereoscopic image quality assessment (SIQA) is still a challenging task. In this paper, combining binocular characteristics, we propose an efficient no-reference stereoscopic image quality assessment according to binocular adding and subtracting channels. Distinguished from other SIQA methods, which pay attention to complex binocular visual properties, the visual information which is closely bound up with image distortion from adding and subtracting channels to describe ocular dominance (alternate name binocularity) is proposed. To estimate the contribution of each channel in SIQA, a dynamic weighting system is proposed for binocular fusion according to local energy. Furthermore, quality awareness features based on multi-scale and multi-orientation are extracted to describe visual degradation. Comparing with existing methods, experimental results on public 3D image databases demonstrate the proposed framework achieves high consistent with the subjective quality scores. [ABSTRACT FROM AUTHOR]

The competitive and inhibitory interactions between the two eyes' images are a pervasive aspect of binocular vision. Over the last decade, our understanding of the neural processes underpinning binocular rivalry (BR) and continuous flash suppression (CFS) has increased substantially, but we still have little understanding of the relationship between these two effects and their variation in the general population. Studies that pool data across individuals and eyes risk masking substantial variations in binocular vision that exist in the general population. To investigate this issue we compared the depth of inter-ocular suppression evoked by BR with that elicited by CFS, in a group (N = 25) of visually normal individuals. A noise pattern (either static for BR or dynamic for CFS) was presented to one eye and its suppressive influence on a probe grating presented simultaneously to the other eye was measured. We found substantial individual differences in the magnitude of suppression (a 10-fold variation in probe detection threshold) evoked by each task, but performance on BR was a significant predictor of performance on the CFS task. However many individuals showed marked asymmetries between the two eyes' ability to detect a suppressed target, that were not necessarily the same for the two tasks. There was a tendency for the magnitude of the asymmetry to increase as the refresh rate of the dynamic noise increased. The results suggest a common underlying mechanism is likely to be responsible, at least in part, for driving inter-ocular suppression under BR and CFS. The marked asymmetries in inter-ocular suppression at higher noise refresh rates, may be indicative of a difference in temporal processing between the eyes. [ABSTRACT FROM AUTHOR]

Short-term monocular deprivation strengthens the contribution of the deprived eye to binocular vision. This change has been observed in adults with normal vision or amblyopia. The change in ocular dominance is transient and recovers over approximately one hour. This shift has been measured with various visual tasks, including binocular rivalry and binocular combination. We investigated whether the ocular dominance shift could be accumulated across multiple periods of monocular deprivation over consecutive days. We used a binocular phase combination task to measure the shift in eye dominance. We patched the dominant eye of ten adults with normal vision for two hours across five consecutive days. Our results show no cumulative effect after repeated sessions of short-term monocular deprivation. [ABSTRACT FROM AUTHOR]

The ocular dominance shift observed after short-term monocular deprivation is a widely used measure of visual homeostatic plasticity in adult humans. Binocular rivalry and binocular combination techniques are used interchangeably to characterize homeostatic plasticity, sometimes leading to contradictory results. Here we directly compare the effect of short-term monocular deprivation on ocular dominance measured by either binocular rivalry or binocular combination and its dependence on the duration of deprivation (15 or 120 min) in the same group of participants. Our results show that both binocular rivalry and binocular combination provide reliable estimates of ocular dominance, which are strongly correlated across techniques both before and after deprivation. Moreover, while 15 min of monocular deprivation induce a larger shift of ocular dominance when measured using binocular combination compared to binocular rivalry, for both techniques, the shift in ocular dominance exhibits a strong dependence on the duration of monocular deprivation, with longer deprivation inducing a larger and longer-lasting shift in ocular dominance. Taken together, our results indicate that both binocular rivalry and binocular combination offer very consistent and reliable measurements of both ocular dominance and the effect short-term monocular deprivation. [ABSTRACT FROM AUTHOR]

Highlights • Whisker deprivation restores "adult-like" ocular dominance plasticity in the primary visual cortex of fully adult mice. • This is accompanied with reduced GABA levels in the visual cortex. • However, re-increasing GABA levels with diazepam does not abolish reactivated ocular dominance plasticity. • Strikingly, this treatment changes the signature of visual cortex plasticity from "adult-like" to "juvenile-like". • This cross-modally restored "juvenile-like" plasticity is NMDA receptor dependent. Abstract In juvenile and young adult mice monocular deprivation (MD) shifts the ocular dominance (OD) of binocular neurons in the primary visual cortex (V1) away from the deprived eye. However, OD plasticity is completely absent in mice older than 110 days, but can be reactivated by treatments which decrease GABA levels in V1. Typically, these OD shifts can be prevented by increasing GABAergic transmission with diazepam. We could recently demonstrate that both bilateral whisker and auditory deprivation (WD, AD), can also restore OD plasticity in mice older than 110 days, since MD for 7 days in WD mice caused a potentiation of V1 input through the ipsilateral (open) eye, the characteristic feature of OD plasticity of "young adult" mice. Here we examined whether WD for 7 days also decreases GABA levels. For this, we performed post mortem HPLC analysis of V1 tissue. Indeed, we found that WD significantly decreased GABA levels in V1. Surprisingly, enhancing GABAergic inhibition by diazepam did not abolish OD shifts in WD mice, as revealed by repeated intrinsic signal imaging. On the contrary, this treatment led to a depression of V1 input through the previously closed contralateral eye, the characteristic signature of OD plasticity in juvenile mice during the critical period. Interestingly, the same result was obtained after AD. Taken together, these results suggest that cross-modally restored OD plasticity does not only depend on reduction of GABA levels in V1, but also requires other, so far unknown mechanisms. [ABSTRACT FROM AUTHOR]

The saccadic system presents asymmetries. Notably, saccadic peak velocity is higher in temporal than in nasal saccades, and in centripetal than in centrifugal saccades. It has already been shown that eye dominance strength relates to naso-temporal asymmetry, but its links with centripetal-centrifugal asymmetry has never been tested. The current study tested both naso-temporal and centripetal-centrifugal asymmetries simultaneously to provide a finer and continuous measure of eye dominance strength. We asked 63 participants to make centripetal and centrifugal saccades from five different locations. Analysis of saccadic peak velocity shows that eye dominance strength modulates every saccadic asymmetry tested. For the first time, we propose a graduated measure of eye dominance strength on a continuum model. The model ranges from weak to very strong eye dominance. Weak eye dominance corresponds to increased saccadic asymmetries whereas strong eye dominance corresponds to no asymmetries. Furthermore, our results provide new insights into the neurophysiological origins of saccadic asymmetries. Modulation of both naso-temporal and centripetal-centrifugal asymmetries by eye dominance strength supports the involvement of V1 in these saccadic asymmetries. [ABSTRACT FROM AUTHOR]

Coupled Generative Adversarial Network (CoGAN) was recently introduced in order to model a joint distribution of a multi modal dataset. The CoGAN model lacks the capability to handle noisy data as well as it is computationally expensive and inefficient for practical applications such as cross-domain image transformation. In this paper, we propose a new method, named the Coupled Generative Adversarial Stacked Auto-encoder (CoGASA), to directly transfer data from one domain to another domain with robustness to noise in the input data as well to as reduce the computation time. We evaluate the proposed model using MNIST and the Large-scale CelebFaces Attributes (CelebA) datasets, and the results demonstrate a highly competitive performance. Our proposed models can easily transfer images into the target domain with minimal effort. [ABSTRACT FROM AUTHOR]

Normal binocular vision emerges from the combination of neural signals arising within separate monocular pathways. It is natural to wonder whether both eyes contribute equally to the unified cyclopean impression we ordinarily experience. Binocular rivalry, which occurs when the inputs to the two eyes are markedly different, affords a useful means for quantifying the balance of influence exerted by the eyes (called sensory eye dominance, SED) and for relating that degree of balance to other aspects of binocular visual function. However, the precise ways in which binocular rivalry dynamics change when the eyes are unbalanced remain uncharted. Relying on widespread individual variability in the relative predominance of the two eyes as demonstrated in previous studies, we found that an observer's overall tendency to see one eye more than the other was driven both by differences in the relative duration and frequency of instances of that eye's perceptual dominance. Specifically, larger imbalances between the eyes were associated with longer and more frequent periods of exclusive dominance for the stronger eye. Increases in occurrences of dominant eye percepts were mediated in part by a tendency to experience "return transitions" to the predominant eye - that is, observers often experienced sequential exclusive percepts of the dominant eye's image with an intervening mixed percept. Together, these results indicate that the often-observed imbalances between the eyes during binocular rivalry reflect true differences in sensory processing, a finding that has implications for our understanding of the mechanisms underlying binocular vision in general. [ABSTRACT FROM AUTHOR]

The integration of hypotheses from Eye-Movement Desensitization and Reprocessing (EMDR) and Saccade Induced Retrieval Enhancement (SIRE), both of which have been met with considerable skepticism, may lead to significant gains in both domains. Cognitive accounts of EMDR, the orienting response (OR) and working memory (WM) hypotheses, and of SIRE, the interhemispheric interaction (IHI) and the top-down attentional control (TDAC) hypotheses, are discussed. The accounts show several blind spots and frictions, for instance, on re-imagining during EMs, on hemispheric lateralization, and on emotional influences of eye movements. The failure to consider these factors across and within domains may well explain the many disparate findings. This perspective aims to remove the artificial separation and seeks a theoretical integration of the domains. It combines elements of OR and TDAC into a new dopaminergic regulation hypothesis while replacing affective (i.e., positive vs. negative) by motivational mechanisms (i.e., fostering approach and recoding). EMs are posited to result in a short-latency, targeted release of dopamine, which is the central neuromodulator in approach tendencies. According to this hypothesis, the largest effects are obtained in individuals with collateralized eye dominance and dopamine dominance. Concrete suggestions are made to improve research conditions and therapeutic efficacy. • The perspective synthesizes hypotheses from EMDR and SIRE into the dopaminergic regulation hypothesis. • Eye movements elicit a dopamine signal from Superior Colliculus to Substantia Nigra. • The signal causes approach to, enhancement, and regulation of negative memories. • Eye movements are most effective with collateralized eye and dopamine dominance. • Optimizations for EMDR and SIRE are suggested. [ABSTRACT FROM AUTHOR]

The visual system can regulate its sensitivity depending on the prevailing contrast conditions. This is known as contrast adaptation and reflects contrast gain changes at different stages along the visual pathway. Recently, it has been shown that depriving an eye of visual stimulation for a short period of time can lead to neuroplastic changes in ocular dominance as the result of homeostatic changes in contrast gain. Here we examine, on the basis of previously published results, whether the neuroplastic ocular dominance changes are just manifestation of the mechanism responsible for contrast adaptation. The evidence suggests that these two visual processes are separate and do not have a common neural substrate. [ABSTRACT FROM AUTHOR]

Exposure to chronic stress following stroke has been shown, both clinically and pre-clinically, to impact negatively on the recovery process. While this phenomenon is well established, the specific mechanisms involved have remained largely unexplored. One obvious signaling pathway through which chronic stress may impact on the recovery process is via corticosterone, and its effects on microglial activity and vascular remodeling. In the current study, we were interested in examining how orally delivered corticosterone at a stress-like concentration impacted on microglial activity and vascular remodeling after stroke. We identified that corticosterone administration for two weeks following stroke significantly increased tissue loss and decreased the weight of the spleen and thymus. We also identified that corticosterone administration significantly altered the expression of the key microglial complement receptor, CD11b after stroke. Corticosterone administration did not alter the expression of the vessel basement membrane protein, Collagen IV after stroke. Together, these results suggest that corticosterone is likely to represent only one of the major stress signals responsible for driving the negative impacts of chronic stress on recovery. [ABSTRACT FROM AUTHOR]

Ocular dominance has been extensively studied, often with the goal to understand neuroplasticity, which is a key characteristic within the critical period. Recent work on monocular deprivation, however, demonstrates residual neuroplasticity in the adult visual cortex. After deprivation of patterned inputs by monocular patching, the patched eye becomes more dominant. Since patching blocks both the Fourier amplitude and phase information of the input image, it remains unclear whether deprivation of the Fourier phase information alone is able to reshape eye dominance. Here, for the first time, we show that removing of the phase regularity without changing the amplitude spectra of the input image induced a shift of eye dominance toward the deprived eye, but only if the eye dominance was measured with a binocular rivalry task rather than an interocular phase combination task. These different results indicate that the two measurements are supported by different mechanisms. Phase integration requires the fusion of monocular images. The fused percept highly relies on the weights of the phase-sensitive monocular neurons that respond to the two monocular images. However, binocular rivalry reflects the result of direct interocular competition that strongly weights the contour information transmitted along each monocular pathway. Monocular phase deprivation may not change the weights in the integration (fusion) mechanism much, but alters the balance in the rivalry (competition) mechanism. Our work suggests that ocular dominance plasticity may occur at different stages of visual processing, and that homeostatic compensation also occurs for the lack of phase regularity in natural scenes. [ABSTRACT FROM AUTHOR]

Unlike handedness, sighting eye dominance, defined as the eye unconsciously chosen when performing monocular tasks, is very rarely considered in studies investigating cerebral asymmetries. We previously showed that sighting eye dominance has an influence on visually triggered manual action with shorter reaction time (RT) when the stimulus appears in the contralateral visual hemifield with respect to the dominant eye (Chaumillon et al. 2014). We also suggested that eye dominance may be more or less pronounced depending on individuals and that this eye dominance strength could be evaluated through saccadic peak velocity analysis in binocular recordings (Vergilino-Perez et al. 2012). Based on these two previous studies, we further examine here whether the strength of the eye dominance can modulate the influence of this lateralization on manual reaction time. Results revealed that participants categorized as having a strong eye dominance, but not those categorized as having a weak eye dominance, exhibited the difference in RT between the two visual hemifields. This present study reinforces that the analysis of saccade peak velocity in binocular recordings provides an effective tool to better categorize the eye dominance. It also shows that the influence of eye dominance in visuo-motor tasks depends on its strength. Our study also highlights the importance of considering the strength of eye dominance in future studies dealing with brain lateralization. [ABSTRACT FROM AUTHOR]

During the visual critical period (CP), sensory experience refines the structure and function of visual circuits. The basis of this plasticity was long thought to be limited to cortical circuits, but recently described thalamic plasticity challenges this dogma and demonstrates greater complexity underlying visual plasticity. Yet how visual experience modulates thalamic neurons or how the thalamus modulates CP timing is incompletely understood. Using a larval zebrafish, thalamus-centric ocular dominance model, we show functional changes in the thalamus and a role of inhibitory signaling to establish CP timing using a combination of functional imaging, optogenetics, and pharmacology. Hemisphere-specific changes in genetically defined thalamic neurons correlate with changes in visuomotor behavior, establishing a role of thalamic plasticity in modulating motor performance. Our work demonstrates that visual plasticity is broadly conserved and that visual experience leads to neuron-level functional changes in the thalamus that require inhibitory signaling to establish critical period timing. [Display omitted] • Ocular dominance plasticity-like changes occur in larval zebrafish • Asymmetric visual experience impacts behavior during a visual critical period • Functional changes in the thalamus correlate with visual experience and behavior • Inhibitory signaling is necessary for visually mediated changes in the thalamus Critical periods are developmental windows of heightened plasticity when sensory experience impacts brain function. Hageter et al. identify a zebrafish visual critical period, where visual experience produces neuronal and behavioral performance changes, dependent on inhibitory signaling. This work provides a model for neuron-level study of sensory-dependent plasticity. [ABSTRACT FROM AUTHOR]

Nitric oxide (NO) has been long recognized as an important modulator of neural plasticity, but characterization of the molecular mechanisms involved - specially the guanylyl cyclase-independent ones - has been challenging. There is evidence that NO could modify BDNF-TRKB signaling, a key mediator of neuronal plasticity. However, the mechanism underlying the interplay of NO and TRKB remains unclear. Here we show that NO induces nitration of the tyrosine 816 in the TRKB receptor in vivo and in vitro , and that post-translational modification inhibits TRKB phosphorylation and binding of phospholipase Cγ1 (PLCγ1) to this same tyrosine residue. Additionally, nitration triggers clathrin-dependent endocytosis of TRKB through the adaptor protein AP-2 and ubiquitination, thereby increasing translocation of TRKB away from the neuronal surface and directing it towards lysosomal degradation. Accordingly, inhibition of nitric oxide increases TRKB phosphorylation and TRKB-dependent neurite branching in neuronal cultures. In vivo , chronic inhibition of neuronal nitric oxide synthase (nNOS) dramatically reduced TRKB nitration and facilitated TRKB signaling in the visual cortex, and promoted a shift in ocular dominance upon monocular deprivation - an indicator of increased plasticity. Altogether, our data describe and characterize a new molecular brake on plasticity, namely nitration of TRKB receptors. [Display omitted] • nNOS-derived NO induces nitration of TRKB at Y816. • Nitration blocks binding of PLCg to TRKB. • Nitration triggers TRKB endocytosis and degradation, and impairs BDNF signaling. • nNOS inhibition decreases nitro- and increases phospho-TRKB, and increases plasticity. [ABSTRACT FROM AUTHOR]

Experiments on the adult visual cortex of cats, ferrets and monkeys have revealed organized spatial relationships between multiple feature maps which can also be reproduced by the Kohonen and elastic net self-organization models. However, attempts to apply these models to simulate the temporal kinetics of monocular deprivation (MD) during the critical period, and their effects on the spatial arrangement of feature maps, have led to conflicting results. In this study, we performed MD and chronic imaging in the ferret visual cortex during the critical period of ocular dominance (OD) plasticity. We also used the Kohonen model to simulate the effects of MD on OD and orientation map development. Both the experiments and simulations demonstrated two general parameter-insensitive findings. Specifically, our first finding demonstrated that the OD index shift resulting from MD, and its subsequent recovery during binocular vision (BV), were both nonlinear, with a significantly stronger shift occurring during the initial period. Meanwhile, spatial reorganization of feature maps led to globally unchanged but locally shifted map patterns. In detail, we found that the periodicity of OD and orientation maps remained unchanged during, and after, deprivation. Relationships between OD and orientation maps remained similar but were significantly weakened due to OD border shifts. These results indicate that orthogonal gradient relationships between maps may be preset and are only mildly modifiable during the critical period. The Kohonen model was able to reproduce these experimental results, hence its role is further extended to the description of cortical feature map dynamics during development. [ABSTRACT FROM AUTHOR]

The input from the two eyes is combined in the brain. In this combination, the relative strength of the input from each eye is determined by the ocular dominance. Recent work has shown that this dominance can be temporarily shifted. Covering one eye with an eye patch for a few hours makes its contribution stronger. It has been proposed that this shift can be enhanced by exercise. Here, we test this hypothesis using a dichoptic surround suppression task, and with exercise performed according to American College of Sport Medicine guidelines. We measured detection thresholds for patches of sinusoidal grating shown to one eye. When an annular mask grating was shown simultaneously to the other eye, thresholds were elevated. The difference in the elevation found in each eye is our measure of relative eye dominance. We made these measurements before and after 120 min of monocular deprivation (with an eye patch). In the control condition, subjects rested during this time. For the exercise condition, 30 min of exercise were performed at the beginning of the patching period. This was followed by 90 min of rest. We find that patching results in a shift in ocular dominance that can be measured using dichoptic surround suppression. However, we find no effect of exercise on the magnitude of this shift. We further performed a meta-analysis on the four studies that have examined the effects of exercise on the dominance shift. Looking across these studies, we find no evidence for such an effect. [ABSTRACT FROM AUTHOR]

Li and Atick (Network: Computation in Neural Systems 5 (1994) 157-174) presented a theory of efficient binocular encoding that explains a number of experimental findings. A binocular neuron is conventionally described in terms of two channels: the left and right eyes. Li and Atick's theory instead describes the neuron in terms of two alternative channels: the binocular sum and difference. The advantage of the latter description is that, unlike the left and right eye channels, the summation and differencing channels are usually uncorrelated; this means that each channel can be optimised independently of the other. The theory shows how to derive optimal receptive fields for the binocular summation and differencing channels; from these, it is easy to derive the neuron's optimal left and right eye receptive fields. The functional reality of the summation and differencing channels is demonstrated by a series of adaptation studies that confirm some counterintuitive predictions of the theory. Here we provide an accessible account of the theory, and review the evidence supporting it. [ABSTRACT FROM AUTHOR]

How the brain combines the neural representations of features that comprise an object in order to activate a coherent object memory is poorly understood, especially when the features are presented in different modalities (visual vs. auditory) and domains (verbal vs. nonverbal). We examined this question using three versions of a modified Semantic Object Retrieval Test, where object memory was probed by a feature presented as a written word, a spoken word, or a picture, followed by a second feature always presented as a visual word. Participants indicated whether each feature pair elicited retrieval of the memory of a particular object. Sixteen subjects completed one of the three versions (N = 48 in total) while their EEG were recorded simultaneously. We analyzed EEG data in four separate frequency bands (delta: 1–4 Hz, theta: 4–7 Hz; alpha: 8–12 Hz; beta: 13–19 Hz) using a multivariate data-driven approach. We found that alpha power time-locked to response was modulated by both cross-modality (visual vs. auditory) and cross-domain (verbal vs. nonverbal) probing of semantic object memory. In addition, retrieval trials showed greater changes in all frequency bands compared to non-retrieval trials across all stimulus types in both response-locked and stimulus-locked analyses, suggesting dissociable neural subcomponents involved in binding object features to retrieve a memory. We conclude that these findings support both modality/domain-dependent and modality/domain-independent mechanisms during semantic object memory retrieval. [ABSTRACT FROM AUTHOR]

In standard cage (SC)-raised mice, ocular dominance (OD) plasticity of the primary visual cortex (V1) induced by monocular deprivation (MD) is maximal in juveniles, declines in adults, and is absent beyond postnatal day (PD) 110. Raising mice in an enriched environment (EE) preserved a juvenile-like OD plasticity after 7 days of MD until at least PD196, mediated by reductions of deprived eye responses in V1. Whether the sensitive phase for OD plasticity can be prolonged into older age and whether long-term EE modifies visual abilities was not yet known. Here, we demonstrate that EE raising enables lifelong OD plasticity. In contrast to PD200 EE-mice, the preserved OD shift in both >PD400 and >PD700 EE-mice was mediated by increases in open eye responses in V1 (adult OD plasticity). When SC-mice were transferred to EE after PD110, OD plasticity was restored until PD922. Moreover, visual abilities tested by both optomotry and the visual water task and interindividual variability were not different between PD700 SC- and EE-mice. Taken together, EE raising enabled a lifelong OD plasticity but did not affect basic visual performance. [ABSTRACT FROM AUTHOR]

Maturation of cortical inhibition just after eye opening is a necessary precedent for the emergence of competitive, experience-dependent ocular dominance plasticity in the visual cortex. What inhibition is doing in this context, though, is not clear. Here I outline new hypotheses on the roles of somatic and dendritic inhibition in the opening and closure of critical periods, and their roles in the competitive processes therein. [ABSTRACT FROM AUTHOR]

Manipulation of the trunk midline has been shown to improve visuospatial performance in patients with unilateral visual neglect. The goal of the present study was to disentangle motor and perceptual components of egocentric midline manipulations and to investigate the contribution of individual hand preference. Two versions of visual temporal order judgment (TOJ) tasks were tested in healthy right- and left-handed subjects while trunk rotation was varied. In the congruent version, subjects were required to execute a saccade to the first of two horizontal stimuli presented with different stimulus onset asynchronies (SOA). In the incongruent version, subjects were required to perform a vertical saccade to a pre-learned color target, thereby dissociating motor response from the perceptual stimulus location. The main findings of this study are a trunk rotation and response direction specific impact on temporal judgments in form of a prior entry bias for right hemifield stimuli during rightward trunk rotation, but only in the congruent task. This trunk rotation-induced spatial bias was most pronounced in left-handed participants but had the same sign in the right-handed group. Results suggest that egocentric midline shifts in healthy subjects induce a spatially-specific motor, but not a perceptual, bias and underline the importance of taking individual differences in functional laterality such as handedness and mode of perceptual report into account when evaluating effects of trunk rotation in either healthy subjects or neurological patients. [ABSTRACT FROM AUTHOR]

A number of previous reports have suggested that the processing of second-order stimuli by the amblyopic eye (AE) is defective and that the fellow non-amblyopic eye (NAE) also exhibits an anomaly. Second-order stimuli involve extra-striate as well as striate processing and provide a means of exploring the extent of the cortical anomaly in amblyopia using psychophysics. We use a range of different second-order stimuli to investigate how general the deficit is for detecting second-order stimuli in adult amblyopes. We compare these results to our previously published adult normative database using the same stimuli and approach to determine the extent to which the detection of these stimuli is defective for both amblyopic and non-amblyopic eye stimulation. The results suggest that the second-order deficit affects a wide range of second-order stimuli, and by implication a large area of extra-striate cortex, both dorsally and ventrally. The NAE is affected only in motion-defined form judgments, suggesting a difference in the degree to which ocular dominance is disrupted in dorsal and ventral extra-striate regions. [ABSTRACT FROM AUTHOR]

Amblyopia is a developmental disorder resulting in poor vision in one eye. The mechanism by which input to the affected eye is prevented from reaching the level of awareness remains poorly understood. We recorded simultaneously from large populations of neurons in the supragranular layers of areas V1 and V2 in 6 macaques that were made amblyopic by rearing with artificial strabismus or anisometropia, and 1 normally reared control. In agreement with previous reports, we found that cortical neuronal signals driven through the amblyopic eyes were reduced, and that cortical neurons were on average more strongly driven by the non-amblyopic than by the amblyopic eyes. We analyzed multiunit recordings using standard population decoding methods, and found that visual signals from the amblyopic eye, while weakened, were not degraded enough to explain the behavioral deficits. Thus additional losses must arise in downstream processing. We tested the idea that under monocular viewing conditions, only signals from neurons dominated by – rather than driven by – the open eye might be used. This reduces the proportion of neuronal signals available from the amblyopic eye, and amplifies the interocular difference observed at the level of single neurons. We conclude that amblyopia might arise in part from degradation in the neuronal signals from the amblyopic eye, and in part from a reduction in the number of signals processed by downstream areas. [ABSTRACT FROM AUTHOR]

In the primary visual cortex (V1), monocular deprivation (MD) induces a shift in the ocular dominance (OD) of binocular neurons towards the open eye (Wiesel and Hubel, 1963; Gordon and Stryker, 1996). In V1 of C57Bl/6J mice, this OD-plasticity is maximal in juveniles, declines in adults and is absent beyond postnatal day (PD) 110 (Lehmann and Löwel, 2008) if mice are raised in standard cages. Since it was recently shown that brief dark exposure (DE) restored OD-plasticity in young adult rats (PD70-100) (He et al., 2006), we wondered whether DE would restore OD-plasticity also in adult and old mice and after a cortical stroke. To this end, we raised mice in standard cages until adulthood and transferred them to a darkroom for 10–14 days. Using intrinsic signal optical imaging we demonstrate that short-term DE can restore OD-plasticity after MD in both adult (PD138) and old mice (PD535), and that OD-shifts were mediated by an increase of open eye responses in V1. Interestingly, restored OD-plasticity after DE was accompanied by a reduction of both parvalbumin expressing cells and perineuronal nets and was prevented by increasing intracortical inhibition with diazepam. DE also maintained OD-plasticity in adult mice (PD150) after a stroke in the primary somatosensory cortex. In contrast, short-term DE did not affect basic visual parameters as measured by optomotry. In conclusion, short-term DE was able to restore OD-plasticity in both adult and aging mice and even preserved plasticity after a cortical stroke, most likely mediated by reducing intracortical inhibition. [ABSTRACT FROM AUTHOR]

Synaptic circuits are highly sensitive to sensory experience during a critical period in early development. The maturation of GABA inhibition in the visual cortex is suggested to be required for both the onset and closure of the critical period for ocular dominance (OD) plasticity, although the underlying mechanism is unclear. This study examines a model of a visual cortical cell to investigate the mechanism by which inhibitory pathway regulates OD plasticity, through the competition between the groups of correlated inputs from two eyes. We show that when feedforward inhibition is at a low level, the activity-dependent competition does not arise. In the lack of competition, synaptic dynamics are monostable, which prevents the sensory experience to be embedded into synaptic weights. When the feedforward inhibition becomes greater than a threshold, the competitive interaction segregates the input groups into dominant and recessive ones. In this case, the synaptic dynamics become bistable, which provides the synaptic pattern with the ability to reflect sensory experience, opening the critical period. When the feedforward inhibition is further increased, a strong stability of synaptic patterns makes it difficult to change according to input stimuli. Therefore, it becomes difficult again for the synaptic weights to reflect the information about sensory stimuli, closing the critical period. Our hypothesis suggests that the start and end of critical period plasticity may be explained by the competitive dynamics of synapses, which is modulated by the feedforward inhibition. [ABSTRACT FROM AUTHOR]

Fast chiral supercritical fluid chromatography (SFC) separations have become important due to the increasing use of high-throughput experimentation (HTE) in organic synthesis. These HTE experiments can generate hundreds of samples for chiral analysis that need to be assayed in a short time. In general, chiral SFC can provide much faster analysis times compared to liquid chromatography (LC). Additionally, columns packed with smaller particles can provide faster and more efficient separations. In this study, the effect of the particle size on the speed and resolution of chiral separations by SFC was evaluated. The performance of Chiralcel OD columns packed with either 5 or 3 μm particles were compared using van Deemter or other kinetic plots. The benefits of using smaller particle columns for chiral SFC analysis are illustrated. [ABSTRACT FROM AUTHOR]

Abstract: Homeostatic synaptic plasticity refers to a set of negative-feedback mechanisms that are used by neurons to maintain activity within a functional range. While it is becoming increasingly clear that homeostatic regulation of synapse function is a key principle in the nervous system, the molecular details of this regulation are only beginning to be uncovered. Recent evidence implicates molecules classically associated with the peripheral immune system in the modulation of homeostatic synaptic plasticity. In particular, the pro-inflammatory cytokine TNFα, class I major histocompatibility complex, and neuronal pentraxin 2 are essential in the regulation of the compensatory synaptic response that occurs in response to prolonged neuronal inactivity. This review will present and discuss current evidence implicating neuroimmune molecules in the homeostatic regulation of synapse function. This article is part of the Special Issue entitled ‘Homeostatic Synaptic Plasticity’. [Copyright &y& Elsevier]

Highlights: [•] Spike correlation at short distances is largely explained by tuning dissimilarity. [•] A generalized linear model measures the contributions of combinations of factors. [•] Ocular dominance similarity is not a significant factor beyond layer 4. [Copyright &y& Elsevier]

Highlights: [•] Different relationships between the inferior and superior RNFLs were observed according to ocular dominance and laterality. [•] The right eyes had a thicker RNFL, except in the superior quadrant, than the left eyes. [•] Regardless of laterality, inferior RNFL was thicker than superior RNFL in the dominant eyes. [•] This is the first reported study demonstrating the RNFL characteristics associated with ocular dominance. [ABSTRACT FROM AUTHOR]

• Maternal separation postpones the onset of ocular dominance plasticity in females. • Female maternal separated mice maintain ocular dominance plasticity into adulthood. • The effect of maternal separation on ocular dominance plasticity is sex-dimorphic. In mammals, maternal separation has been reported to affect brain structure and function in various brain regions; however, its effect on visual system development is largely unknown. In this study, we established a repeated maternal separation (RMS) model in C57BL/6 mice, where the mice pups were separated from their mothers 1 h per day from postnatal day 2 to 8. Ocular dominance plasticity (ODP) was measured at different developmental ages. Interestingly, RMS delayed the opening of critical period (CP) of ODP in female, but not in male mice, while postponed the closure of CP in both sexes. Only female RMS mice maintained the juvenile-like ODP into adulthood. Neither the protein expressions of neither glutamate decarboxylase 65 (GAD65) nor N-methyl-D-aspartate receptor NR2B subunit were altered in visual cortex of RMS mice. No depression/anxiety-like behaviors were detected in RMS mice. These results for the first time reveal that RMS alters the development of ODP. [ABSTRACT FROM AUTHOR]

Abstract: A novel analogue CMOS design of a cortical cell, that computes weighted sum of inputs, is presented. The cell’s feedback regime exploits the adaptation dynamics of floating gate FET ‘synapse’ to perform competitive learning amongst input weights as time-staggered winner take all. A learning rate parameter regulates adaptation time and a bias enforces resource limitation by restricting the number of input branches and winners in a competition. When learning ends, the cell’s response favours one input pattern over others to exhibit feature selectivity. Embedded in a 2-D RC grid, these feature selective cells are capable of performing a symmetry breaking pattern formation, observed in some reaction–diffusion models of cortical feature map formation, e.g. ocular dominance. Close similarity with biological networks in terms of adaptability and long term memory indicates that the cell’s design is ideally suited for analogue VLSI implementation of Self-Organizing Feature Map (SOFM) models of cortical feature maps. [Copyright &y& Elsevier]

Abstract: The roles of the central noradrenergic and serotonergic system in the activity-dependent regulation of ocular dominance plasticity have been a contentious issue. Using c-Fos activity mapping, we have developed a new, straightforward method to measure the strength of ocular dominance plasticity: the number of c-Fos-immunopositive cells in layer IV of rat visual cortex (Oc1B), ipsilateral to the stimulated eye, is a sensitive and reliable measure of the effects of monocular deprivation. Applying this new method, here we studied the unique modification of the degree of c-Fos expression induced in the visual cortex, in that endogenous noradrenaline (NA) and serotonin (5HT) in the cortex were significantly reduced, respectively by specific pharmacological agents. Intraperitoneal injections of N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine (DSP4) and p-chlorophenylalanine (pCPA) selectively impair NA- and 5HT-containing nerve terminals and fibers, respectively. In the visual cortex with strongly reduced NA, the number of c-Fos-immunopositive cells was found remaining significantly decreased in response to stimulation of the deprived eye, while by open eye stimulation the expected increase in c-Fos-immunoreactivity was strongly suppressed, showing values not different from those obtained by monocular stimulation in the normal rats. In contrast, in the visual cortex with strongly reduced 5HT no expected decrease was found in response to stimulation of the deprived eye, while, as is usually the case for the normal animals, a significant increase was still induced in response to open eye stimulation. These findings suggest that the noradrenergic and serotonergic system regulate ocular dominance (OD) plasticity differently: in the NA-depleted cortex the expected increase in c-Fos expression by open eye stimulation was not seen due to strong suppression, whereas in 5HT-depletion, the expected decrease in c-Fos expression was not materialized due to strong suppression. The present findings with c-Fos activity mapping method indicated a novel possibility of the differential regulation of OD plasticity by two types of common monoaminergic systems. [Copyright &y& Elsevier]

Abstract: Objective: Some neurologic and psychiatric disorders such as schizophrenia, depression, autism and migraine are referred to as cerebral lateralization abnormalities. In this study the possible relationships among handedness, eye dominance, and crossed hand–eye dominance in patients with different addictions mentioned above are investigated. Methods: Thirty three patients with cigarette, 35 patients with alcohol, 133 patients with heroin, 117 patients with hashish, 13 patients with drug addictions and 102 age matched controls were included in the study. Six of 13 patients with drug addictions were addicted to diazepam, 5 to pethidine and 2 to clonazepam. The patient group included 307 men and 24 women who ranged in age from 15 to 70 years. Handedness was ascertained by using the Edinburgh Handedness Inventory. Eye dominance was measured only by the near-far alignment test. Diagnoses were made on the basis of information provided from clinical interviews and Structured Clinical Interview for DSM-IV. Results: Patients with heroin and hashish had a significantly increased frequency of left-handedness in comparison with the other patients and controls (chi square=29.36, p <0.001). Patients with cigarette, alcohol, heroin and hashish addictions had a significantly increased frequency of left-eyedness in comparison with controls (chi square=25.24, p <0.01). Also, patients with cigarette, alcohol, heroin and hashish addictions had a significantly increased frequency of the crossed hand–eye dominance in comparison with controls (chi square=19.11, p <0.01). Conclusions: Different addictions such as cigarette, alcohol, heroin and hashish may be associated with abnormal handedness distribution and accepted as cerebral lateralization abnormalities. [Copyright &y& Elsevier]

Abstract: Amblyopia is one of the most common forms of visual impairment, arising from an early functional imbalance between the two eyes. It is currently accepted that, due to a lack of neural plasticity, amblyopia is an untreatable pathology in adults. Environmental enrichment (EE) emerged as a strategy highly effective in restoring plasticity in adult animals, eliciting recovery from amblyopia through a reduction of intracortical inhibition. It is unknown whether single EE components are able to promote plasticity in the adult brain, crucial information for designing new protocols of environmental stimulation suitable for amblyopic human subjects. Here, we assessed the effects of enhanced physical exercise, increased social interaction, visual enrichment or perceptual learning on visual function recovery in adult amblyopic rats. We report a complete rescue of both visual acuity and ocular dominance in exercised rats, in animals exposed to visual enrichment and in animals engaged in perceptual learning. These effects were accompanied by a reduced inhibition/excitation balance in the visual cortex. In contrast, we did not detect any sign of recovery in socially enriched rats or in animals practicing a purely associative visual task. These findings could have a bearing in orienting clinical research in the field of amblyopia therapy. [Copyright &y& Elsevier]