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Handbook of Clinical Neurology 2022Blindness is a common sequela after stroke affecting the primary visual cortex, presenting as a contralesional, homonymous, visual field cut. This can occur unilaterally... (Review)
Review
Blindness is a common sequela after stroke affecting the primary visual cortex, presenting as a contralesional, homonymous, visual field cut. This can occur unilaterally or, less commonly, bilaterally. While it has been widely assumed that after a brief period of spontaneous improvement, vision loss becomes stable and permanent, accumulating data show that visual training can recover some of the vision loss, even long after the stroke. Here, we review the different approaches to rehabilitation employed in adult-onset cortical blindness (CB), focusing on visual restoration methods. Most of this work was conducted in chronic stroke patients, partially restoring visual discrimination and luminance detection. However, to achieve this, patients had to train for extended periods (usually many months), and the vision restored was not entirely normal. Several adjuvants to training such as noninvasive, transcranial brain stimulation, and pharmacology are starting to be investigated for their potential to increase the efficacy of training in CB patients. However, these approaches are still exploratory and require considerably more research before being adopted. Nonetheless, having established that the adult visual system retains the capacity for restorative plasticity, attention recently turned toward the subacute poststroke period. Drawing inspiration from sensorimotor stroke rehabilitation, visual training was recently attempted for the first time in subacute poststroke patients. It improved vision faster, over larger portions of the blind field, and for a larger number of visual discrimination abilities than identical training initiated more than 6 months poststroke (i.e., in the chronic period). In conclusion, evidence now suggests that visual neuroplasticity after occipital stroke can be reliably recruited by a range of visual training approaches. In addition, it appears that poststroke visual plasticity is dynamic, with a critical window of opportunity in the early postdamage period to attain more rapid, more extensive recovery of a larger set of visual perceptual abilities.
Topics: Adult; Blindness, Cortical; Humans; Primary Visual Cortex; Stroke; Stroke Rehabilitation; Vision, Ocular; Visual Perception
PubMed: 35034749
DOI: 10.1016/B978-0-12-819410-2.00030-8 -
Nature Nov 2022Neuropsychiatric disorders classically lack defining brain pathologies, but recent work has demonstrated dysregulation at the molecular level, characterized by...
Neuropsychiatric disorders classically lack defining brain pathologies, but recent work has demonstrated dysregulation at the molecular level, characterized by transcriptomic and epigenetic alterations. In autism spectrum disorder (ASD), this molecular pathology involves the upregulation of microglial, astrocyte and neural-immune genes, the downregulation of synaptic genes, and attenuation of gene-expression gradients in cortex. However, whether these changes are limited to cortical association regions or are more widespread remains unknown. To address this issue, we performed RNA-sequencing analysis of 725 brain samples spanning 11 cortical areas from 112 post-mortem samples from individuals with ASD and neurotypical controls. We find widespread transcriptomic changes across the cortex in ASD, exhibiting an anterior-to-posterior gradient, with the greatest differences in primary visual cortex, coincident with an attenuation of the typical transcriptomic differences between cortical regions. Single-nucleus RNA-sequencing and methylation profiling demonstrate that this robust molecular signature reflects changes in cell-type-specific gene expression, particularly affecting excitatory neurons and glia. Both rare and common ASD-associated genetic variation converge within a downregulated co-expression module involving synaptic signalling, and common variation alone is enriched within a module of upregulated protein chaperone genes. These results highlight widespread molecular changes across the cerebral cortex in ASD, extending beyond association cortex to broadly involve primary sensory regions.
Topics: Humans; Autism Spectrum Disorder; Cerebral Cortex; Neurons; RNA; Transcriptome; Autopsy; Sequence Analysis, RNA; Primary Visual Cortex; Neuroglia; Genetic Variation
PubMed: 36323788
DOI: 10.1038/s41586-022-05377-7 -
Nature May 2023Sensory processing in the neocortex requires both feedforward and feedback information flow between cortical areas. In feedback processing, higher-level representations...
Sensory processing in the neocortex requires both feedforward and feedback information flow between cortical areas. In feedback processing, higher-level representations provide contextual information to lower levels, and facilitate perceptual functions such as contour integration and figure-ground segmentation. However, we have limited understanding of the circuit and cellular mechanisms that mediate feedback influence. Here we use long-range all-optical connectivity mapping in mice to show that feedback influence from the lateromedial higher visual area (LM) to the primary visual cortex (V1) is spatially organized. When the source and target of feedback represent the same area of visual space, feedback is relatively suppressive. By contrast, when the source is offset from the target in visual space, feedback is relatively facilitating. Two-photon calcium imaging data show that this facilitating feedback is nonlinearly integrated in the apical tuft dendrites of V1 pyramidal neurons: retinotopically offset (surround) visual stimuli drive local dendritic calcium signals indicative of regenerative events, and two-photon optogenetic activation of LM neurons projecting to identified feedback-recipient spines in V1 can drive similar branch-specific local calcium signals. Our results show how neocortical feedback connectivity and nonlinear dendritic integration can together form a substrate to support both predictive and cooperative contextual interactions.
Topics: Animals; Mice; Calcium; Dendrites; Visual Cortex; Visual Pathways; Feedback, Physiological; Primary Visual Cortex; Pyramidal Cells; Optogenetics; Calcium Signaling
PubMed: 37138089
DOI: 10.1038/s41586-023-06007-6 -
Current Biology : CB May 2021How many thalamic neurons converge onto a cortical cell? This is an important question, because the organization of thalamocortical projections can influence the...
How many thalamic neurons converge onto a cortical cell? This is an important question, because the organization of thalamocortical projections can influence the cortical architecture. Here, we estimate the degree of thalamocortical convergence in primary visual cortex by taking advantage of the cortical expansion-neurons within a restricted volume in primary visual cortex have overlapping receptive fields driven by a smaller set of inputs from the lateral geniculate nucleus. Under these conditions, the measurements of cortical receptive fields in a population can be used to infer the receptive fields of their geniculate inputs and the weights of their projections using non-negative matrix factorization. The analysis reveals sparse connectivity, where a handful (~2-6) of thalamic inputs account for 90% of the total synaptic weight to a cortical neuron. Together with previous findings, these results paint a picture consistent with the idea that convergence of a few inputs partly determine the retinotopy and tuning properties of cortical cells..
Topics: Animals; Geniculate Bodies; Neurons; Primary Visual Cortex; Thalamus
PubMed: 33705713
DOI: 10.1016/j.cub.2021.02.032 -
ELife Aug 2018The ongoing debate on the neural basis of orientation selectivity in the primary visual cortex continues.
The ongoing debate on the neural basis of orientation selectivity in the primary visual cortex continues.
Topics: Orientation; Orientation, Spatial; Photic Stimulation; Visual Cortex; Visual Perception
PubMed: 30106374
DOI: 10.7554/eLife.39762 -
Frontiers in Neural Circuits 2021Lesion or damage to the primary visual cortex (V1) results in a profound loss of visual perception in humans. Similarly, in mice, optogenetic silencing of V1 profoundly... (Review)
Review
Lesion or damage to the primary visual cortex (V1) results in a profound loss of visual perception in humans. Similarly, in mice, optogenetic silencing of V1 profoundly impairs discrimination of orientated gratings. V1 is thought to have such a critical role in perception in part due to its position in the visual processing hierarchy. It is the first brain area in the neocortex to receive visual input, and it distributes this information to more than 18 brain areas. Here I review recent advances in our understanding of the organization and function of the V1 projections in the mouse. This progress is in part due to new anatomical and viral techniques that allow for efficient labeling of projection neurons. In the final part of the review, I conclude by highlighting challenges and opportunities for future research.
Topics: Animals; Mice; Neurons; Optogenetics; Primary Visual Cortex; Visual Cortex; Visual Pathways; Visual Perception
PubMed: 34867213
DOI: 10.3389/fncir.2021.751331 -
The Journal of Neuroscience : the... Nov 2022How variable is the functionally defined structure of early visual areas in human cortex and how much variability is shared between twins? Here we quantify individual...
How variable is the functionally defined structure of early visual areas in human cortex and how much variability is shared between twins? Here we quantify individual differences in the best understood functionally defined regions of cortex: V1, V2, V3. The Human Connectome Project 7T Retinotopy Dataset includes retinotopic measurements from 181 subjects (109 female, 72 male), including many twins. We trained four "anatomists" to manually define V1-V3 using retinotopic features. These definitions were more accurate than automated anatomical templates and showed that surface areas for these maps varied more than threefold across individuals. This threefold variation was little changed when normalizing visual area size by the surface area of the entire cerebral cortex. In addition to varying in size, we find that visual areas vary in how they sample the visual field. Specifically, the cortical magnification function differed substantially among individuals, with the relative amount of cortex devoted to central vision varying by more than a factor of 2. To complement the variability analysis, we examined the similarity of visual area size and structure across twins. Whereas the twin sample sizes are too small to make precise heritability estimates (50 monozygotic pairs, 34 dizygotic pairs), they nonetheless reveal high correlations, consistent with strong effects of the combination of shared genes and environment on visual area size. Collectively, these results provide the most comprehensive account of individual variability in visual area structure to date, and provide a robust population benchmark against which new individuals and developmental and clinical populations can be compared. Areas V1, V2, and V3 are among the best studied functionally defined regions in human cortex. Using the largest retinotopy dataset to date, we characterized the variability of these regions across individuals and the similarity between twin pairs. We find that the size of visual areas varies dramatically (up to 3.5×) across healthy young adults, far more than the variability of the cerebral cortex size as a whole. Much of this variability appears to arise from inherited factors, as we find very high correlations in visual area size between monozygotic twin pairs, and lower but still substantial correlations between dizygotic twin pairs. These results provide the most comprehensive assessment of how functionally defined visual cortex varies across the population to date.
Topics: Female; Humans; Male; Young Adult; Brain Mapping; Magnetic Resonance Imaging; Primary Visual Cortex; Visual Cortex; Visual Fields; Visual Pathways
PubMed: 36180226
DOI: 10.1523/JNEUROSCI.0690-21.2022 -
Frontiers in Neural Circuits 2021Stimulus-selective response plasticity (SRP) is a robust and lasting modification of primary visual cortex (V1) that occurs in response to exposure to novel visual... (Review)
Review
Stimulus-selective response plasticity (SRP) is a robust and lasting modification of primary visual cortex (V1) that occurs in response to exposure to novel visual stimuli. It is readily observed as a pronounced increase in the magnitude of visual evoked potentials (VEPs) recorded in response to phase-reversing grating stimuli in neocortical layer 4. The expression of SRP at the individual neuron level is equally robust, but the qualities vary depending on the neuronal type and how activity is measured. This form of plasticity is highly selective for stimulus features such as stimulus orientation, spatial frequency, and contrast. Several key insights into the significance and underlying mechanisms of SRP have recently been made. First, it occurs concomitantly and shares core mechanisms with behavioral habituation, indicating that SRP reflects the formation of long-term familiarity that can support recognition of innocuous stimuli. Second, SRP does not manifest within a recording session but only emerges after an off-line period of several hours that includes sleep. Third, SRP requires not only canonical molecular mechanisms of Hebbian synaptic plasticity within V1, but also the opposing engagement of two key subclasses of cortical inhibitory neuron: the parvalbumin- and somatostatin-expressing GABAergic interneurons. Fourth, pronounced shifts in the power of cortical oscillations from high frequency (gamma) to low frequency (alpha/beta) oscillations provide respective readouts of the engagement of these inhibitory neuronal subtypes following familiarization. In this article we will discuss the implications of these findings and the outstanding questions that remain to gain a deeper understanding of this striking form of experience-dependent plasticity.
Topics: Evoked Potentials, Visual; Interneurons; Neuronal Plasticity; Primary Visual Cortex; Visual Cortex
PubMed: 35173586
DOI: 10.3389/fncir.2021.815554