Balancing plasticity and stability in neural circuits is essential for an animal\'s ability to learn from its environment while preserving proper processing and perception of sensory information. However, unlike the mechanisms that drive plasticity in neural circuits, the activity-induced molecular mechanisms that convey functional stability remain poorly understood. Focusing on the visual cortex of adult mice and combining transcriptomics, electrophysiology, and in vivo calcium imaging, we find that the daily appearance of light induces, in excitatory neurons, a large gene program along with rapid and transient increases in the ratio of excitation and inhibition (E/I ratio) and neural activity. Furthermore, we find that the light-induced transcription factor NPAS4 drives these daily normalizations of the E/I ratio and neural activity rates and that it stabilizes the neurons\' response properties. These findings indicate that daily sensory-induced transcription normalizes the E/I ratio and drives downward firing rate homeostasis to maintain proper sensory processing and perception.

While executive functions (EFs) have traditionally been linked to the cerebral cortex, our understanding of EFs has evolved with increasing evidence pointing to the involvement of cortico-subcortical networks. Despite the importance of investigating EFs within this broader context, the functional contributions of subcortical regions to these processes remain largely unexplored. This study addresses this gap by specifically examining the involvement of subcortical regions in executive inhibition, as measured by the classic Eriksen flanker task. In this study, we used a stereoscope to differentiate between subcortical (monocular) and cortical (mostly binocular) visual pathways in EF processes. Our findings indicate that monocular visual pathways play a crucial role in representing executive conflict, which necessitates cortical involvement. The persistence of a monoptic advantage in conflict representation highlights the substantial contribution of subcortical regions to these executive processes. This exploration of subcortical involvement in executive inhibition provides valuable insights into the intricate relationships between cortical and subcortical regions in EFs.

Neuronal activation sequence information is essential for understanding brain functions. Extracting such timing information from blood-oxygenation-level-dependent functional magnetic resonance imaging (fMRI) signals is confounded by local cerebral vascular reactivity (CVR), which varies across brain locations. Thus, detecting neuronal synchrony as well as inferring inter-regional causal modulation using fMRI signals can be biased. Here we used fast fMRI measurements sampled at 10 Hz to measure the fMRI latency difference between visual and sensorimotor areas when participants engaged in a visuomotor task. The regional fMRI timing was calibrated by subtracting the CVR latency measured by a breath-holding task. After CVR calibration, the fMRI signal at the lateral geniculate nucleus (LGN) preceded that at the visual cortex by 496 ms, followed by the fMRI signal at the sensorimotor cortex with a latency of 464 ms. Sequential LGN, visual, and sensorimotor cortex activations were found in each participant after the CVR calibration. These inter-regional fMRI timing differences across and within participants were more closely related to the reaction time after the CVR calibration. Our results suggested the feasibility of mapping brain activity using fMRI with accuracy in hundreds of milliseconds.

Color is an important visual feature that informs behavior, and the retinal basis for color vision has been studied across various vertebrate species. While many studies have investigated how color information is processed in visual brain areas of primate species, we have limited understanding of how it is organized beyond the retina in other species, including most dichromatic mammals. In this study, we systematically characterized how color is represented in the primary visual cortex (V1) of mice. Using large-scale neuronal recordings and a luminance and color noise stimulus, we found that more than a third of neurons in mouse V1 are color-opponent in their receptive field center, while the receptive field surround predominantly captures luminance contrast. Furthermore, we found that color-opponency is especially pronounced in posterior V1 that encodes the sky, matching the statistics of natural scenes experienced by mice. Using unsupervised clustering, we demonstrate that the asymmetry in color representations across cortex can be explained by an uneven distribution of green-On/UV-Off color-opponent response types that are represented in the upper visual field. Finally, a simple model with natural scene-inspired parametric stimuli shows that green-On/UV-Off color-opponent response types may enhance the detection of \'predatory\'-like dark UV-objects in noisy daylight scenes. The results from this study highlight the relevance of color processing in the mouse visual system and contribute to our understanding of how color information is organized in the visual hierarchy across species.

It is known that the primate amygdala forms projections to many areas of the ipsilateral cortex, but the extent to which it forms connections with the contralateral visual cortex remains less understood. Based on retrograde tracer injections in marmoset monkeys, we report that the amygdala forms widespread projections to the ipsilateral extrastriate cortex, including V1 and areas in both the dorsal (MT, V4T, V3a, 19M, and PG/PFG) and the ventral (VLP and TEO) streams. In addition, contralateral projections were found to target each of the extrastriate areas, but not V1. In both hemispheres, the tracer-labeled neurons were exclusively located in the basolateral nuclear complex. The number of labeled neurons in the contralateral amygdala was small relative to the ipsilateral connection (1.2% to 5.8%). The percentage of contralateral connections increased progressively with hierarchical level. An injection in the corpus callosum demonstrated that at least some of the amygdalo-cortical connections cross through this fiber tract, in addition to the previously documented path through the anterior commissure. Our results expand knowledge of the amygdalofugal projections to the extrastriate cortex, while also revealing pathways through which visual stimuli conveying affective content can directly influence early stages of neural processing in the contralateral visual field.

Paired-pulse transcranial magnetic stimulation is a valuable tool for investigating inhibitory mechanisms in motor cortex. We recently demonstrated its use in measuring cortical inhibition in visual cortex, using an approach in which participants trace the size of phosphenes elicited by stimulation to occipital cortex. Here, we investigate age-related differences in primary visual cortical inhibition and the relationship between primary visual cortical inhibition and local GABA+ in the same region, estimated using magnetic resonance spectroscopy. GABA+ was estimated in 28 young (18 to 28 years) and 47 older adults (65 to 84 years); a subset (19 young, 18 older) also completed a paired-pulse transcranial magnetic stimulation session, which assessed visual cortical inhibition. The paired-pulse transcranial magnetic stimulation measure of inhibition was significantly lower in older adults. Uncorrected GABA+ in primary visual cortex was also significantly lower in older adults, while measures of GABA+ that were corrected for the tissue composition of the magnetic resonance spectroscopy voxel were unchanged with age. Furthermore, paired-pulse transcranial magnetic stimulation-measured inhibition and magnetic resonance spectroscopy-measured tissue-corrected GABA+ were significantly positively correlated. These findings are consistent with an age-related decline in cortical inhibition in visual cortex and suggest paired-pulse transcranial magnetic stimulation effects in visual cortex are driven by GABAergic mechanisms, as has been demonstrated in motor cortex.

OBJECTIVE: Recovery of vision after acute optic neuritis (AON) is critical to improving the quality of life of people with demyelinating diseases. The objective of the study was to prospectively assess the changes in visual acuity, retinal layer thickness, and cortical visual network in patients with AON to identify the predictors of permanent visual disability.
METHODS: We studied a prospective cohort of 88 consecutive patients with AON with 6-month follow-up using high and low-contrast (2.5%) visual acuity, color vision, retinal thickness from optical coherence tomography, latencies and amplitudes of multifocal visual evoked potentials, mean deviation of visual fields, and diffusion-based structural (n = 53) and functional (n = 19) brain MRI to analyze the cortical visual network. The primary outcome was 2.5% low-contrast vision, and data were analyzed with mixed-effects and multivariate regression models.
RESULTS: We found that after 6 months, low-contrast vision and quality of vision remained moderately impaired. The thickness of the ganglion cell layer at baseline was a predictor of low-contrast vision 6 months later (ß = 0.49 [CI 0.11-0.88], p = 0.012). The structural cortical visual network at baseline predicted low-contrast vision, the best predictors being the betweenness of the right parahippocampal cortex (ß = -036 [CI -0.66 to 0.06], p = 0.021), the node strength of the right V3 (ß = 1.72 [CI 0.29-3.15], p = 0.02), and the clustering coefficient of the left intraparietal sulcus (ß = 57.8 [CI 12.3-103.4], p = 0.015). The functional cortical visual network at baseline also predicted low-contrast vision, the best predictors being the betweenness of the left ventral occipital cortex (ß = 8.6 [CI: 4.03-13.3], p = 0.009), the node strength of the right intraparietal sulcus (ß = -2.79 [CI: -5.1-0.4], p = 0.03), and the clustering coefficient of the left superior parietal lobule (ß = 501.5 [CI 50.8-952.2], p = 0.03).
CONCLUSIONS: The assessment of the visual pathway at baseline predicts permanent vision disability after AON, indicating that damage is produced early after disease onset and that it can be used for defining vision impairment and guiding therapy.

Complex visual stimuli evoke diverse patterns of gaze, but previous research suggests that their neural representations are shared across brains. Here, we used hyperalignment to compare visual responses between observers viewing identical stimuli. We find that individual eye movements enhance cortical visual responses but also lead to representational divergence. Pairwise differences in the spatial distribution of gaze and in semantic salience predict pairwise representational divergence in V1 and inferior temporal cortex, respectively. This suggests that individual gaze sculpts individual visual worlds.

An extended four-dimensional version of the traditional Petitot-Citti-Sarti model on contour completion in the visual cortex is examined. The neural configuration space is considered as the group of similarity transformations, denoted as M=SIM(2). The left-invariant subbundle of the tangent bundle models possible directions for establishing neural communication. The sub-Riemannian distance is proportional to the energy expended in interneuron activation between two excited border neurons. According to the model, the damaged image contours are restored via sub-Riemannian geodesics in the space M of positions, orientations and thicknesses (scales). We study the geodesic problem in M using geometric control theory techniques. We prove the existence of a minimal geodesic between arbitrary specified boundary conditions. We apply the Pontryagin maximum principle and derive the geodesic equations. In the special cases, we find explicit solutions. In the general case, we provide a qualitative analysis. Finally, we support our model with a simulation of the association field.

Jean-Martin Charcot, often lauded for his seminal contributions, is seldom critiqued for his blunders. One such blunder was his double-semidecussation scheme for the retinocortical visual pathways, proposed in 1875 to explain, on neuroanatomic grounds, cases of hysteria that manifest hysterical amblyopia accompanied with ipsilateral hemianaesthesia. Charcot\'s scheme was inconsistent with the older, broadly correct scheme of Prussian ophthalmologist Albrecht von Gräfe. Charcot failed to perform clinicopathologic correlation studies. His analysis relied on a series of mistaken conclusions he made in conjunction with Swiss-French ophthalmologist Edmund Landolt: (1) only an optic tract lesion could produce a homonymous hemianopsia; (2) cerebral lesions, if they ever produced homonymous hemianopsia, did so by secondary effects (e.g. pressure) on the optic tracts; and (3) damage to the cortical projections from the lateral geniculate produces a crossed amblyopia. Challenges to Charcot\'s theory came from within France by 1880. By 1882, Charcot recognized that his scheme was erroneous, and he approved a thesis by his pupil Charles Féré that reverted to Gräfe\'s scheme with an ill-conceived modification to accommodate Charcot\'s concept of hysterical cerebral amblyopia. A critique by American neurologist Moses Starr in 1884 argued for Gräfe\'s scheme and refuted Charcot\'s erroneous scheme and its subsequent derivatives.