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In primary visual cortex (V1), neuronal receptive fields are generally thought to be fully established prior to eye-opening, with subsequent experience-dependent refinement controlled by GABAergic inhibition and regulated by homeostatic mechanisms. However, GABAergic interneurons (INs) are diverse and relatively little is known about the early postnatal roles of dendrite-targeting interneurons. Surprisingly, we find that somatostatin-expressing interneurons (SST-INs) in mouse V1 are not visually responsive at eye opening, instead developing visual sensitivity during the third postnatal week. Over the same period, SST-INs exhibit a rapid increase in excitatory innervation without compensatory synaptic scaling. Simultaneous imaging and optogenetic manipulation in juvenile animals reveals that SST-INs largely exert a multiplicative modulation of nearby excitatory neuron responses at all ages, but this effect increases over time. Our results identify a uniquely delayed developmental window for maturation of this inhibitory circuit and its contribution to visual gain normalization. The early postnatal roles of dendrite-targeting interneurons in primary visual cortex (V1) remain elusive. Here, the authors find that somatostatin interneurons in mouse V1 exhibit a uniquely delayed developmental trajectory for innervation and sensory responses, highlighting a window for the emergence of a key mechanism for normalization in cortical circuits.

The brain adapts to the sensory environment. For example, simple sensory exposure can modify the response properties of early sensory neurons. How these changes affect the overall encoding and maintenance of stimulus information across neuronal populations remains unclear. We perform parallel recordings in the primary visual cortex of anesthetized cats and find that brief, repetitive exposure to structured visual stimuli enhances stimulus encoding by decreasing the selectivity and increasing the range of the neuronal responses that persist after stimulus presentation. Low-dimensional projection methods and simple classifiers demonstrate that visual exposure increases the segregation of persistent neuronal population responses into stimulus-specific clusters. These observed refinements preserve the representational details required for stimulus reconstruction and are detectable in postexposure spontaneous activity. Assuming response facilitation and recurrent network interactions as the core mechanisms underlying stimulus persistence, we show that the exposure-driven segregation of stimulus responses can arise through strictly local plasticity mechanisms, also in the absence of firing rate changes. Our findings provide evidence for the existence of an automatic, unguided optimization process that enhances the encoding power of neuronal populations in early visual cortex, thus potentially benefiting simple readouts at higher stages of visual processing.

Background Migraine episodes are known to induce heightened photosensitivity. Neuroimaging investigations have revealed that the primary visual cortex exhibits abnormal activation patterns both during and between migraine attacks. Growing evidence suggests that altered cortical activity patterns may underlie the pathophysiology of neurological disorders. This study explored whether and how chronic migraine affects cortical activity patterns at single-cell resolution in the primary visual cortex during its progression. Methods Longitudinal in vivo two-photon calcium imaging was performed in the primary visual cortex of a chronic migraine mouse model across multiple time points. Cortical circuit activity patterns and behavioral correlates were assessed through combined chemogenetic manipulation and pharmacological interventions, with a particular focus on primary visual cortex functional modulation. Results Following chronic migraine induction, spontaneous hyperactivation emerged in cortical activity patterns within the primary visual cortex. Layer II/III neurons appeared as major contributors to this neural dysregulation, with layer V neurons showing less pronounced involvement. Prophylactic topiramate treatment attenuated allodynia and light aversion behaviors while reducing pathological cortical hyperactivity. Chemogenetic inhibition of primary visual cortex layer II/III neurons ameliorated light aversion without attenuating pain sensitization, while modulating aberrant spontaneous cortical activity patterns. Conclusions These findings provide preliminary evidence for dynamic alterations in spontaneous cortical neural signatures within the primary visual cortex throughout chronic migraine progression. Modulation of these neural adaptations appears to show the potential to alleviate associated light sensitivity, providing insight into potential pathophysiological mechanisms underlying light sensitivity in chronic migraine. Graphical abstract

This paper offers a theory for the origin of direction selectivity (DS) in the macaque primary visual cortex, V1. DS is essential for the perception of motion and control of pursuit eye movements. In the macaque visual pathway, neurons with DS first appear in V1, in the Simple cell population of the Magnocellular input layer 4Cα. The lateral geniculate nucleus (LGN) cells that project to these cortical neurons, however, are not direction selective. We hypothesize that DS is initiated in feed-forward LGN input, in the summed responses of LGN cells afferent to a cortical cell, and it is achieved through the interplay of 1) different visual response dynamics of ON and OFF LGN cells and 2) the wiring of ON and OFF LGN neurons to cortex. We identify specific temporal differences in the ON/OFF pathways that, together with item 2, produce distinct response time courses in separated subregions; analysis and simulations confirm the efficacy of the mechanisms proposed. To constrain the theory, we present data on Simple cells in layer 4Cα in response to drifting gratings. About half of the cells were found to have high DS, and the DS was broadband in spatial and temporal frequency (SF and TF). The proposed theory includes a complete analysis of how stimulus features such as SF and TF interact with ON/OFF dynamics and LGN-to-cortex wiring to determine the preferred direction and magnitude of DS.

Neurons respond selectively to stimuli, and thereby define a code that associates stimuli with population response patterns. Certain correlations within population responses (noise correlations) significantly impact the information content of the code, especially in large populations. Understanding the neural code thus necessitates response models that quantify the coding properties of modelled populations, while fitting large-scale neural recordings and capturing noise correlations. In this paper, we propose a class of response model based on mixture models and exponential families. We show how to fit our models with expectation-maximization, and that they capture diverse variability and covariability in recordings of macaque primary visual cortex. We also show how they facilitate accurate Bayesian decoding, provide a closed-form expression for the Fisher information, and are compatible with theories of probabilistic population coding. Our framework could allow researchers to quantitatively validate the predictions of neural coding theories against both large-scale neural recordings and cognitive performance.

Neural networks are crucial for brain function, but the relationship between functional and structural networks remains unclear, hindering disease understanding and treatment. This study employs AAVs, MRI reporter gene (AQP1), and chemogenetic-fMRI to explore the relationship between structural and functional connectivity in the mouse primary visual cortex (V1), offering a novel approach to study abnormal brain functions. The rAAV-PHP.eB-DIO vector encoding AQP1 was used to cross the blood-brain barrier and infect the brain, enabling diffusion-weighted imaging (DWI-MRI) to assess the anterograde structural connectivity network of V1. Additionally, chemogenetic activation of V1 using a Cre-dependent system was performed, and the whole-brain BOLD responses were evaluated using fMRI. The integration of these techniques provided a comprehensive analysis of the relationship between functional and structural connectivity. This study successfully achieved the combined detection of structural and functional connectivity in the V1 of mice. The rAAV1-hSyn-Cre virus was utilized for monosynaptic anterograde tracing. Additionally, a blood-brain barrier-crossing serotype viral vector, rAAV-PHP.eB-DIO-AQP1-EGFP, was intravenously injected to effectively transduce AQP1 into the V1 region and its downstream areas. The results indicated that regions expressing AQP1 under the control of Cre recombinase, including V1, LGN, CPu, and SC, exhibited significant alterations in DWI signal intensity (SI) and apparent diffusion coefficient (ADC). DREADD-fMRI analysis revealed that chemogenetic activation of the V1 region significantly enhanced neural activity in related brain regions, accompanied by a notable increase in BOLD signals. These regions included CPu, HIP, TH, SC, and PAG. decoding of neuronal activity and structural connectivity provides insights into brain structure-function interplay, which was important for understanding the cerebral function.

Objective According to a seminal hypothesis stated by Crick and Koch in 1995, one is not aware of neural activity in primary visual cortex (V1) because this region lacks reciprocal connections with prefrontal cortex (PFC). Methods We provide here a neuropsychological illustration of this hypothesis in a patient with a very rare form of cortical blindness: ventral and dorsal cortical pathways were lesioned bilaterally while V1 areas were partially preserved. Results Visual stimuli escaped conscious perception but still activated V1 regions that were functionally disconnected from PFC. Interpretation These results are consistent with the hypothesis of a causal role of PFC in visual awareness.

As the main cause of visual function deficits in children and adolescents worldwide, amblyopia causes serious impairment of monocular visual acuity and stereopsis. The recovery of visual functions from amblyopia beyond the critical period is slow and incomplete due to the limited plasticity of the mature cortex; notably, visual stimulation training seems to be an effective therapeutic strategy in clinical practice. However, the precise neural basis and cellular mechanisms that underlie amblyopia and visual stimulation treatment remain to be elucidated. Using monocular deprivation in juvenile mice to model amblyopia, we employed two-photon calcium imaging and chemogenetic techniques to investigate the visual responses of individual excitatory neurons and parvalbumin (PV + ) interneurons in the primary visual cortex (V1) of amblyopic mice. We demonstrate that amblyopic mice exhibit an excitation/inhibition (E/I) imbalance. Moreover, visual stimulation decreases the response of PV + interneurons, reactivates the ocular dominance plasticity of excitatory neurons, and promotes vision recovery in adult amblyopic mice. Our results reveal a dynamic E/I balance between excitatory neurons and PV + interneurons that may underlie the neural mechanisms of amblyopia during cortical development and visual stimulation-mediated functional recovery from adult amblyopia, providing evidence for therapeutic applications that rely on reactivating adult cortical plasticity. A dynamic excitation and inhibition (E/I) balance between excitatory neurons and PV+ interneurons in the primary visual cortex underlying the neural mechanisms of amblyopia during cortical development and visual stimulation-mediated functional recovery from adult amblyopia.

Sensory processing in the neocortex requires both feedforward and feedback information flow between cortical areas 1 . In feedback processing, higher-level representations provide contextual information to lower levels, and facilitate perceptual functions such as contour integration and figure–ground segmentation 2 , 3 . 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. Feedback influence from a higher visual area to primary visual cortex in mice engages nonlinear dendritic integration.

A well-known example of filling-in involves the blind spot, a region in the back of the eye that is devoid of photoreceptors. The term blind spot is somewhat of a misnomer, because the corresponding region of visual space is not simply perceived as dark, as one would expect. Instead, it is “filled-in” with the same color and texture as the surrounding background. This phenomenon is often considered as little more than a curiosity. However, this book argues that completion mechanisms similar to those that fill in the blind spot are pervasive and necessary for normal perception. The book reviews evidence suggesting a link between particular neural processes and the perception of filling-in. It then introduces the idea that these processes can instigate various types of long-term neural plasticity, which may underlie recovery and rehabilitation after peripheral injury, as well as other types of skill learning. The connection between completion phenomena and long-term plasticity is explored not only in the visual system, but also in the auditory, somatosensory, and motor systems.