The visual cortex is an essential part of the brain for processing visual information. It exhibits structural and functional plasticity, which is crucial for adapting to complex visual environments. The quintessential manifestation of visual cortical plasticity is ocular dominance plasticity during the critical period, which involves numerous cellular and molecular events. While previous studies have emphasized the role of visual cortical neurons and their associated functional molecules in visual plasticity, recent findings have revealed that structural factors such as the extracellular matrix and glia are also involved. Investigating how these molecules interact to form a complex network that facilitates plasticity in the visual cortex is crucial to our understanding of the development of the visual system and the advancement of therapeutic strategies for visual disorders like amblyopia.
Neuronal Plasticity/physiology* ; Dominance, Ocular/physiology* ; Visual Cortex/physiology* ; Humans ; Animals ; Neurons/physiology*

The thalamic reticular nucleus (TRN) plays a crucial role in regulating sensory encoding, even at the earliest stages of visual processing, as evidenced by numerous studies. Orientation selectivity, a vital neural response, is essential for detecting objects through edge perception. Here, we demonstrate that somatostatin (SOM)-expressing and parvalbumin (PV)-expressing neurons in the TRN project to the dorsal lateral geniculate nucleus and modulate orientation selectivity and the capacity for visual information processing in the primary visual cortex (V1). These findings show that SOM-positive and PV-positive neurons in the TRN are powerful modulators of visual information encoding in V1, revealing a novel role for this thalamic nucleus in influencing visual processing.
Animals ; Somatostatin/metabolism* ; Parvalbumins/metabolism* ; Neurons/physiology* ; Thalamic Nuclei/physiology* ; Visual Pathways/physiology* ; Mice ; Mice, Inbred C57BL ; Visual Perception/physiology* ; Male ; Mice, Transgenic ; Visual Cortex/physiology* ; Primary Visual Cortex/cytology*

Low-intensity ultrasound stimulation of the retina has the ability to modulate neural activity in the primary visual cortex (V1), however, it is currently unclear how different intensities and durations of ultrasonic stimulation of the retina modulate neural activity in V1. In this paper, we recorded local field potential (LFP) signals in the V1 brain region of mice under different ultrasound intensities and different stimulation times. The amplitude of LFP corresponding to 1 s before ultrasound stimulation to 2 s after stimulation (-1-2 s) was analyzed, including the power and sample entropy of delta, theta, alpha beta, and low gamma frequency bands. The experimental results showed that, as the stimulation intensity increased, the peak value of the LFP in the visual cortex showed a linear upward trend; the power in the delta and theta frequency bands showed a linear upward trend, and the sample entropy showed a linear downward trend. With increases of stimulation duration, the peak value of the LFP in the visual cortex showed an upward trend, and the upward trend gradually weakened; the power in the delta frequency band showed an upward trend, the sample entropy showed a linear upward trend, and the sample entropy in the theta frequency band showed a downward trend. The results show that low-intensity ultrasonic stimulation of the retina has a significant modulatory effect on neural activity in the visual cortex. The study provides insights into the mechanisms by which ultrasonic stimulation regulates visual system function. Furthermore, it clarifies the patterns of parameter selection, facilitating the development of personalized multi-parameter modulation for the treatment of visual neural degeneration, retinal disorders and related research areas.
Animals ; Visual Cortex/radiation effects* ; Retina/radiation effects* ; Mice ; Ultrasonic Waves ; Primary Visual Cortex/physiology*

Major depressive disorder (MDD) is a highly heterogeneous mental disorder, and its complex etiology and unclear mechanism are great obstacles to the diagnosis and treatment of the disease. Studies have shown that abnormal functions of the visual cortex have been reported in MDD patients, and the actions of several antidepressants coincide with improvements in the structure and synaptic functions of the visual cortex. In this review, we critically evaluate current evidence showing the involvement of the malfunctioning visual cortex in the pathophysiology and therapeutic process of depression. In addition, we discuss the molecular mechanisms of visual cortex dysfunction that may underlie the pathogenesis of MDD. Although the precise roles of visual cortex abnormalities in MDD remain uncertain, this undervalued brain region may become a novel area for the treatment of depressed patients.
Humans ; Depressive Disorder, Major/pathology* ; Brain/pathology* ; Antidepressive Agents/therapeutic use* ; Visual Cortex/pathology*

Fear memory contextualization is critical for selecting adaptive behavior to survive. Contextual fear conditioning (CFC) is a classical model for elucidating related underlying neuronal circuits. The primary visual cortex (V1) is the primary cortical region for contextual visual inputs, but its role in CFC is poorly understood. Here, our experiments demonstrated that bilateral inactivation of V1 in mice impaired CFC retrieval, and both CFC learning and extinction increased the turnover rate of axonal boutons in V1. The frequency of neuronal Ca²⁺ activity decreased after CFC learning, while CFC extinction reversed the decrease and raised it to the naïve level. Contrary to control mice, the frequency of neuronal Ca²⁺ activity increased after CFC learning in microglia-depleted mice and was maintained after CFC extinction, indicating that microglial depletion alters CFC learning and the frequency response pattern of extinction-induced Ca²⁺ activity. These findings reveal a critical role of microglia in neocortical information processing in V1, and suggest potential approaches for cellular-based manipulation of acquired fear memory.
Mice ; Animals ; Primary Visual Cortex ; Extinction, Psychological/physiology* ; Learning/physiology* ; Fear/physiology* ; Hippocampus/physiology*

How the brain perceives objects and classifies perceived objects is one of the important goals of visual cognitive neuroscience. Previous research has shown that when we see objects, the brain's ventral visual pathway recognizes and classifies them, leading to different ways of interacting with them. In this paper, we summarize the latest research progress of the ventral visual pathway related to the visual classification of objects. From the perspective of the neural representation of objects and its underlying mechanisms in the visual cortex, we summarize the current research status of the two important organizational dimensions of object animacy and real-world size, provide new insights, and point out the direction of further research.
Brain Mapping/methods* ; Magnetic Resonance Imaging ; Pattern Recognition, Visual ; Photic Stimulation ; Visual Cortex ; Visual Pathways

Studies have shown that spatial attention remarkably affects the trial-to-trial response variability shared between neurons. Difficulty in the attentional task adjusts how much concentration we maintain on what is currently important and what is filtered as irrelevant sensory information. However, how task difficulty mediates the interactions between neurons with separated receptive fields (RFs) that are attended to or attended away is still not clear. We examined spike count correlations between single-unit activities recorded simultaneously in the primary visual cortex (V1) while monkeys performed a spatial attention task with two levels of difficulty. Moreover, the RFs of the two neurons recorded were non-overlapping to allow us to study fluctuations in the correlated responses between competing visual inputs when the focus of attention was allocated to the RF of one neuron. While increasing difficulty in the spatial attention task, spike count correlations were either decreased to become negative between neuronal pairs, implying competition among them, with one neuron (or none) exhibiting attentional enhancement of firing rate, or increased to become positive, suggesting inter-neuronal cooperation, with one of the pair showing attentional suppression of spiking responses. Besides, the modulation of spike count correlations by task difficulty was independent of the attended locations. These findings provide evidence that task difficulty affects the functional interactions between different neuronal pools in V1 when selective attention resolves the spatial competition.
Animals ; Attention/physiology* ; Macaca mulatta ; Neurons/physiology* ; Photic Stimulation ; Primary Visual Cortex ; Visual Cortex/physiology*

OBJECTIVES: To study the mechanism of retinoic acid receptor α (RARα) signal change to regulate neurexin 1 (NRXN1) in the visual cortex and participate in the autistic-like behavior in rats with vitamin A deficiency (VAD). METHODS: The models of vitamin A normal (VAN) and VAD pregnant rats were established, and some VAD maternal and offspring rats were given vitamin A supplement (VAS) in the early postnatal period. Behavioral tests were performed on 20 offspring rats in each group at the age of 6 weeks. The three-chamber test and the open-field test were used to observe social behavior and repetitive stereotyped behavior. High-performance liquid chromatography was used to measure the serum level of retinol in the offspring rats in each group. Electrophysiological experiments were used to measure the long-term potentiation (LTP) level of the visual cortex in the offspring rats. Quantitative real-time PCR and Western blot were used to measure the expression levels of RARα, NRXN1, and N-methyl-D-aspartate receptor 1 (NMDAR1). Chromatin co-immunoprecipitation was used to measure the enrichment of RARα transcription factor in the promoter region of the NRXN1 gene. RESULTS: The offspring rats in the VAD group had autistic-like behaviors such as impaired social interactions and repetitive stereotypical behaviors, and VAS started immediately after birth improved most of the behavioral deficits in offspring rats. The offspring rats in the VAD group had a significantly lower serum level of retinol than those in the VAN and VAS groups (P<0.05). Compared with the offspring rats in the VAN and VAS groups, the offspring rats in the VAD group had significant reductions in the mRNA and protein expression levels of NMDAR1, RARα, and NRXN1 and the LTP level of the visual cortex (P<0.05). The offspring rats in the VAD group had a significant reduction in the enrichment of RARα transcription factor in the promoter region of the NRXN1 gene in the visual cortex compared with those in the VAN and VAS groups (P<0.05). CONCLUSIONS RARα affects the synaptic plasticity of the visual cortex in VAD rats by regulating NRXN1, thereby participating in the formation of autistic-like behaviors in VAD rats.
Animals ; Autistic Disorder ; Female ; Pregnancy ; Rats ; Rats, Sprague-Dawley ; Receptors, N-Methyl-D-Aspartate ; Retinoic Acid Receptor alpha ; Visual Cortex ; Vitamin A ; Vitamin A Deficiency

Crossmodal information processing in sensory cortices has been reported in sparsely distributed neurons under normal conditions and can undergo experience- or activity-induced plasticity. Given the potential role in brain function as indicated by previous reports, crossmodal connectivity in the sensory cortex needs to be further explored. Using perforated whole-cell recording in anesthetized adult rats, we found that almost all neurons recorded in the primary somatosensory, auditory, and visual cortices exhibited significant membrane-potential responses to crossmodal stimulation, as recorded when brain activity states were pharmacologically down-regulated in light anesthesia. These crossmodal cortical responses were excitatory and subthreshold, and further seemed to be relayed primarily by the sensory thalamus, but not the sensory cortex, of the stimulated modality. Our experiments indicate a sensory cortical presence of widespread excitatory crossmodal inputs, which might play roles in brain functions involving crossmodal information processing or plasticity.
Animals ; Auditory Cortex/physiology* ; Neuronal Plasticity/physiology* ; Neurons ; Rats ; Thalamus ; Visual Cortex/physiology*

BACKGROUND: This study assessed the therapeutic effect of adjunctive bifrontal transcranial direct current stimulation (tDCS) in patients with tinnitus. METHODS: Forty-four patients who visited our university hospital with a complaint of non-pulsatile subjective tinnitus in January through December 2016 were enrolled. All patients received directive counseling and sound therapy, such as a sound generator or hearing aids, and/or oral clonazepam. Patients who agreed to undergo additional bifrontal tDCS were classified as the study group (n = 26). For tDCS, 1.5 mA of direct current was applied to the prefrontal cortex with a 10–20 EEG system for 20 minutes per session. RESULTS: The Tinnitus Handicap Inventory (THI), Beck Depression Inventory, and Visual Analog Scale (VAS) scores decreased significantly after treatment (P < 0.001). Patients who had a moderate or catastrophic handicap were significantly more likely to respond favorably to bifrontal tDCS (P = 0.026). There was no correlation of number of tDCS sessions with change in the THI or VAS score (P > 0.05). Logistic regression analysis revealed that the initial THI score was independently associated with improvement in the THI. However, tDCS was not a significant determinant of recovery. CONCLUSION: tDCS can be used as an adjunctive treatment in patients with severe tinnitus. Although tDCS did not decrease the loudness of tinnitus, it could alleviate the distress associated with the condition in some patients with a moderate or catastrophic handicap.
Clonazepam ; Depression ; Directive Counseling ; Electroencephalography ; Hearing Aids ; Humans ; Logistic Models ; Prefrontal Cortex ; Tinnitus* ; Transcranial Direct Current Stimulation* ; Visual Analog Scale