Stimulus-specific enhancement in mouse visual cortex requires GABA but not VIP-peptide release from VIP interneurons.

When adult mice are repeatedly exposed to a particular visual stimulus for as little as 1 h per day for several days while their visual cortex (V1) is in the high-gain state produced by locomotion, that specific stimulus elicits much stronger responses in V1 neurons for the following several weeks, even when measured in anesthetized animals. Such stimulus-specific enhancement (SSE) is not seen if locomotion is prevented. The effect of locomotion on cortical responses is mediated by vasoactive intestinal peptide (VIP) positive interneurons, which can release both the peptide and the inhibitory neurotransmitter GABA. Previous studies have examined the role of VIP-ergic interneurons, but none have distinguished the individual roles of peptide from GABA release. Here, we used genetic ablation to determine which of those molecules secreted by VIP-ergic neurons is responsible for SSE. SSE was not impaired by VIP deletion but was prevented by compromising release of GABA from VIP cells. This finding suggests that SSE may result from Hebbian mechanisms that remain present in adult V1.NEW & NOTEWORTHY Many neurons package and release a peptide along with a conventional neurotransmitter. The conventional view is that such peptides exert late, slow effects on plasticity. We studied a form of cortical plasticity that depends on the activity of neurons that express both vasoactive intestinal peptide (VIP) and the inhibitory neurotransmitter GABA. GABA release accounted for their action on plasticity, with no effect of deleting the peptide on this phenomenon.

Feedforward and disinhibitory circuits differentially control activity of cortical somatostatin interneurons during behavioral state transitions.

Interneurons (INs), specifically those in disinhibitory circuits like somatostatin (SST) and vasoactive intestinal peptide (VIP)-INs, are strongly modulated by the behavioral context. Yet, the mechanisms by which these INs are recruited during active states and whether their activity is consistent across sensory cortices remain unclear. We now report that in mice, locomotor activity strongly recruits SST-INs in the primary somatosensory (S1) but not the visual (V1) cortex. This diverse engagement of SST-INs cannot be explained by differences in VIP-IN function but is absent in the presence of visual input, suggesting the involvement of feedforward sensory pathways. Accordingly, inactivating the somatosensory thalamus, but not decreasing VIP-IN activity, significantly reduces the modulation of SST-INs by locomotion. Model simulations suggest that the differences in SST-INs across behavioral states can be explained by varying ratios of VIP- and thalamus-driven activity. By integrating feedforward activity with neuromodulation, SST-INs are anticipated to be crucial for adapting sensory processing to behavioral states.

Behavioral strategy shapes activation of the Vip-Sst disinhibitory circuit in visual cortex.

In complex environments, animals can adopt diverse strategies to find rewards. How distinct strategies differentially engage brain circuits is not well understood. Here, we investigate this question, focusing on the cortical Vip-Sst disinhibitory circuit between vasoactive intestinal peptide-postive (Vip) interneurons and somatostatin-positive (Sst) interneurons. We characterize the behavioral strategies used by mice during a visual change detection task. Using a dynamic logistic regression model, we find that individual mice use mixtures of a visual comparison strategy and a statistical timing strategy. Separately, mice also have periods of task engagement and disengagement. Two-photon calcium imaging shows large strategy-dependent differences in neural activity in excitatory, Sst inhibitory, and Vip inhibitory cells in response to both image changes and image omissions. In contrast, task engagement has limited effects on neural population activity. We find that the diversity of neural correlates of strategy can be understood parsimoniously as the increased activation of the Vip-Sst disinhibitory circuit during the visual comparison strategy, which facilitates task-appropriate responses.

A clinico-anatomical dissection of the magnocellular and parvocellular pathways in a patient with the Riddoch syndrome.

KEY MESSAGE: The Riddoch syndrome is thought to be caused by damage to the primary visual cortex (V1), usually following a vascular event. This study shows that damage to the anatomical input to V1, i.e., the optic radiations, can result in selective visual deficits that mimic the Riddoch syndrome. The results also highlight the differential susceptibility of the magnocellular and parvocellular visual systems to injury. Overall, this study offers new insights that will improve our understanding of the impact of brain injury and neurosurgery on the visual pathways. The Riddoch syndrome, characterised by the ability to perceive, consciously, moving visual stimuli but not static ones, has been associated with lesions of primary visual cortex (V1). We present here the case of patient YL who, after a tumour resection surgery that spared his V1, nevertheless showed symptoms of the Riddoch syndrome. Based on our testing, we postulated that the magnocellular (M) and parvocellular (P) inputs to his V1 may be differentially affected. In a first experiment, YL was presented with static and moving checkerboards in his blind field while undergoing multimodal magnetic resonance imaging (MRI), including structural, functional, and diffusion, acquired at 3 T. In a second experiment, we assessed YL's neural responses to M and P visual stimuli using psychophysics and high-resolution fMRI acquired at 7 T. YL's optic radiations were partially damaged but not severed. We found extensive activity in his visual cortex for moving, but not static, visual stimuli, while our psychophysical tests revealed that only low-spatial frequency moving checkerboards were perceived. High-resolution fMRI revealed strong responses in YL's V1 to M stimuli and very weak ones to P stimuli, indicating a functional P lesion affecting V1. In addition, YL frequently reported seeing moving stimuli and discriminating their direction of motion in the absence of visual stimulation, suggesting that he was experiencing visual hallucinations. Overall, this study highlights the possibility of a selective loss of P inputs to V1 resulting in the Riddoch syndrome and in hallucinations of visual motion.

A multicolor suite for deciphering population coding of calcium and cAMP in vivo.

cAMP is a universal second messenger regulated by various upstream pathways including Ca2+ and G-protein-coupled receptors (GPCRs). To decipher in vivo cAMP dynamics, we rationally designed cAMPinG1, a sensitive genetically encoded green cAMP indicator that outperformed its predecessors in both dynamic range and cAMP affinity. Two-photon cAMPinG1 imaging detected cAMP transients in the somata and dendritic spines of neurons in the mouse visual cortex on the order of tens of seconds. In addition, multicolor imaging with a sensitive red Ca2+ indicator RCaMP3 allowed simultaneous measurement of population patterns in Ca2+ and cAMP in hundreds of neurons. We found Ca2+-related cAMP responses that represented specific information, such as direction selectivity in vision and locomotion, as well as GPCR-related cAMP responses. Overall, our multicolor suite will facilitate analysis of the interaction between the Ca2+, GPCR and cAMP signaling at single-cell resolution both in vitro and in vivo.

Ethanol Differentially Affects Excitatory and Inhibitory Synaptic Transmission in Visual Cortex of Wild-type and Adenosine A1R Knock-out Mice.

Ethanol is one of the most commonly used and abused substances in the world. While the behavioral effects of ethanol are well characterized, mechanisms of its action on neurons and synapses remain elusive. Prior research suggested that ethanol could affect neurons by interfering with metabolism of biologically active molecules, such as adenosine. Here, we explored the involvement of adenosine A1 receptors (A1R) in mediating ethanol's effects on synaptic transmission to layer 2/3 pyramidal neurons of visual cortex using wild type (WT) and A1R knock-out (KO) mice. Ethanol differentially affected excitatory and inhibitory transmission in WT and KO mice. In slices from WT mice ethanol had heterogeneous effects on excitatory transmission (facilitation, suppression or no change), with no net change. Ethanol's effects remained heterogeneous during acute blockade of A1Rs with a selective antagonist DPCPX. However, in A1RKO mice ethanol consistently suppressed excitatory transmission, with no cases of enhancement observed. Inhibitory transmission was suppressed by ethanol in both WT and A1RKO mice. At both excitatory and inhibitory synapses, changes of response amplitude correlated with changes of paired-pulse ratio, suggesting involvement of presynaptic mechanisms. We conclude that A1Rs are not involved in mediating effects of ethanol on synaptic transmission in mouse visual cortex. However, A1Rs are necessary for development of mechanisms mediating facilitation at some excitatory synapses. Our results add evidence for the diversity of ethanol's effects and mechanisms of action on synaptic transmission in different brain structures, and even in the same brain area (visual cortex) in different species, rats vs mice.

Distinct patterns of spatial attentional modulation of steady-state visual evoked magnetic fields (SSVEFs) in subdivisions of the human early visual cortex.

In recent years, steady-state visual evoked potentials (SSVEPs) became an increasingly valuable tool to investigate neural dynamics of competitive attentional interactions and brain-computer interfaces. This is due to their good signal-to-noise ratio, allowing for single-trial analysis, and their ongoing oscillating nature that enables to analyze temporal dynamics of facilitation and suppression. Given the popularity of SSVEPs, it is surprising that only a few studies looked at the cortical sources of these responses. This is in particular the case when searching for studies that assessed the cortical sources of attentional SSVEP amplitude modulations. To address this issue, we used a typical spatial attention task and recorded neuromagnetic fields (MEG) while presenting frequency-tagged stimuli in the left and right visual fields, respectively. Importantly, we controlled for attentional deployment in a baseline period before the shifting cue. Subjects either attended to a central fixation cross or to two peripheral stimuli simultaneously. Results clearly showed that signal sources and attention effects were restricted to the early visual cortex: V1, V2, hMT+, precuneus, occipital-parietal, and inferior-temporal cortex. When subjects attended to central fixation first, shifting attention to one of the peripheral stimuli resulted in a significant activation increase for the to-be-attended stimulus with no activation decrease for the to-be-ignored stimulus in hMT+ and inferio-temporal cortex, but significant SSVEF decreases from V1 to occipito-parietal cortex. When attention was first deployed to both rings, shifting attention away from one ring basically resulted in a significant activation decrease in all areas for the then-to-be-ignored stimulus.

The Impact of the Wavelength and Its Transmittance on the Visual Evoked Potentials, at Baseline, and under the Effect of Six Monochromatic Filters Used for Visual Treatments.

PURPOSE: This is an observational, non-invasive study which measures the VEPs of twelve individuals, at baseline, and under the effect of six monochromatic filters used in visual therapy, to understand their effect on neural activity to propose successful treatments. METHODS: Monochromatic filters were chosen to represent the visible light spectrum, going from red to violet color, 440.5-731 nm, and light transmittance from 19 to 89.17%. Two of the participants presented accommodative esotropia. The impact of each filter, differences, and similarities among them, were analyzed using non-parametric statistics. RESULTS: There was an increase on the N75 and P100 latency of both eyes and a decrease was on the VEP amplitude. The neurasthenic (violet), omega (blue), and mu (green) filter had the biggest effects on the neural activity. Changes may primarily be attributable to transmittance (%) for blue-violet colors, wavelength (nm) for yellow-red colors, and a combination of both for the green color. No significant VEPs differences were seen in accommodative strabismic patients, which reflects the good integrity and functionality of their visual pathway. CONCLUSIONS: Monochromatic filters, influenced the axonal activation and the number of fibers that get connected after stimulating the visual pathway, as well as the time needed for the stimulus to reach the visual cortex and thalamus. Consequently, modulations to the neural activity could be due to the visual and non-visual pathway. Considering the different types of strabismus and amblyopia, and their cortical-visual adaptations, the effect of these wavelengths should be explored in other categories of visual dysfunctions, to understand the neurophysiology underlying the changes on neural activity.

Putting the brakes on synchrony: VIP interneurons tune visually evoked rhythmic activity.

Visually evoked synchrony in the primary visual cortex has proven to be a robust model for examining circuit interactions. In this issue of Neuron, Veit et al.1 highlight a previously unappreciated role for VIP interneurons in regulating local and long-range patterns of coordinated neural activity.

Dual-polarity voltage imaging of the concurrent dynamics of multiple neuron types.

Genetically encoded fluorescent voltage indicators are ideally suited to reveal the millisecond-scale interactions among and between targeted cell populations. However, current indicators lack the requisite sensitivity for in vivo multipopulation imaging. We describe next-generation green and red voltage sensors, Ace-mNeon2 and VARNAM2, and their reverse response-polarity variants pAce and pAceR. Our indicators enable 0.4- to 1-kilohertz voltage recordings from >50 spiking neurons per field of view in awake mice and ~30-minute continuous imaging in flies. Using dual-polarity multiplexed imaging, we uncovered brain state-dependent antagonism between neocortical somatostatin-expressing (SST+) and vasoactive intestinal peptide-expressing (VIP+) interneurons and contributions to hippocampal field potentials from cell ensembles with distinct axonal projections. By combining three mutually compatible indicators, we performed simultaneous triple-population imaging. These approaches will empower investigations of the dynamic interplay between neuronal subclasses at single-spike resolution.

Juvenile depletion of microglia reduces orientation but not high spatial frequency selectivity in mouse V1.

Microglia contain multiple mechanisms that shape the synaptic landscape during postnatal development. Whether the synaptic changes mediated by microglia reflect the developmental refinement of neuronal responses in sensory cortices, however, remains poorly understood. In postnatal life, the development of increased orientation and spatial frequency selectivity of neuronal responses in primary visual cortex (V1) supports the emergence of high visual acuity. Here, we used the colony-stimulating factor 1 receptor (CSF1R) inhibitor PLX5622 to rapidly and durably deplete microglia in mice during the juvenile period in which increased orientation and spatial frequency selectivity emerge. Excitatory and inhibitory tuning properties were measured simultaneously using multi-photon calcium imaging in layer II/III of mouse V1. We found that microglia depletion generally increased evoked activity which, in turn, reduced orientation selectivity. Surprisingly, microglia were not required for the emergence of high spatial frequency tuned responses. In addition, microglia depletion did not perturb cortical binocularity, suggesting normal depth processing. Together, our finding that orientation and high spatial frequency selectivity in V1 are differentially supported by microglia reveal that microglia are required normal sensory processing, albeit selectively.

Response Selectivity of the Lateral Posterior Nucleus Axons Projecting to the Mouse Primary Visual Cortex.

Neurons in the mouse primary visual cortex (V1) exhibit characteristic response selectivity to visual stimuli, such as orientation, direction and spatial frequency selectivity. Since V1 receives thalamic visual inputs from the lateral geniculate nucleus (LGN) and lateral posterior nucleus (LPN), the response selectivity of the V1 neurons could be influenced mostly by these inputs. However, it remains unclear how these two thalamic inputs contribute to the response selectivity of the V1 neurons. In this study, we examined the orientation, direction and spatial frequency selectivity of the LPN axons projecting to V1 and compared their response selectivity with our previous results of the LGN axons in mice. For this purpose, the genetically encoded calcium indicator, GCaMP6s, was locally expressed in the LPN using the adeno-associated virus (AAV) infection method. Visual stimulations were presented, and axonal imaging was conducted in V1 by two-photon calcium imaging in vivo. We found that LPN axons primarily terminate in layers 1 and 5 and, to a lesser extent, in layers 2/3 and 4 of V1, while LGN axons mainly terminate in layer 4 and, to a lesser extent, in layers 1 and 2/3 of V1. LPN axons send highly orientation- and direction-selective inputs to all the examined layers in V1, whereas LGN axons send highly orientation- and direction-selective inputs to layers 1 and 2/3 but low orientation and direction selective inputs to layer 4 in V1. The distribution of preferred orientation and direction was strongly biased toward specific orientations and directions in LPN axons, while weakly biased to cardinal orientations and directions in LGN axons. In spatial frequency tuning, both the LPN and LGN axons send selective inputs to V1. The distribution of preferred spatial frequency was more diverse in the LPN axons than in the LGN axons. In conclusion, LPN inputs to V1 are functionally different from LGN inputs and may have different roles in the orientation, direction and spatial frequency tuning of the V1 neurons.

Hidden in plain sight.

Context controls the activity of sensory neurons.

A strategy for mapping biophysical to abstract neuronal network models applied to primary visual cortex.

A fundamental challenge for the theoretical study of neuronal networks is to make the link between complex biophysical models based directly on experimental data, to progressively simpler mathematical models that allow the derivation of general operating principles. We present a strategy that successively maps a relatively detailed biophysical population model, comprising conductance-based Hodgkin-Huxley type neuron models with connectivity rules derived from anatomical data, to various representations with fewer parameters, finishing with a firing rate network model that permits analysis. We apply this methodology to primary visual cortex of higher mammals, focusing on the functional property of stimulus orientation selectivity of receptive fields of individual neurons. The mapping produces compact expressions for the parameters of the abstract model that clearly identify the impact of specific electrophysiological and anatomical parameters on the analytical results, in particular as manifested by specific functional signatures of visual cortex, including input-output sharpening, conductance invariance, virtual rotation and the tilt after effect. Importantly, qualitative differences between model behaviours point out consequences of various simplifications. The strategy may be applied to other neuronal systems with appropriate modifications.

Spontaneous modulations of high-frequency cortical activity.

OBJECTIVE: We clarified the clinical and mechanistic significance of physiological modulations of high-frequency broadband cortical activity associated with spontaneous saccadic eye movements during a resting state. METHODS: We studied 30 patients who underwent epilepsy surgery following extraoperative electrocorticography and electrooculography recordings. We determined whether high-gamma activity at 70-110 Hz preceding saccade onset would predict upcoming ocular behaviors. We assessed how accurately the model incorporating saccade-related high-gamma modulations would localize the primary visual cortex defined by electrical stimulation. RESULTS: The dynamic atlas demonstrated transient high-gamma suppression in the striatal cortex before saccade onset and high-gamma augmentation subsequently involving the widespread posterior brain regions. More intense striatal high-gamma suppression predicted the upcoming saccade directed to the ipsilateral side and lasting longer in duration. The bagged-tree-ensemble model demonstrated that intense saccade-related high-gamma modulations localized the visual cortex with an accuracy of 95%. CONCLUSIONS: We successfully animated the neural dynamics supporting saccadic suppression, a principal mechanism minimizing the perception of blurred vision during rapid eye movements. The primary visual cortex per se may prepare actively in advance for massive image motion expected during upcoming prolonged saccades. SIGNIFICANCE: Measuring saccade-related electrocorticographic signals may help localize the visual cortex and avoid misperceiving physiological high-frequency activity as epileptogenic.

Synaptosomal Actin Dynamics in the Developmental Visual Cortex Regulate Behavioral Visual Acuity in Rats.

Purpose: Synaptosomal actin dynamics are essential for synaptic structural stability. Whether actin dynamics are involved in structural and functional synaptic plasticity within the primary visual cortex (V1) or behavioral visual acuity in rats has still not been thoroughly investigated. Methods: Synaptosome preparation and western blot analysis were used to analyze synaptosomal actin dynamics. Transmission electron microscopy was used to detect synaptic density and mitochondrial area alterations. A visual water maze task was applied to assess behavioral visual acuity. Microinjection of the actin polymerization inhibitor or stabilizer detected the effect of actin dynamics on visual function. Results: Actin dynamics, the mitochondrial area, and synaptic density within the area of V1 are increased during the critical period for the development of binocularity. Microinjection of the actin polymerization inhibitor cytochalasin D into the V1 decreased the mitochondrial area, synaptic density, and behavioral visual acuity. Long-term monocular deprivation reduced actin dynamics, the mitochondrial area, and synaptic density within the V1 contralateral to the deprived eye compared with those ipsilateral to the deprived eye and impaired visual acuity in the amblyopic eye. In addition, the mitochondrial area, synaptic density, and behavioral visual acuity were improved by stabilization of actin polymerization by jasplakinolide microinjection. Conclusions: During the critical period of visual development of binocularity, synaptosomal actin dynamics regulate synaptic structure and function and play roles in behavioral visual acuity in rats.

Partial recovery of visual function in a blind patient after optogenetic therapy.

Optogenetics may enable mutation-independent, circuit-specific restoration of neuronal function in neurological diseases. Retinitis pigmentosa is a neurodegenerative eye disease where loss of photoreceptors can lead to complete blindness. In a blind patient, we combined intraocular injection of an adeno-associated viral vector encoding ChrimsonR with light stimulation via engineered goggles. The goggles detect local changes in light intensity and project corresponding light pulses onto the retina in real time to activate optogenetically transduced retinal ganglion cells. The patient perceived, located, counted and touched different objects using the vector-treated eye alone while wearing the goggles. During visual perception, multichannel electroencephalographic recordings revealed object-related activity above the visual cortex. The patient could not visually detect any objects before injection with or without the goggles or after injection without the goggles. This is the first reported case of partial functional recovery in a neurodegenerative disease after optogenetic therapy.

Bariatric surgery restores visual cortical plasticity in nondiabetic subjects with obesity.

BACKGROUND/OBJECTIVES: Obesity leads to changes in synaptic plasticity. We aimed at investigating the impact of bariatric surgery (RYGB) on visual neural plasticity (NP) and its relationship with the main gut peptides, leptin, and brain-derived neurotrophic factor (BDNF). SUBJECTS/METHODS: NP was assessed testing binocular rivalry before and after 2 h of monocular deprivation (index of visual brain plasticity) in 15 subjects with obesity (age 42.3 ± 9.8 years; BMI 46.1 ± 4.9 kg/m2) before and after RYGB. Gut peptides, leptin, and BDNF were obtained at baseline and 6 months after surgery in 13 subjects. RESULTS: A significant reduction in BMI (p < 0.001 vs. baseline) and a significant increase of disposition index (DI, p = 0.02 vs baseline) were observed after RYGB. Total and active GLP-1 release in response to glucose ingestion significantly increased after RYGB, while no changes occurred in VIP, GIP, and BDNF levels. Fasting leptin concentration was lower after RYGB (p = 0.001 vs. baseline). Following RYGB, NP was progressively restored (p < 0.002). NP was correlated with DI and fasting glucose at baseline (r = 0.75, p = 0.01; r = -0.7, p = 0.02; respectively), but not with BMI. A positive correlation between post-pre-RYGB changes in AUCactive GLP-1 and NP was observed (r = 0.70, p < 0.01). Leptin was inversely correlated with NP 6 months after surgery (r = -0.63, p = 0.02). No correlation was observed between GIP, VIP, BDNF, and NP. CONCLUSIONS: Visual plasticity is altered in subjects with obesity, and it can be restored after RYGB. The improvement may be mediated by amelioration of insulin sensitivity, increased GLP-1 levels, and reduced leptin levels.

Altered Heterosynaptic Plasticity Impairs Visual Discrimination Learning in Adenosine A1 Receptor Knock-Out Mice.

Theoretical and modeling studies demonstrate that heterosynaptic plasticity-changes at synapses inactive during induction-facilitates fine-grained discriminative learning in Hebbian-type systems, and helps to achieve a robust ability for repetitive learning. A dearth of tools for selective manipulation has hindered experimental analysis of the proposed role of heterosynaptic plasticity in behavior. Here we circumvent this obstacle by testing specific predictions about the behavioral consequences of the impairment of heterosynaptic plasticity by experimental manipulations to adenosine A1 receptors (A1Rs). Our prior work demonstrated that the blockade of adenosine A1 receptors impairs heterosynaptic plasticity in brain slices and, when implemented in computer models, selectively impairs repetitive learning on sequential tasks. Based on this work, we predict that A1R knock-out (KO) mice will express (1) impairment of heterosynaptic plasticity and (2) behavioral deficits in learning on sequential tasks. Using electrophysiological experiments in slices and behavioral testing of animals of both sexes, we show that, compared with wild-type controls, A1R KO mice have impaired synaptic plasticity in visual cortex neurons, coupled with significant deficits in visual discrimination learning. Deficits in A1R knockouts were seen specifically during relearning, becoming progressively more apparent with learning on sequential visual discrimination tasks of increasing complexity. These behavioral results confirm our model predictions and provide the first experimental evidence for a proposed role of heterosynaptic plasticity in organism-level learning. Moreover, these results identify heterosynaptic plasticity as a new potential target for interventions that may help to enhance new learning on a background of existing memories.SIGNIFICANCE STATEMENT Understanding how interacting forms of synaptic plasticity mediate learning is fundamental for neuroscience. Theory and modeling revealed that, in addition to Hebbian-type associative plasticity, heterosynaptic changes at synapses that were not active during induction are necessary for stable system operation and fine-grained discrimination learning. However, lacking tools for selective manipulation prevented behavioral analysis of heterosynaptic plasticity. Here we circumvent this barrier: from our prior experimental and computational work we predict differential behavioral consequences of the impairment of Hebbian-type versus heterosynaptic plasticity. We show that, in adenosine A1 receptor knock-out mice, impaired synaptic plasticity in visual cortex neurons is coupled with specific deficits in learning sequential, increasingly complex visual discrimination tasks. This provides the first evidence linking heterosynaptic plasticity to organism-level learning.

Reorganization of auditory-visual network interactions in long-term unilateral postlingual hearing loss.

Long-term unilateral hearing loss could reorganize the functional network association between the bilateral auditory cortices, while alterations of other functional networks need to be further explored. We attempted to investigate the pattern of the reorganization of functional network associations between the auditory and visual cortex caused by long-term postlingual unilateral hearing loss (UHI) and its relationship with clinical characteristics. Therefore, 48 patients with hearing loss caused by unilateral acoustic tumors and 52 matched healthy controls were enrolled, and their high-resolution structural MRI and resting-state functional MRI data were also collected to depict the brain network. Degree centrality (DC) was employed to evaluate the functional network association of the auditory-visual network interaction. Group comparisons were performed to investigate the network reorganization, and its correlations with clinical data were calculated. Compared with the healthy control group, patients with UHI showed significantly increased DC between the auditory network (superior temporal gyrus and the medial geniculate body) and the visual network. Meanwhile, this difference was positively correlated with the extent of hearing impairment, and the correlation was more significant with the ipsilateral superior temporal gyrus in cases of acoustic neuroma. These results suggest that long-term unilateral hearing impairment may lead to enhancement of the visual-auditory network interactions and that the degree of reorganization is positively correlated with the pure tone average (PTA) and is more significant for the ipsilateral superior temporal gyrus, which provides clinical evidence regarding cross-modal plasticity in the UHI and its lateralization.