Automated registration-based skull stripping procedure for feline neuroimaging.

Skull stripping is a fundamental preprocessing step in modern neuroimaging analyses that consists of removing non-brain voxels from structural images. When performed entirely manually, this laborious step can be rate-limiting for analyses, with the potential to influence the population size chosen. This emphasizes the need for a fully- or semi-automated masking procedure to decrease man-hours without an associated decline in accuracy. These algorithms are plentiful in human neuroimaging but are relatively lacking for the plethora of animal species used in research. Unfortunately, software designed for humans cannot be easily transformed for animal use due to the high amount of tailoring required to accurately account for the considerable degree of variation within the highly folded human cortex. As most animals have a relatively less complex cerebral morphology, intersubject variability is consequently decreased, presenting the possibility to simply warp the brain mask of a template image into subject space for the purpose of skull stripping. This study presents the use of the Cat Automated Registration-based Skull Stripper (CARSS) tool on feline structural images. Validation metrics revealed that this method was able to perform on par with manual raters on >90 % of scans tested, and that its consistency across multiple runs was superior to that of masking performed by two independent raters. Additionally, CARSS outperformed three well-known skull stripping programs on the validation dataset. Despite a handful of manual interventions required, the presented tool reduced the man-hours required to skull strip 60 feline images over tenfold when compared to a fully manual approach, proving to be invaluable for feline neuroimaging studies, particularly those with large population sizes.

Gray matter volume of the feline cerebral cortex and structural plasticity following perinatal deafness.

In response to sensory deprivation, the brain adapts according to contemporary demands to efficiently navigate a modified perceptual environment. This reorganization may result in improved processing of the remaining senses-a phenomenon referred to as compensatory crossmodal plasticity. One approach to explore this neuroplasticity is to consider the macrostructural changes in neural tissue that mirror this functional optimization. The current study is the first of its kind to measure MRI-derived gray matter (GM) volumes of control felines (n=30), while additionally identifying volumetric differences in response to perinatal deafness (30 ototoxically-deafened cats). To accomplish this purpose, regional and morphometric methods were performed in parallel. The regional analysis evaluated volumetric alterations of global GM, as well as the volumes of 146 regions of interest (ROIs) and 12 functional subgroupings of these ROIs. Results revealed whole-brain GM preservation; however, somatosensory and visual cortices exhibited an overall increase in volume. On a smaller scale, this analysis uncovered two auditory ROIs (second auditory cortex, A2, and ventral auditory field, VAF) that decreased in volume alongside two visual regions (anteromedial lateral suprasylvian area, AMLS and splenial visual area, SVA) that increased-all localized within the right hemisphere. Comparatively, the findings of tensor-based morphometry (TBM) generally aligned with those of the ROI-based method, as this voxel-wise approach demonstrated clusters of expansion coincident with visual- and somatosensory-related loci; although, it failed to detect any GM reductions following deafness. As distinct differences were identified in each analysis, the current study highlights the importance of employing multiple methods when exploring MRI volumetry. Overall, this study proposes that volumetric alterations within sensory loci allude to a redistribution of cortical space arising from modified perceptual demands following auditory deprivation.

Connectome alterations following perinatal deafness in the cat.

Following sensory deprivation, areas and networks in the brain may adapt and reorganize to compensate for the loss of input. These adaptations are manifestations of compensatory crossmodal plasticity, which has been documented in both human and animal models of deafness-including the domestic cat. Although there are abundant examples of structural plasticity in deaf felines from retrograde tracer-based studies, there is a lack of diffusion-based knowledge involving this model compared to the current breadth of human research. The purpose of this study was to explore white matter structural adaptations in the perinatally-deafened cat via tractography, increasing the methodological overlap between species. Plasticity was examined by identifying unique group connections and assessing altered connectional strength throughout the entirety of the brain. Results revealed a largely preserved connectome containing a limited number of group-specific or altered connections focused within and between sensory networks, which is generally corroborated by deaf feline anatomical tracer literature. Furthermore, five hubs of cortical plasticity and altered communication following perinatal deafness were observed. The limited differences found in the present study suggest that deafness-induced crossmodal plasticity is largely built upon intrinsic structural connections, with limited remodeling of underlying white matter.

The gradient in gray matter thickness across auditory cortex and differential cortical thickness changes following perinatal deafness.

In the absence of hearing during development, the brain adapts and repurposes what was destined to become auditory cortex. As cortical thickness is commonly used as a proxy to identify cortical regions that have undergone plastic changes, the purpose of this investigation was to compare cortical thickness patterns between hearing and deaf cats. In this study, normal hearing (n = 29) and deaf (n = 26) cats were scanned to examine cortical thickness in hearing controls, as well as differential changes in thickness as a consequence of deafness. In hearing cats, a gradient in cortical thickness was identified across auditory cortex in which it is thinner in more dorsal regions and thicker in more ventral regions. Compared with hearing controls, differential thickening and thinning was observed in specific regions of deaf auditory cortex. More dorsal regions were found to be bilaterally thicker in the deaf group, while more ventral regions in the left hemisphere were thinner. The location and nature of these changes creates a gradient along the dorsoventral axis, wherein dorsal auditory cortical fields are thicker, whereas more ventral fields are thinner in deaf animals compared with hearing controls.

Resilience of FEF neuronal saccade code to V4 perturbations.

The frontal eye field (FEF) plays a key role in initiating rapid eye movements known as saccades. Accumulation models have been proposed to explain the dynamic of these neurons and how they may enable the initiation of saccades. To update the scope of the viability of this model, we studied single neurons recorded from the FEF of two rhesus monkeys while they performed a memory-guided saccade task. We evaluated the degree to which each type of FEF neuron complied with these models by quantifying how precisely their discharge predicted an imminent saccade based on their immediate presaccadic activity. We found that decoders trained on single neurons with a stronger motor component performed better than decoders trained on neurons with a stronger visual component in predicting the saccade. Importantly, despite a dramatic effect on the reaction times, the perturbations delivered to the FEF neurons via area V4 did not impact their saccade predictability. Our results demonstrate a high degree of resilience of the FEF neuronal presaccadic discharge patterns, fulfilling the predictions of accumulation models.NEW & NOTEWORTHY We studied neurons in the brain's frontal eye field (FEF) to understand how these neurons predict swift eye shifts called saccades. We found that neurons with more movement-related activity were better at predicting saccades than those with sensory-related activity. Interestingly, electrical disruptions of this region strongly impacted saccade onset times but did not affect the individual neuron's saccade predictability, consistent with models suggesting that a specific threshold in neural activity triggers the saccade.

Deafness induces complete crossmodal plasticity in a belt region of dorsal auditory cortex.

Many neural areas, where patterned activity is lost following deafness, have the capacity to become activated by the remaining sensory systems. This crossmodal plasticity can be measured at perceptual/behavioural as well as physiological levels. The dorsal zone (DZ) of auditory cortex of deaf cats is involved in supranormal visual motion detection, but its physiological level of crossmodal reorganisation is not well understood. The present study of early-deaf DZ (and hearing controls) used multiple single-channel recording methods to examine neuronal responses to visual, auditory, somatosensory and combined stimulation. In early-deaf DZ, no auditory activation was observed, but 100% of the neurons were responsive to visual cues of which 21% were also influenced by somatosensory stimulation. Visual and somatosensory responses were not anatomically organised as they are in hearing cats, and fewer multisensory neurons were present in the deaf condition. These crossmodal physiological results closely correspond with and support the perceptual/behavioural enhancements that occur following hearing loss.

Multisensory responses in a belt region of the dorsal auditory cortical pathway.

A basic function of the cerebral cortex is to receive and integrate information from different sensory modalities into a comprehensive percept of the environment. Neurons that demonstrate multisensory convergence occur across the necortex but are especially prevalent in higher order association areas. However, a recent study of a cat higher order auditory area, the dorsal zone (DZ) of auditory cortex, did not observe any multisensory features. Therefore, the goal of the present investigation was to address this conflict using recording and testing methodologies that are established for exposing and studying multisensory neuronal processing. Among the 482 neurons studied, we found that 76.6% were influenced by non-auditory stimuli. Of these neurons, 99% were affected by visual stimulation, but only 11% by somatosensory. Furthermore, a large proportion of the multisensory neurons showed integrated responses to multisensory stimulation, constituted a majority of the excitatory and inhibitory neurons encountered (as identified by the duration of their waveshape) and exhibited a distinct spatial distribution within DZ. These findings demonstrate that the DZ of auditory cortex robustly exhibits multisensory properties and that the proportions of multisensory neurons encountered are consistent with those identified in other higher order cortices.

Macaque anterior cingulate cortex deactivation impairs performance and alters lateral prefrontal oscillatory activities in a rule-switching task.

In primates, both the dorsal anterior cingulate cortex (dACC) and the dorsolateral prefrontal cortex (dlPFC) are key regions of the frontoparietal cognitive control network. To study the role of the dACC and its communication with the dlPFC in cognitive control, we recorded local field potentials (LFPs) from the dlPFC before and during the reversible deactivation of the dACC, in macaque monkeys engaging in uncued switches between 2 stimulus-response rules, namely prosaccade and antisaccade. Cryogenic dACC deactivation impaired response accuracy during maintenance of-but not the initial switching to-the cognitively demanding antisaccade rule, which coincided with a reduction in task-related theta activity and the correct-error (C-E) difference in dlPFC beta-band power. During both rule switching and maintenance, dACC deactivation prolonged the animals' reaction time and reduced task-related alpha power in the dlPFC. Our findings support a role of the dACC in prefrontal oscillatory activities that are involved the maintenance of a new, challenging task rule.

Early hearing loss induces plasticity within extra-striate visual cortex.

Supranormal perceptual performance has been observed within the intact senses of early-deaf or blind humans and animals. For cortical areas deprived of their normal sensory input, numerous studies have shown that the lesioned modality is replaced by that of the intact sensory modalities through a process termed crossmodal plasticity. In contrast, little is known about the effects of loss of a particular sensory modality on the cortical representations of the remaining, intact sensory modalities. In the present study, an area of extrastriate visual cortex from early-deaf adult cats was examined for features of dendritic plasticity known to occur after early-deafness. Using light-microscopy of Golgi-stained pyramidal neurons from the posterolateral lateral suprasylvian (PLLS) cortex, dendritic spine density significantly increased (~19%), while spine head size was slightly but significantly decreased (~9%) following early hearing loss. Curiously, these changes were not localized to regions of the visual PLLS known to receive auditory inputs, but instead showed a broad pattern more reflective of the distribution of the area's visual features. Whereas hearing loss results in crossmodal plasticity in auditory cortices, the same peripheral lesion can also induce intramodal plasticity within representations of the intact sensory systems that may also contribute to supranormal performance.

Frontal eye field inactivation alters the readout of superior colliculus activity for saccade generation in a task-dependent manner.

Saccades require a spatiotemporal transformation of activity between the intermediate layers of the superior colliculus (iSC) and downstream brainstem burst generator. The dynamic linear ensemble-coding model (Goossens and Van Opstal 2006) proposes that each iSC spike contributes a fixed mini-vector to saccade displacement. Although biologically-plausible, this model assumes cortical areas like the frontal eye fields (FEF) simply provide the saccadic goal to be executed by the iSC and brainstem burst generator. However, the FEF and iSC operate in unison during saccades, and a pathway from the FEF to the brainstem burst generator that bypasses the iSC exists. Here, we investigate the impact of large yet reversible inactivation of the FEF on iSC activity in the context of the model across four saccade tasks. We exploit the overlap of saccade vectors generated when the FEF is inactivated or not, comparing the number of iSC spikes for metrically-matched saccades. We found that the iSC emits fewer spikes for metrically-matched saccades during FEF inactivation. The decrease in spike count is task-dependent, with a greater decrease accompanying more cognitively-demanding saccades. Our results show that FEF integrity influences the readout of iSC activity in a task-dependent manner. We propose that the dynamic linear ensemble-coding model be modified so that FEF inactivation increases the gain of a readout parameter, effectively increasing the influence of a single iSC spike. We speculate that this modification could be instantiated by FEF and iSC pathways to the cerebellum that could modulate the excitability of the brainstem burst generator.

Impairment but not abolishment of express saccades after unilateral or bilateral inactivation of the frontal eye fields.

Express saccades are a manifestation of a visual grasp reflex triggered when visual information arrives in the intermediate layers of the superior colliculus (SCi), which in turn orchestrates the lower level brainstem saccade generator to evoke a saccade with a very short latency (~100 ms or less). A prominent theory regarding express saccades generation is that they are facilitated by preparatory signals, presumably from cortical areas, which prime the SCi before the arrival of visual information. Here, we test this theory by reversibly inactivating a key cortical input to the SCi, the frontal eye fields (FEF), while monkeys perform an oculomotor task that promotes express saccades. Across three tasks with a different combination of potential target locations and unilateral or bilateral FEF inactivation, we found a spared ability for monkeys to generate express saccades, despite decreases in express saccade frequency during FEF inactivation. This result is consistent with the FEF having a facilitatory but not critical role in express saccade generation, likely because other cortical areas compensate for the loss of preparatory input to the SCi. However, we also found decreases in the accuracy and peak velocity of express saccades generated during FEF inactivation, which argues for an influence of the FEF on the saccadic burst generator even during express saccades. Overall, our results shed further light on the role of the FEF in the shortest-latency visually-guided eye movements.NEW & NOTEWORTHY Express saccades are the shortest-latency saccade. The frontal eye fields (FEF) are thought to promote express saccades by presetting the superior colliculus. Here, by reversibly inactivating the FEF either unilaterally or bilaterally via cortical cooling, we support this by showing that the FEF plays a facilitative but not critical role in express saccade generation. We also found that FEF inactivation lowered express saccade peak velocity, emphasizing a contribution of the FEF to express saccade kinematics.

The limited capacity of visual temporal integration in cats.

It has been long known that prolonging stimulus duration may increase the perceived brightness of a visual stimulus. The interaction between intensity and duration generally follows a rule, such as that described in Bloch's law. This visual temporal integration relationship has been identified in human subjects and in non-human primates. However, although auditory temporal integration has been extensively studied in the cat, visual temporal integration has not. Therefore, the goal of this study was to examine visual temporal integration in the cat. We trained five cats to respond when a brief luminance change was detected in a fixation dot. After training, we measured the success rate of detecting the luminance change with varying durations at threshold, subthreshold, and suprathreshold luminance levels. Psychometric functions showed that prolonging stimulus duration improved task performance, more noticeably for stimuli below 100 ms than beyond. Most psychometric functions were better fit to an exponential model than to a linear model. The gradually saturated performance observed here, as in previous studies, can be explained by the "leaky integrator" hypothesis, that is, temporal integration is only valid below a critical duration. Overall, we developed a task whereby visual temporal integration was successfully demonstrated in the cat. The effect of stimulus duration on detection success rate displayed a pattern generally consistent with previous human and non-human primate findings on visual temporal integration.

Modified Origins of Cortical Projections to the Superior Colliculus in the Deaf: Dispersion of Auditory Efferents.

Following the loss of a sensory modality, such as deafness or blindness, crossmodal plasticity is commonly identified in regions of the cerebrum that normally process the deprived modality. It has been hypothesized that significant changes in the patterns of cortical afferent and efferent projections may underlie these functional crossmodal changes. However, studies of thalamocortical and corticocortical connections have refuted this hypothesis, instead revealing a profound resilience of cortical afferent projections following deafness and blindness. This report is the first study of cortical outputs following sensory deprivation, characterizing cortical projections to the superior colliculus in mature cats (N = 5, 3 female) with perinatal-onset deafness. The superior colliculus was exposed to a retrograde pathway tracer, and subsequently labeled cells throughout the cerebrum were identified and quantified. Overall, the percentage of cortical projections arising from auditory cortex was substantially increased, not decreased, in early-deaf cats compared with intact animals. Furthermore, the distribution of labeled cortical neurons was no longer localized to a particular cortical subregion of auditory cortex but dispersed across auditory cortical regions. Collectively, these results demonstrate that, although patterns of cortical afferents are stable following perinatal deafness, the patterns of cortical efferents to the superior colliculus are highly mutable.SIGNIFICANCE STATEMENT When a sense is lost, the remaining senses are functionally enhanced through compensatory crossmodal plasticity. In deafness, brain regions that normally process sound contribute to enhanced visual and somatosensory perception. We demonstrate that hearing loss alters connectivity between sensory cortex and the superior colliculus, a midbrain region that integrates sensory representations to guide orientation behavior. Contrasting expectation, the proportion of projections from auditory cortex increased in deaf animals compared with normal hearing, with a broad distribution across auditory fields. This is the first description of changes in cortical efferents following sensory loss and provides support for models predicting an inability to form a coherent, multisensory percept of the environment following periods of abnormal development.

What and How the Deaf Brain Sees.

Over the past decade, there has been an unprecedented level of interest and progress into understanding visual processing in the brain of the deaf. Specifically, when the brain is deprived of input from one sensory modality (such as hearing), it often compensates with supranormal performance in one or more of the intact sensory systems (such as vision). Recent psychophysical, functional imaging, and reversible deactivation studies have converged to define the specific visual abilities that are enhanced in the deaf, as well as the cortical loci that undergo crossmodal plasticity in the deaf and are responsible for mediating these superior visual functions. Examination of these investigations reveals that central visual functions, such as object and facial discrimination, and peripheral visual functions, such as motion detection, visual localization, visuomotor synchronization, and Vernier acuity (measured in the periphery), are specifically enhanced in the deaf, compared with hearing participants. Furthermore, the cortical loci identified to mediate these functions reside in deaf auditory cortex: BA 41, BA 42, and BA 22, in addition to the rostral area, planum temporale, Te3, and temporal voice area in humans; primary auditory cortex, anterior auditory field, dorsal zone of auditory cortex, auditory field of the anterior ectosylvian sulcus, and posterior auditory field in cats; and primary auditory cortex and anterior auditory field in both ferrets and mice. Overall, the findings from these studies show that crossmodal reorganization in auditory cortex of the deaf is responsible for the superior visual abilities of the deaf.

A Causal Role for the Cortical Frontal Eye Fields in Microsaccade Deployment.

Microsaccades aid vision by helping to strategically sample visual scenes. Despite the importance of these small eye movements, no cortical area has ever been implicated in their generation. Here, we used unilateral and bilateral reversible inactivation of the frontal eye fields (FEF) to identify a cortical drive for microsaccades. Unexpectedly, FEF inactivation altered microsaccade metrics and kinematics. Such inactivation also impaired microsaccade deployment following peripheral cue onset, regardless of cue side or inactivation configuration. Our results demonstrate that the FEF provides critical top-down drive for microsaccade generation, particularly during the recovery of microsaccades after disruption by sensory transients. Our results constitute the first direct evidence, to our knowledge, for the contribution of any cortical area to microsaccade generation, and they provide a possible substrate for how cognitive processes can influence the strategic deployment of microsaccades.

Memory-Guided Stumbling Correction in the Hindlimb of Quadrupeds Relies on Parietal Area 5.

In complex environments, tripping over an unexpected obstacle evokes the stumbling corrective reaction, eliciting rapid limb hyperflexion to lift the leg over the obstruction. While stumbling correction has been characterized within a single limb in the cat, this response must extend to both forelegs and hindlegs for successful avoidance in naturalistic settings. Furthermore, the ability to remember an obstacle over which the forelegs have tripped is necessary for hindleg clearance if locomotion is delayed. Therefore, memory-guided stumbling correction was studied in walking cats after the forelegs tripped over an unexpected obstacle. Tactile input to only one foreleg was often sufficient in modulating stepping of all four legs when locomotion was continuous, or when hindleg clearance was delayed. When obstacle height was varied, animals appropriately scaled step height to obstacle height. As tactile input without foreleg clearance was insufficient in reliably modulating stepping, efference, or proprioceptive information about modulated foreleg stepping may be important for producing a robust, long-lasting memory. Finally, cooling-induced deactivation of parietal area 5 altered hindleg stepping in a manner indicating that animals no longer recalled the obstacle over which they had tripped. Altogether, these results demonstrate the integral role area 5 plays in memory-guided stumbling correction.

Contributions of Parietal Cortex to the Working Memory of an Obstacle Acquired Visually or Tactilely in the Locomoting Cat.

A working memory of obstacles is essential for navigating complex, cluttered terrain. In quadrupeds, it has been proposed that parietal cortical areas related to movement planning and working memory may be important for guiding the hindlegs over an obstacle previously cleared by the forelegs. To test this hypothesis, parietal areas 5 and 7 were reversibly deactivated in walking cats. The working memory of an obstacle was assessed in both a visually dependent and tactilely dependent paradigm. Reversible bilateral deactivation of area 5, but not area 7, altered hindleg stepping in a manner indicating that the animals did not recall the obstacle over which their forelegs had stepped. Similar deficits were observed when area 5 deactivation was restricted to the delay during which obstacle memory must be maintained. Furthermore, partial memory recovery observed when area 5 function was deactivated and restored within this maintenance period suggests that the deactivation may suppress, but not eliminate, the working memory of an obstacle. As area 5 deactivations incurred similar memory deficits in both visual and tactile obstacle working memory paradigms, parietal area 5 is critical for maintaining the working memory of an obstacle acquired via vision or touch that is used to modify stepping for avoidance.

Posterior Inferotemporal Cortex Cells Use Multiple Input Pathways for Shape Encoding.

In the macaque monkey brain, posterior inferior temporal (PIT) cortex cells contribute to visual object recognition. They receive concurrent inputs from visual areas V4, V3, and V2. We asked how these different anatomical pathways shape PIT response properties by deactivating them while monitoring PIT activity in two male macaques. We found that cooling of V4 or V2|3 did not lead to consistent changes in population excitatory drive; however, population pattern analyses showed that V4-based pathways were more important than V2|3-based pathways. We did not find any image features that predicted decoding accuracy differences between both interventions. Using the HMAX hierarchical model of visual recognition, we found that different groups of simulated "PIT" units with different input histories (lacking "V2|3" or "V4" input) allowed for comparable levels of object-decoding performance and that removing a large fraction of "PIT" activity resulted in similar drops in performance as in the cooling experiments. We conclude that distinct input pathways to PIT relay similar types of shape information, with V1-dependent V4 cells providing more quantitatively useful information for overall encoding than cells in V2 projecting directly to PIT.SIGNIFICANCE STATEMENT Convolutional neural networks are the best models of the visual system, but most emphasize input transformations across a serial hierarchy akin to the primary "ventral stream" (V1 → V2 → V4 → IT). However, the ventral stream also comprises parallel "bypass" pathways: V1 also connects to V4, and V2 to IT. To explore the advantages of mixing long and short pathways in the macaque brain, we used cortical cooling to silence inputs to posterior IT and compared the findings with an HMAX model with parallel pathways.

Frontal Eye Field Inactivation Diminishes Superior Colliculus Activity, But Delayed Saccadic Accumulation Governs Reaction Time Increases.

Stochastic accumulator models provide a comprehensive framework for how neural activity could produce behavior. Neural activity within the frontal eye fields (FEFs) and intermediate layers of the superior colliculus (iSC) support such models for saccade initiation by relating variations in saccade reaction time (SRT) to variations in such parameters as baseline, rate of accumulation of activity, and threshold. Here, by recording iSC activity during reversible cryogenic inactivation of the FEF in four male nonhuman primates, we causally tested which parameter(s) best explains concomitant increases in SRT. While FEF inactivation decreased all aspects of ipsilesional iSC activity, decreases in accumulation rate and threshold poorly predicted accompanying increases in SRT. Instead, SRT increases best correlated with delays in the onset of saccade-related accumulation. We conclude that FEF signals govern the onset of saccade-related accumulation within the iSC, and that the onset of accumulation is a relevant parameter for stochastic accumulation models of saccade initiation.SIGNIFICANCE STATEMENT The superior colliculus (SC) and frontal eye fields (FEFs) are two of the best-studied areas in the primate brain. Surprisingly, little is known about what happens in the SC when the FEF is temporarily inactivated. Here, we show that temporary FEF inactivation decreases all aspects of functionally related activity in the SC. This combination of techniques also enabled us to relate changes in SC activity to concomitant increases in saccadic reaction time (SRT). Although stochastic accumulator models relate SRT increases to reduced rates of accumulation or increases in threshold, such changes were not observed in the SC. Instead, FEF inactivation delayed the onset of saccade-related accumulation, emphasizing the importance of this parameter in biologically plausible models of saccade initiation.

Effects of neonatal deafness on resting-state functional network connectivity.

Normal brain development depends on early sensory experience. Behavioral consequences of brain maturation in the absence of sensory input early in life are well documented. For example, experiments with mature, neonatally deaf human or animal subjects have revealed improved peripheral visual motion detection and spatial localization abilities. Such supranormal behavioral abilities in the nondeprived sensory modality are evidence of compensatory plasticity occurring in deprived brain regions at some point or throughout development. Sensory deprived brain regions may simply become unused neural real-estate resulting in a loss of function. Compensatory plasticity and loss of function are likely reflected in the differences in correlations between brain networks in deaf compared with hearing subjects. To address this, we used resting-state functional magnetic resonance imaging (fMRI) in lightly anesthetized hearing and neonatally deafened cats. Group independent component analysis (ICA) was used to identify 20 spatially distinct brain networks across all animals including auditory, visual, somatosensory, cingulate, insular, cerebellar, and subcortical networks. The resulting group ICA components were back-reconstructed to individual animal brains. The maximum correlations between the time-courses associated with each spatial component were computed using functional network connectivity (FNC). While no significant differences in the delay to peak correlations were identified between hearing and deaf cats, we observed 10 (of 190) significant differences in the amplitudes of between-network correlations. Six of the significant differences involved auditory-related networks and four involved visual, cingulate, or somatosensory networks. The results are discussed in context of known behavioral, electrophysiological, and anatomical differences following neonatal deafness. Furthermore, these results identify novel targets for future investigations at the neuronal level.