Common Neural Substrates Research Articles

Dose–response of tDCS effects on motor learning and cortical excitability: A preregistered study

Abstract Multiple studies have demonstrated that transcranial direct current stimulation (tDCS) of the primary motor cortex (M1) can influence corticospinal excitability and motor skill acquisition. However, the evidence for these effects is inconsistent, and a common neural substrate for these effects has not been directly demonstrated. To address this, we hypothesized that higher tDCS intensities would produce more robust effects, and uncover their relationship. In this preregistered study, 120 participants engaged in a motor skill learning task while receiving tDCS with posterior-to-anterior currents through M1. We employed a double-blind, between-subjects design, with groups of 4 mA, 6 mA, or sham stimulation, while ensuring balanced groups in terms of typing speed. Cortical excitability was assessed via motor-evoked potentials (MEPs) and TMS-evoked potentials (TEPs) before and after motor skill learning with concurrent tDCS. tDCS at these higher intensities was well tolerated, and motor learning correlated with pretraining typing speed. Planned analyses found no dose–response effect of tDCS on motor skill performance or MEP amplitude. This suggests that, under our experimental conditions, tDCS did not significantly modulate motor skill learning or corticospinal excitability. Furthermore, there was no correlation between motor performance and MEP, and thus no evidence for a common neural substrate. Exploratory analyses found an increase in MEP and TEP amplitudes following the sequence learning task. Motor skill gains positively correlated with TEP changes over the stimulated M1, which were more negative with increasing tDCS intensity. The effects of tDCS on motor skill learning and MEPs, if they exist, may require particular experimental conditions that have not been tested here. Preregistration: https://osf.io/jyuev (in-principle acceptance: 2024/06/05)

Neural correlates of phonetic categorization under auditory (phoneme) and visual (grapheme) modalities

This study assessed the neural mechanisms and relative saliency of categorization for speech sounds and comparable graphemes (i.e., visual letters) of the same phonetic label. Given that linguistic experience shapes categorical processing, and letter-speech sound matching plays a crucial role during early reading acquisition, we hypothesized sound phoneme and visual grapheme tokens representing the same linguistic identity might recruit common neural substrates, despite originating from different sensory modalities. Behavioral and neuroelectric brain responses (ERPs) were acquired as participants categorized stimuli from sound (phoneme) and homologous letter (grapheme) continua each spanning a /da/−/ga/ gradient. Behaviorally, listeners were faster and showed stronger categorization of phoneme compared to graphemes. At the neural level, multidimensional scaling of the EEG revealed responses self-organized in a categorial fashion such that tokens clustered within their respective modality beginning ∼150–250 ms after stimulus onset. Source-resolved ERPs further revealed modality-specific and overlapping brain regions supporting phonetic categorization. Left inferior frontal gyrus and auditory cortex showed stronger responses for sound category members compared to phonetically ambiguous tokens, whereas early visual cortices paralleled this categorical organization for graphemes. Auditory and visual categorization also recruited common visual association areas in extrastriate cortex but in opposite hemispheres (auditory = left; visual = right). Our findings reveal both auditory and visual sensory cortex supports categorical organization for phonetic labels within their respective modalities. However, a partial overlap in phoneme and grapheme processing among occipital brain areas implies the presence of an isomorphic, domain-general mapping for phonetic categories in dorsal visual system

General anesthesia activates a central anxiolytic center in the BNST

Low doses of general anesthetics like ketamine and dexmedetomidine have anxiolytic properties independent of their sedative effects, but the underlying mechanisms remain unclear. We discovered a population of GABAergic neurons in the oval division of the bed nucleus of the stria terminalis that are activated by multiple anesthetics and the anxiolytic drug diazepam (ovBNSTGA). The majority of ovBNSTGA neurons express neurotensin receptor 1 (Ntsr1) and form circuits with brain regions known to regulate anxiety and stress responses. Optogenetic activation of ovBNSTGA or ovBNSTNtsr1 neurons significantly attenuated anxiety-like behaviors in both naive animals and mice with inflammatory pain, while inhibition of these cells elevated anxiety. Activation of these neurons decreased heart rate and increased heart rate variability, suggesting that they reduce anxiety by modulating autonomic responses. Our study identifies ovBNSTGA/ovBNSTNtsr1 neurons as a common neural substrate mediating the anxiolytic effect of low-dose anesthetics and a potential therapeutic target for treating anxiety-related disorders.

The shared neurobiological basis of developmental dyslexia and developmental stuttering: A meta-analysis of functional and structural MRI studies

BackgroundDevelopmental dyslexia (DD) and persistent developmental stuttering (PDS) are the most representative written and spoken language disorders, respectively, and both significantly hinder life success. Although widespread brain alterations are evident in both DD and PDS, it remains unclear to what extent these two language disorders share common neural substrates. MethodsA systematic review and meta-analysis of task-based functional magnetic resonance imaging (fMRI) and voxel-based morphometry (VBM) studies of PDS and DD were conducted to explore the shared functional and anatomical alterations across these disorders. ResultsThe results of fMRI studies indicated shared hypoactivation in the left inferior temporal gyrus and inferior parietal gyrus across PDS and DD compared to healthy controls. When examined separately for children and adults, we found that child participants exhibited reduced activation in the left inferior temporal gyrus, inferior parietal gyrus, precentral gyrus, middle temporal gyrus, and inferior frontal gyrus, possibly reflecting the universal causes of written and spoken language disorders. In contrast, adult participants exhibited hyperactivation in the right precentral gyrus and left cingulate motor cortex, possibly reflecting common compensatory mechanisms. Anatomically, the analysis of VBM studies revealed decreased gray matter volume in the left inferior frontal gyrus across DD and PDS, which was exclusively observed in children. Finally, meta-analytic connectivity modeling and brain-behavior correlation analyses were conducted to explore functional connectivity patterns and related cognitive functions of the brain regions commonly involved in DD and PDS. ConclusionsThis study identified concordances in brain abnormalities across DD and PDS, suggesting common neural substrates for written and spoken language disorders and providing new insights into the transdiagnostic neural signatures of language disorders.

Functional diversity along the anteroposterior axis of the ventromedial hypothalamus.

Innate behaviors ensure animal survival and reproductive success. Defending their territory, escaping from predators or mating with a sexual partner, are fundamental behaviors determining the ecological fitness of individuals. Remarkably, all these behaviors share a common neural substrate, as they are under the control of the ventromedial hypothalamus (VMH). Decades of research have contributed to understanding the exquisite diversity of functional ensembles underlying the wide array of functions that the VMH carries out. These functional ensembles are usually distributed throughout the dorsoventral and mediolateral axes of this nucleus. However, increasing evidence is bringing to attention the functional diversity of the VMH across its anteroposterior axis. In this review, we will overview our current understanding of how different ensembles within the VMH control a wide array of animal behaviors, emphasizing the newly discovered roles for its anterior subdivision in the context of conspecific self-defense.

Unique Functional Neuroimaging Signatures of Genetic Versus Clinical High Risk for Psychosis

Background22q11.2 deletion syndrome (22qDel) is a copy number variant that is associated with psychosis and other neurodevelopmental disorders. Adolescents who are at clinical high risk for psychosis (CHR) are identified based on the presence of subthreshold psychosis symptoms. Whether common neural substrates underlie these distinct high-risk populations is unknown. We compared functional brain measures in 22qDel and CHR cohorts and mapped the results to biological pathways. MethodsWe analyzed 2 large multisite cohorts with resting-state functional magnetic resonance imaging data: 1) a 22qDel cohort (n = 164, 47% female) and typically developing (TD) control participants (n = 134, 56% female); and 2) a cohort of CHR individuals (n = 240, 41% female) and TD control participants (n = 149, 46% female) from the NAPLS-2 (North American Prodrome Longitudinal Study-2). We computed global brain connectivity (GBC), local connectivity (LC), and brain signal variability (BSV) across cortical regions and tested case-control differences for 22qDel and CHR separately. Group difference maps were related to published brain maps using autocorrelation-preserving permutation. ResultsBSV, LC, and GBC were significantly disrupted in individuals with 22qDel compared with TD control participants (false discovery rate–corrected q < .05). Spatial maps of BSV and LC differences were highly correlated with each other, unlike GBC. In the CHR group, only LC was significantly altered versus the control group, with a different spatial pattern than the 22qDel group. Group differences mapped onto biological gradients, with 22qDel effects being strongest in regions with high predicted blood flow and metabolism. Conclusions22qDel carriers and CHR individuals exhibited different effects on functional magnetic resonance imaging temporal variability and multiscale functional connectivity. In 22qDel carriers, strong and convergent disruptions in BSV and LC that were not seen in CHR individuals suggest distinct functional brain alterations.

Neural correlates of phonetic categorization under auditory (phoneme) and visual (grapheme) modalities.

We tested whether the neural mechanisms of phonetic categorization are specific to speech sounds or generalize to graphemes (i.e., visual letters) of the same phonetic label. Given that linguistic experience shapes categorical processing, and letter-speech sound matching plays a crucial role during early reading acquisition, we hypothesized sound phoneme and visual grapheme tokens representing the same linguistic identity might recruit common neural substrates, despite originating from different sensory modalities. Behavioral and neuroelectric brain responses (ERPs) were acquired as participants categorized stimuli from sound (phoneme) and homologous letter (grapheme) continua each spanning a /da/ - /ga/ gradient. Behaviorally, listeners were faster and showed stronger categorization of phoneme compared to graphemes. At the neural level, multidimensional scaling of the EEG revealed responses self-organized in a categorial fashion such that tokens clustered within their respective modality beginning ∼150-250 ms after stimulus onset. Source-resolved ERPs further revealed modality-specific and overlapping brain regions supporting phonetic categorization. Left inferior frontal gyrus and auditory cortex showed stronger responses for sound category members compared to phonetically ambiguous tokens, whereas early visual cortices paralleled this categorical organization for graphemes. Auditory and visual categorization also recruited common visual association areas in extrastriate cortex but in opposite hemispheres (auditory = left; visual=right). Our findings reveal both auditory and visual sensory cortex supports categorical organization for phonetic labels within their respective modalities. However, a partial overlap in phoneme and grapheme processing among occipital brain areas implies the presence of an isomorphic, domain-general mapping for phonetic categories in dorsal visual system.

Precision mapping of the default network reveals common and distinct (inter) activity for autobiographical memory and theory of mind.

The default network is widely implicated as a common neural substrate for self-generated thought, such as remembering one's past (autobiographical memory) and imagining the thoughts and feelings of others (theory of mind). Findings that the default network comprises subnetworks of regions, some commonly and some distinctly involved across processes, suggest that one's own experiences inform their understanding of others. With the advent of precision functional MRI (fMRI) methods, however, it is unclear if this shared substrate is observed instead due to traditional group analysis methods. We investigated this possibility using a novel combination of methodological strategies. Twenty-three participants underwent multi-echo resting-state and task fMRI. We used their resting-state scans to conduct cortical parcellation sensitive to individual variation while preserving our ability to conduct group analysis. Using multivariate analyses, we assessed the functional activation and connectivity profiles of default network regions while participants engaged in autobiographical memory, theory of mind, or a sensorimotor control condition. Across the default network, we observed stronger activity associated with both autobiographical memory and theory of mind compared to the control condition. Nonetheless, we also observed that some regions showed preferential activity to either experimental condition, in line with past work. The connectivity results similarly indicated shared and distinct functional profiles. Our results support that autobiographical memory and theory of mind, two theoretically important and widely studied domains of social cognition, evoke common and distinct aspects of the default network even when ensuring high fidelity to individual-specific characteristics.NEW & NOTEWORTHY We used cutting-edge precision functional MRI (fMRI) methods such as multi-echo fMRI acquisition and denoising, a robust experimental paradigm, and individualized cortical parcellation across 23 participants to provide evidence that remembering one's past experiences and imagining the thoughts and feelings of others share a common neural substrate. Evidence from activation and connectivity analyses indicate overlapping and distinct functional profiles of these widely studied episodic and social processes.

Neural correlates of semantic-driven syntactic parsing in sentence comprehension

For sentence comprehension, information carried by semantic relations between constituents must be combined with other information to decode the constituent structure of a sentence, due to atypical and noisy situations of language use. Neural correlates of decoding sentence structure by semantic information have remained largely unexplored. In this functional MRI study, we examine the neural basis of semantic-driven syntactic parsing during sentence reading and compare it with that of other types of syntactic parsing driven by word order and case marking. Chinese transitive sentences of various structures were investigated, differing in word order, case making, and agent-patient semantic relations (i.e., same vs. different in animacy). For the non-canonical unmarked sentences without usable case marking, a semantic-driven effect triggered by agent-patient ambiguity was found in the left inferior frontal gyrus opercularis (IFGoper) and left inferior parietal lobule, with the activity not being modulated by naturalness factors of the sentences. The comparison between each type of non-canonical sentences with canonical sentences revealed that the non-canonicity effect engaged the left posterior frontal and temporal regions, in line with previous studies. No extra neural activity was found responsive to case marking within the non-canonical sentences. A word order effect across all types of sentences was also found in the left IFGoper, suggesting a common neural substrate between different types of parsing. The semantic-driven effect was also observed for the non-canonical marked sentences but not for the canonical sentences, suggesting that semantic information is used in decoding sentence structure in addition to case marking. The current findings illustrate the neural correlates of syntactic parsing with semantics, and provide neural evidence of how semantics facilitates syntax together with other information.

Aphasia improvement without logotherapy during motor neurorehabilitation of post-stroke hemiparesis using virtual reality or modified constraint-induced movement therapy: A retrospective cohort.

Some research suggests that post-stroke aphasia can recover "on its own", however, there is evidence of a common neural substrate for motor and language systems. We hypothesize, that motor neurorehabilitation of hemiparesis could be related to simultaneous improvement in aphasia. To measure changes in post-stroke aphasia and its relation with hemiparesis treated with different therapies. Database information (n = 32) on post-stroke hemiparesis (Fugl-Meyer Scale evaluated) managed with virtual reality (VR) versus modified constraint-induced movement therapy (mCIMT) or regular therapy (rPT/OT) was analyzed. None received logotherapy (LT) by appointment at four months. < 3 months after the stroke, aphasia severe (Boston Aphasia Intensity Scale), and all three evaluations. Twenty-one patient records met inclusion criteria (71,4% women and mean age 66,67±3,13 years) who received VR, mCIMT, or rPT/OT (n = 6, 8, and 7, respectively). There was continuous intra-groups improvement in aphasia (p < 0.05), but inter-groups the greater aphasia recovery (p = 0.05) and hemiparesis (p = 0.02) were in VR, with a high correlation in evolution between them (r = 0.73; p = 0.047). High clinical correlation between aphasia, without LT, and hemiparesis evolution during motor neurorehabilitation would support common neural connections stimulation. We will conduct a clinical trial, with a larger sample size to contrast our hypothesis.

2 Associations Between Motor Functioning and Intellectual Abilities in Pediatric Arterial Ischemic Stroke

Objective:Motor impairments are one of the most common adverse outcomes after pediatric arterial ischemic stroke (AIS), affecting approximately half of survivors. The development of motor and cognitive skills is closely interrelated, and they share common neural substrates. The objective of this study was to examine whether motor functioning after the acute phase of stroke is associated with school-age intellectual abilities. We also examined associations between concurrent motor functioning and intellectual abilities. Finally, we explored clinical features associated with motor impairments.Participants and Methods:Participants were 64 children, 34 childhood AIS (Meanage= 11.90[2.38]); 30 perinatal AIS (Meanage= 8.75[2.22]), from the Children’s Stroke Program at SickKids Hospital. Motor functioning was assessed with the Pediatric Stroke Outcome Measure sensorimotor subscale at two timepoints, Time 1 or early recovery (childhood group between 30 days post-stroke to 1 year; perinatal group between 2-5 years of age) and Time 2, closest to neuropsychological testing. Intellectual abilities were measured using the Wechsler Intelligence Scale for Children 4th or 5th edition. Associations between motor and intellectual functioning were examined separately in childhood and perinatal AIS groups. Clinical features associated with motor impairment were examined across the full sample.Results:Motor functioning during early recovery was significantly associated with processing speed (r= -.391, p= .036) in the perinatal group and with overall intellectual functioning (r= -.414, p= .018) verbal intellectual abilities (r= -.444, p= .011), working memory (r= .393, p= .026), and processing speed (r= -.351, p= .042) in the childhood group. There were no associations between concurrent motor and intellectual functioning in the perinatal group, and only with processing speed (r= -.525, p= .002) in the childhood group. When motor functioning was dichotomized as no/mild motor deficit and moderate/severe motor deficit at Time 1, children in the perinatal group with moderate/severe motor deficit had significantly lower perceptual reasoning scores (f[28]= 2.15, p= .040) and participants in the childhood group with moderate/severe motor deficit had significantly lower perceptual reasoning (f[32]= 2.35, p= .025) and processing speed (f[32]= 2.14, p= 0.41) scores. There were no differences between no/mild and moderate/severe motor deficit groups for either perinatal or childhood AIS at Time 2. Clinical features associated with moderate/severe motor deficit at Time 1 were cortical+subcortical infarcts, large lesions, presenting with hemiparesis and seizures at time of neuropsychological assessment, and accessing occupational therapy and physical therapy.Conclusions:Results suggest that motor functioning during early stroke recovery is associated with intellectual outcome, whereas motor functioning at time closest to neuropsychological assessment is not. This may be related neuroplastic changes post-injury, likely in frontal-subcortical connections, that result in observable motor deficits after stroke and affect subsequent hierarchal brain maturational processes thereby impacting later cognitive outcome. Different patterns of associations between motor functioning and specific intellectual abilities in perinatal and childhood groups suggest possible age-mediated effects on this relationship.

Symposium 01: Neuropsychological Outcomes Following Pediatric Stroke: Research Trends and Advances

Summary Abstract:Stroke is an important cause of acquired brain injury in youth and a significant source of childhood disability. Up to 80% of survivors suffer long-term neurological deficits, including impairments across a range of neuropsychological domains. An improved understanding of neuropsychological outcomes is key to optimizing clinical care, improving evaluation of prognosis, and developing effective rehabilitation and intervention strategies. The proposed symposium will begin with a literature review on neuropsychological outcomes following pediatric stroke. Next, four studies will be presented, each posing distinct and complementary research questions regarding predictors of outcomes. The roles of both clinical (e.g., lesion size, motor impairment, inflammatory response) and environmental factors (e.g., socioeconomic status, family functioning) will be explored regarding cognitive, social-emotional, and behavioral outcomes. The symposium will end with a Q&amp;A period.Attendees will leave with an in-depth understanding of recent trends and scientific advances in research on neuropsychological outcomes in pediatric stroke, which should inform clinical practice and research directions. The first presentation examines predictors of neuropsychological outcomes following pediatric stroke. Findings have often conflicted, and more research is needed to disentangle the effects of predictors on specific domains. Explored predictors include: age at stroke; stroke subtype (hemorrhagic vs. ischemic); lesion location; lesion size; time since stroke; neurologic severity; seizure disorder; and socioeconomic status. This study examines the impact of these predictors on distinct neuropsychological domains. The next presentation addresses associations between neuropsychological outcomes and motor functioning following pediatric stroke. The development of cognitive and motor skills is interrelated and they share common neural substrates. In other populations, motor functioning predicts intellectual ability, and brain connectivity underlies this association. This study investigates associations between motor functioning and global neuropsychological outcomes in children with stroke and explores clinical features associated with motor impairments. The third presentation explores mental health outcomes. Neuropsychological deficits can hinder academic advancement and social-emotional development and may place youth at increased risk for psychological concerns. An increased focus on mental health is warranted given that psychosocial and behavioral issues are often the most concerning problems for parents and teachers. This study uses a qualitative paradigm to shed light on lived experience of youth with stroke with a focus on mental health, relationships, and social competence. The fourth presentation consists of a systematic review exploring the association between inflammatory response and neuropsychological outcome. Stroke induces an inflammation in the central and peripheral nervous systems, and high levels of inflammatory markers following stroke have been associated with poorer cognitive outcomes. This study reviews the state of research on this topic with a focus on pro-inflammatory cytokines and c-reactive protein. The symposium topics covered lie at the heart of the INS mission to study brain-behavior relationships using a multidisciplinary lens, with an emphasis on sharing and applying scientific knowledge. The symposium seeks to inform professionals working with youth with stroke about cutting-edge research, clinically applicable and novel insights, and ideas for future research directions. In this way, our symposium contributes to evidence-based care and the advancement of research.

Perceived plausibility modulates hippocampal activity in episodic counterfactual thinking.

Episodic counterfactual thinking (ECT) consists of imagining alternative outcomes to past personal events. Previous research has shown that ECT shares common neural substrates with episodic future thinking (EFT): our ability to imagine possible future events. Both ECT and EFT have been shown to critically depend on the hippocampus, and past research has explored hippocampal engagement as a function of the perceived plausibility of an imagined future event. However, the extent to which the hippocampus is modulated by perceived plausibility during ECT is unknown. In this study, we combine two functional magnetic resonance imaging datasets to investigate whether perceived plausibility modulates hippocampal activity during ECT. Our results indicate that plausibility parametrically modulates hippocampal activity during ECT, and that such modulation is confined to the left anterior portion of the hippocampus. Moreover, our results indicate that this modulation is positive, such that increased activity in the left anterior hippocampus is associated with higher ratings of ECT plausibility. We suggest that neither effort nor difficulty alone can account for these results, and instead suggest possible alternatives to explain the role of the hippocampus during the construction of plausible and implausible ECT.

Are False Memory and Creative Thinking Mediated by Common Neural Substrates? An fMRI Meta-Analysis

ABSTRACT Episodic retrieval plays a functional-adaptive role in supporting divergent creative thinking, the ability to creatively combine different pieces of information. However, the same constructive memory process that provides this benefit can also lead to memory errors. Prior behavioral work has shown that there is a positive correlation between the false recognition of lure items in the Deese-Roediger-McDermott paradigm, and divergent creative thinking as assessed on the alternate uses task. Here, we conducted a meta-analysis of functional magnetic resonance imaging studies to test for convergence in the neural substrates associated with these cognitive linkages. Our individual meta-analyses of false recognition-related activity as well as divergent thinking-related neural activity replicated prior meta-analyses. However, there was no significant statistical overlap across the neural regions associated with false recognition and divergent creative thinking. These null findings may reflect the operation of distinct generative retrieval processes engaged during divergent thinking relative to false recognition.

The perceptual consequences and neurophysiology of eye blinks.

A hand passing in front of a camera produces a large and obvious disruption of a video. Yet the closure of the eyelid during a blink, which lasts for hundreds of milliseconds and occurs thousands of times per day, typically goes unnoticed. What are the neural mechanisms that mediate our uninterrupted visual experience despite frequent occlusion of the eyes? Here, we review the existing literature on the neurophysiology, perceptual consequences, and behavioral dynamics of blinks. We begin by detailing the kinematics of the eyelid that define a blink. We next discuss the ways in which blinks alter visual function by occluding the pupil, decreasing visual sensitivity, and moving the eyes. Then, to anchor our understanding, we review the similarities between blinks and other actions that lead to reductions in visual sensitivity, such as saccadic eye movements. The similarity between these two actions has led to suggestions that they share a common neural substrate. We consider the extent of overlap in their neural circuits and go on to explain how recent findings regarding saccade suppression cast doubt on the strong version of the shared mechanism hypothesis. We also evaluate alternative explanations of how blink-related processes modulate neural activity to maintain visual stability: a reverberating corticothalamic loop to maintain information in the face of lid closure; and a suppression of visual transients related to lid closure. Next, we survey the many areas throughout the brain that contribute to the execution of, regulation of, or response to blinks. Regardless of the underlying mechanisms, blinks drastically attenuate our visual abilities, yet these perturbations fail to reach awareness. We conclude by outlining opportunities for future work to better understand how the brain maintains visual perception in the face of eye blinks. Future work will likely benefit from incorporating theories of perceptual stability, neurophysiology, and novel behavior paradigms to address issues central to our understanding of natural visual behavior and for the clinical rehabilitation of active vision.

Neural Representations in Visual and Parietal Cortex Differentiate between Imagined, Perceived, and Illusory Experiences.

Humans constantly receive massive amounts of information, both perceived from the external environment and imagined from the internal world. To function properly, the brain needs to correctly identify the origin of information being processed. Recent work has suggested common neural substrates for perception and imagery. However, it has remained unclear how the brain differentiates between external and internal experiences with shared neural codes. Here we tested this question in human participants (male and female) by systematically investigating the neural processes underlying the generation and maintenance of visual information from voluntary imagery, veridical perception, and illusion. The inclusion of illusion allowed us to differentiate between objective and subjective internality: while illusion has an objectively internal origin and can be viewed as involuntary imagery, it is also subjectively perceived as having an external origin like perception. Combining fMRI, eye-tracking, multivariate decoding, and encoding approaches, we observed superior orientation representations in parietal cortex during imagery compared with perception, and conversely in early visual cortex. This imagery dominance gradually developed along a posterior-to-anterior cortical hierarchy from early visual to parietal cortex, emerged in the early epoch of imagery and sustained into the delay epoch, and persisted across varied imagined contents. Moreover, representational strength of illusion was more comparable to imagery in early visual cortex, but more comparable to perception in parietal cortex, suggesting content-specific representations in parietal cortex differentiate between subjectively internal and external experiences, as opposed to early visual cortex. These findings together support a domain-general engagement of parietal cortex in internally generated experience.SIGNIFICANCE STATEMENT How does the brain differentiate between imagined and perceived experiences? Combining fMRI, eye-tracking, multivariate decoding, and encoding approaches, the current study revealed enhanced stimulus-specific representations in visual imagery originating from parietal cortex, supporting the subjective experience of imagery. This neural principle was further validated by evidence from visual illusion, wherein illusion resembled perception and imagery at different levels of cortical hierarchy. Our findings provide direct evidence for the critical role of parietal cortex as a domain-general region for content-specific imagery, and offer new insights into the neural mechanisms underlying the differentiation between subjectively internal and external experiences.

Heterogeneity of social cognition between visual perspective-taking and theory of mind in the temporo-parietal junction

Visual perspective taking (VPT), particularly level 2 VPT (VPT2), which allows an individual to understand that the same object can be seen differently by others, is related to the theory of mind (ToM), because both functions require a decoupled representation from oneself. Although previous neuroimaging studies have shown that VPT2 and ToM activate the temporo-parietal junction (TPJ), it is unclear whether common neural substrates are involved in both functions. To clarify this point, we directly compared the TPJ activation patterns of individual participants performing VPT2 and ToM tasks using functional magnetic resonance imaging and within-subjects design. A whole-brain analysis revealed that VPT2 and ToM activated overlapping areas in the posterior part of the TPJ. In addition, we found that both the peak coordinates and activated regions for ToM were located significantly more anteriorly and dorsally within the bilateral TPJ than those measured during the VPT2 task. We further confirmed that these activated areas were spatially distinct from the nearby extrastriate body area (EBA), visual motion area (MT+), and the posterior superior temporal sulcus (pSTS) using independent localizer scans. Our findings revealed that VPT2 and ToM have gradient representations, indicating the functional heterogeneity of social cognition within the TPJ.

Distraction and cognitive control independently impact parietal and prefrontal response to pain.

Previous studies have found that distracting someone through a challenging activity leads to hypoalgesia, an effect mediated by parietal and prefrontal processes. Other studies suggest that challenging activities affect the ability to regulate one's aching experiences, due to the partially common neural substrate between cognitive control and pain at the level of the medial prefrontal cortex. We investigated the effects of distraction and cognitive control on pain by delivering noxious stimulations during or after a Stroop paradigm (requiring high cognitive load) or a neutral condition. We found less-intense and unpleasant subjective pain ratings during (compared to after) task execution. This hypoalgesia was associated with enhanced activity at the level of the dorsolateral prefrontal cortex and the posterior parietal cortex, which also showed negative connectivity with the insula. Furthermore, multivariate pattern analysis revealed that distraction altered the neural response to pain, by making it more similar to that associated with previous Stroop tasks. All these effects were independent of the nature of the task, which, instead, led to a localized neural modulation around the anterior cingulate cortex. Overall, our study underscores the role played by two facets of human executive functions, which exert an independent influence on the neural response to pain.

Is ocular dominance plasticity a special case of contrast adaptation?

The visual system can regulate its sensitivity depending on the prevailing contrast conditions. This is known as contrast adaptation and reflects contrast gain changes at different stages along the visual pathway. Recently, it has been shown that depriving an eye of visual stimulation for a short period of time can lead to neuroplastic changes in ocular dominance as the result of homeostatic changes in contrast gain. Here we examine, on the basis of previously published results, whether the neuroplastic ocular dominance changes are just manifestation of the mechanism responsible for contrast adaptation. The evidence suggests that these two visual processes are separate and do not have a common neural substrate.

The impact of loneliness and social adaptation on depressive symptoms: Behavioral and brain measures evidence from a brain health perspective.

Early detection of depression is a cost-effective way to prevent adverse outcomes on brain physiology, cognition, and health. Here we propose that loneliness and social adaptation are key factors that can anticipate depressive symptoms. We analyzed data from two separate samples to evaluate the associations between loneliness, social adaptation, depressive symptoms, and their neural correlates. For both samples, hierarchical regression models on self-reported data showed that loneliness and social adaptation have negative and positive effects on depressive symptoms. Moreover, social adaptation reduces the impact of loneliness on depressive symptoms. Structural connectivity analysis showed that depressive symptoms, loneliness, and social adaptation share a common neural substrate. Furthermore, functional connectivity analysis demonstrated that only social adaptation was associated with connectivity in parietal areas. Altogether, our results suggest that loneliness is a strong risk factor for depressive symptoms while social adaptation acts as a buffer against the ill effects of loneliness. At the neuroanatomical level, loneliness and depression may affect the integrity of white matter structures known to be associated to emotion dysregulation and cognitive impairment. On the other hand, socio-adaptive processes may protect against the harmful effects of loneliness and depression. Structural and functional correlates of social adaptation could indicate a protective role through long and short-term effects, respectively. These findings may aid approaches to preserve brain health via social participation and adaptive social behavior.