Cerebral cortex最新文献

The microgravity environment results in transient changes in sensorimotor behavior upon astronauts' return to Earth; the effects on behavior inflight are less understood. We examined whether adaptation to sensory conflict is disrupted in microgravity, suggesting competition for adaptive resources. We evaluated sensorimotor adaptation pre-, in-, and post-flight, as well as functional brain changes at pre- and post-flight, in astronauts participating in International Space Station missions. Astronauts (n = 13) performed this task pre- and four times post-flight within an MRI scanner and performed the task three times in microgravity during a 6-mo mission. We collected behavioral data from Earth-bound controls (n = 13) along the same timeline. Astronauts displayed no change in adaptation from pre- to inflight or following their return to Earth. They showed greater aftereffects of adaptation inflight; controls did not. Astronauts also displayed increased brain activity from pre- to post-flight. These increases did not return to baseline levels until 90 d post-flight. This pattern of brain activity may reflect compensation, allowing astronauts to maintain pre-flight performance levels. These findings indicate that microgravity does not alter short-term visuomotor adaptation; however, it does affect de-adaptation, and post-flight sensorimotor neural activation can take up to 90 d to return to pre-flight levels.

Concurrent application of transcranial alternating current stimulation over distant cortical regions has been shown to modulate functional connectivity between stimulated regions; however, the precise mechanisms remain unclear. Here, we investigated how bifocal transcranial alternating current stimulation applied over the bilateral primary sensorimotor cortices modulates connectivity between the left and right primary motor cortices (M1). Using a cross-over sham-controlled triple-blind design, 37 (27 female, age: 18 to 37 yrs) healthy participants received transcranial alternating current stimulation (1.0 mA, 20 Hz, 20 min) over the bilateral sensorimotor cortices. Before and after transcranial alternating current stimulation, functional connectivity between the left and right M1s was assessed using imaginary coherence measured via resting-state electroencephalography and interhemispheric inhibition via dual-site transcranial magnetic stimulation protocol. Additionally, manual dexterity was assessed using the Purdue pegboard task. While imaginary coherence remained unchanged after stimulation, beta (20 Hz) power decreased during the transcranial alternating current stimulation session. Bifocal transcranial alternating current stimulation but not sham strengthened interhemispheric inhibition between the left and right M1s and improved bimanual assembly performance. These results suggest that improvement in bimanual performance may be explained by modulation in interhemispheric inhibition, rather than by coupling in the oscillatory activity. As functional connectivity underlies many clinical symptoms in neurological and psychiatric disorders, these findings are invaluable in developing noninvasive therapeutic interventions that target neural networks to alleviate symptoms.

The prefrontal cortex regulates emotions and is influenced by serotonin. Rodents lacking the serotonin transporter (5-HTT) show increased anxiety and changes in excitatory and inhibitory cell markers in the prefrontal cortex. However, these observations are constrained by limitations in brain representation and cell segmentation, as standard immunohistochemistry is inadequate to consider volume variations in regions of interest. We utilized the deep learning network of the StarDist method in combination with novel open-source methods for automated cell counts in a wide range of prefrontal cortex subregions. We found that 5-HTT knockout rats displayed increased anxiety and diminished relative numbers of subclass excitatory VGluT2+ and activated ΔFosB+ cells in the infralimbic and prelimbic cortices and of inhibitory GAD67+ cells in the prelimbic cortex. Anxiety levels and ΔFosB cell counts were positively correlated in wild-type, but not in knockout, rats. In conclusion, we present a novel method to quantify whole brain subregions of multilabeled cells in animal models and demonstrate reduced excitatory and inhibitory neuronal marker expression in prefrontal cortex subregions of 5-HTT knockout rats.

Maple syrup urine disease is a rare metabolic disorder that results in neurodevelopmental injury despite dietary therapy. While structural neuroimaging has shown a characteristic pattern of edema and white matter injury, no functional neuroimaging studies of maple syrup urine disease have been performed. Using widefield optical imaging, we investigated resting-state functional connectivity in two brain-specific mouse models of maple syrup urine disease (an astrocyte-specific knockout and a whole-brain knockout). At 8 weeks, mouse functional neuroimaging was performed using a custom-built widefield optical imaging system. Imaging was performed before and after initiation of a high-protein diet for 1 week to mimic metabolic crisis, which we hypothesized would result in decreased functional connectivity strength. Data were analyzed using seed-based functional connectivity and cluster-based inference. Astrocyte-specific knockout mice developed increased contralateral functional connectivity within the posteromedial somatosensory cortex after diet initiation. Whole-brain knockout mice had a similar pattern present at baseline, which persisted after diet initiation. Thus, contrary to expectations, maple syrup urine disease resulted in increased functional connectivity strength, especially after diet initiation. While the underlying etiology of these changes is unclear, these results demonstrate that inborn errors of metabolism result in changes to functional connectivity networks. Further research may demonstrate functional neuroimaging biomarkers that could be translated to clinical care.

Qualitatively different topographical patterns of connections are thought to underlie individual differences in thought and behavior, particularly at heteromodal association areas. As such, we hypothesized that connections unique to 16p11.2 deletion carriers compared to controls, rather than hyper- or hypo-connectivity, would serve as a better model to explain the cognitive and behavioral changes observed in individuals carrying this autism-risk copy number variation. Using a spatially-unbiased, data-driven approach we found that differential links clustered non-uniformly across the cortex-particularly at the superior temporal gyrus and sulcus, posterior insula, cingulate sulcus, and inferior parietal lobule bilaterally. At these hotspots, altered local connectivity that spanned across the borders of cortical large-scale networks coincided with aberrant distant interconnectivity between large-scale networks. This was most evident between the auditory and the dorsomedial default (DNb) networks-such that greater between-network interconnectivity was associated with greater communication and social impairment. Entangled connectivity between large-scale networks may preclude each network from having the necessary fidelity to operate properly, particularly when the 2 networks have opposing organization principles-namely, local specialization (segregation) versus global coherency (integration).

Subchronic administration of the psychotomimetic drug phencyclidine is known to exacerbate serotonin 5-HT2A receptor-relevant behavioral abnormalities. However, the effects of subchronic phencyclidine on 5-HT2A receptors remain unclear. Here, we investigated the effects of subchronic phencyclidine on the binding potential (BPND) of 5-HT2A receptors in the rat brain using positron emission tomography. Adult male Sprague-Dawley rats received intraperitoneal injection of either phencyclidine (10 mg/kg) or physiological saline once daily, a total of 15 times. positron emission tomography scans were performed twice, before and after drug administration, using 18F-altanserin, a selective 5-HT2A receptor radioactive marker. Two behavioral tests, the sociability test and the social interaction test, were performed before each positron emission tomography scan. The social interaction time was significantly shortened by subchronic phencyclidine. The BPND of the 5-HT2A receptors was significantly increased after subchronic phencyclidine administration in the medial prefrontal cortex, ventral hippocampus, motor cortex, and somatosensory cortex. The BPND change between the pre- and postdrug periods in the ventral hippocampus showed a significant negative correlation (r = 0.73) with that of the social interaction time change. Our results suggest that upregulation of 5-HT2A receptors in the ventral hippocampus may play a role in disturbed social ability and the development of negative symptoms.

Alzheimer's disease is an irreversible central neurodegenerative disease, and early diagnosis of Alzheimer's disease is beneficial for its prevention and early intervention treatment. In this study, we propose a novel framework, FusionNet-ISBOA-MK-SVM, which integrates a fusion network (FusionNet) and improved secretary bird optimization algorithm to optimize multikernel support vector machine for Alzheimer's disease diagnosis. The model leverages multimodality data, including functional magnetic resonance imaging and genetic information (single-nucleotide polymorphisms). Specifically, FusionNet employs U-shaped hierarchical graph convolutional networks and sparse graph attention networks to select feature effectively. Extensive validation using the Alzheimer's Disease Neuroimaging Initiative dataset demonstrates the model's superior interpretability and classification performance. Compared to other state-of-the-art machine learning methods, FusionNet-ISBOA-MK-SVM achieves classification accuracies of 98.6%, 95.7%, 93.0%, 91.8%, 93.1%, and 95.4% for HC vs. AD, EMCI vs. AD, LMCI vs. AD, EMCI vs. AD, HC vs. EMCI, and HC vs. LMCI, respectively. Moreover, the proposed model identifies affected brain regions and pathogenic genes, offering deeper insights into the mechanisms and progression of Alzheimer's disease. These findings provide valuable scientific evidence to support early diagnosis and preventive strategies for Alzheimer's disease.

Major depressive disorder (MDD) is a psychiatric disorder characterized by persistent lethargy that can lead to suicide in severe cases. Hence, timely and accurate diagnosis and treatment are crucial. Previous neuroscience studies have demonstrated that major depressive disorder subjects exhibit topological brain network changes and different temporal electroencephalography (EEG) characteristics compared to healthy controls. Based on these phenomena, we proposed a novel model, termed as MDD-SSTNet, for detecting major depressive disorder by exploring spectral-spatial-temporal information from resting-state EEG with deep convolutional neural network. Firstly, MDD-SSTNet used the Sinc filter to obtain specific frequency band features from pre-processed EEG data. Secondly, two parallel branches were used to extract temporal and spatial features through convolution and other operations. Finally, the model was trained with a combined loss function of center loss and Binary Cross-Entropy Loss. Using leave-one-subject-out cross-validation on the HUSM dataset and MODMA dataset, the MDD-SSTNet model outperformed six baseline models, achieving average classification accuracies of 93.85% and 65.08%, respectively. These results indicate that MDD-SSTNet could effectively mine spatial-temporal difference information between major depressive disorder subjects and healthy control subjects, and it holds promise to provide an efficient approach for MDD detection with EEG data.

The link between hemispheric asymmetry and auditory verbal hallucinations in schizophrenia is underexplored with neuroimaging evidence. This study examined white matter asymmetries in schizophrenia patients. Diffusion tensor imaging data from 52 patients with persistent auditory verbal hallucinations, 33 who never experienced auditory verbal hallucinations, and 40 healthy controls were analyzed. Asymmetry indices for fractional anisotropy, axial diffusivity, radial diffusivity, and mean diffusivity were calculated for the whole-brain white matter skeleton and 22 pairs of regions of interest. The persistent auditory verbal hallucination group showed reduced fractional anisotropy asymmetry index in the whole-brain white matter skeleton compared to healthy control and never experienced auditory verbal hallucination groups, indicating altered asymmetry. Region of interest analysis revealed decreased fractional anisotropy asymmetry index in nine pairs and increased mean diffusivity AI in two pairs in the persistent auditory verbal hallucination group. Greater rightward asymmetry in the superior longitudinal fasciculus correlated with more severe auditory verbal hallucinations in persistent auditory verbal hallucination patients. No significant asymmetry differences were found between never experienced auditory verbal hallucinations and healthy control groups. Ridge regression analysis demonstrated that including the fractional anisotropy asymmetry index of the superior longitudinal fasciculus increased the explained variance in auditory verbal hallucination severity. These findings highlight distinct white matter asymmetry patterns in persistent auditory verbal hallucination patients, suggesting that hemispheric asymmetry plays a key role in the pathology of auditory verbal hallucinations in schizophrenia.

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In the current issue of Cerebral Cortex, Lorenzi et al. (2025) discuss evidence for an innate sense of object number (numerosity) in the brains of many species, without the need for visual experience. This commentary discusses how numerosity processing can be understood as an innate property of vision, derived from the spatial frequency-based representation of images in the visual systems of many animals.