Neuroscience
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Understanding brain processing mechanisms from the perception of speech sounds to high-level semantic processing is vital for effective human-robot communication. In this study, 128-channel electroencephalograph (EEG) signals were recorded when subjects were listening to real and pseudowords in Mandarin. By using an EEG source reconstruction method and a sliding-window Granger causality analysis, we analyzed the dynamic brain connectivity patterns. ⋯ This may be related to semantic processing and integration. The involvement of both bottom-up input and top-down modulation in real word processing may support the previously proposed TRACE model. In sum, the findings of this study suggest that representations of speech involve dynamic interactions among distributed brain regions that communicate through time-specific functional networks.
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Signal processing in the principal neurons of the anteroventral cochlear nucleus (AVCN) is modulated by glycinergic inhibition. The kinetics of IPSCs are specific to the target neurons. It remains unclear what glycine receptor subunits are involved in generating such target-specific IPSC kinetics in AVCN principal neurons. ⋯ To further identify the cell type-specific expression patterns of GlyRα subunits, we combined whole-cell patch clamp recording with immunohistochemistry by recording from all three types of AVCN principal neurons, characterizing the synaptic properties of their glycinergic inhibition, dye-filling the neurons, and processing the slice for immunostaining of different GlyRα subunits. We found that AVCN bushy neurons express both GlyRα1 and GlyRα4 subunits that underlie their slow IPSC kinetics, whereas both T-stellate and D-stellate neurons express only GlyRα1 subunit that underlies their fast IPSC kinetics. In conclusion, AVCN principal neurons express cell-type specific GlyRα subunits that underlie their distinct IPSC kinetics, which enables glycinergic inhibition from the same source to exert target cell-specific modulation of activity to support the unique physiological function of these neurons.
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Sushi repeat-containing protein X-linked 2 (SRPX2) is a novel hypothalamic protein and a ligand of the urokinase-type plasminogen activator receptor (uPAR), which is essential for proteolysis of extracellular matrix and tissue remodeling after an insult to the brain. However, little is known about regulation of SRPX2. Our objective was to investigate if SRPX2 expression is altered by (i) the deficiency of uPAR or uPA (urokinase-type plasminogen activator), and (ii) traumatic brain injury (TBI). ⋯ Unsupervised hierarchical clustering using SRPX2 expression did not identify genotype or injury-specific clusters. Our data demonstrate that SRPX2 expression in the hypothalamus is resistant to genetic deficiencies in the urokinase-system or to the hypothalamus-affecting TBI. The contribution of elevated Srpx2 gene expression in perilesional cortex to post-TBI recovery process, however, requires further exploration.
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The striatum mediates habit formation and reward association. The striatum can be divided into the patch and matrix compartment, which are two distinct regions that sub-serve different aspects of behavior. The patch compartment may mediate reward-related behaviors, while the matrix compartment may mediate adaptive motor functions. ⋯ Our data showed that patch compartment lesions in the dorsolateral striatum reduced the reinstatement of sucrose self-administration after sucrose devaluation, indicating that destruction of this region prevented the development of habitual behavior. Additionally, in animals with patch compartment lesions in the DLS that did not develop habitual behavior, activation of the dorsolateral striatum and sensorimotor cortex was diminished, while activity in the dorsomedial striatum and prefrontal cortex was increased, suggesting less engagement of regions that mediate habitual behaviors and heightened engagement of regions that mediate goal-directed behaviors occurs with reduced habit formation. These data indicate that the dorsolateral patch compartment may mediate habit formation by altering information flow through basal ganglia circuits.
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Cortical spreading depolarization (CSD) is the electrophysiological substrate of migraine aura, and a putative trigger of trigeminovascular activation and migraine headache. Many migraineurs report stress or relief after a stress triggers an attack. We tested whether various stress conditions might modulate CSD susceptibility and whether this is dependent on genetic factors. ⋯ Stress status did not affect CSD propagation speed, duration or amplitude. In summary, relief after chronic stress, but not acute or chronic stress alone, augments CSD in genetically susceptible mice. Therefore, enhanced CSD susceptibility may explain why, in certain patients, migraine attacks typically occur during a period of stress relief such as weekends or holidays.