Neuroscience
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Altered functional networks in attention deficit/hyperactivity disorder (ADHD) have been frequently reported, but effective connectivity has hardly been studied. Especially the differences of effective connectivity in children with ADHD after receiving neurofeedback (NF) training have been merely reported. Therefore, this study aimed to explore the effective networks of ADHD and the positive influence of NF on the effective networks. ⋯ Moreover, parent's SWAN presented significant improvements of ADHD symptoms after NF. Our findings revealed that the effective connectivity of ADHD was altered and that NF could improve the brain function of ADHD. The present study provided the first evidence that children with ADHD differed from healthy children in phase-based effective connectivity and that NF could reduce the differences.
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Working memory (WM) capacity, the amount of information one can hold online in mind, has a central role in cognition. Previous electrophysiological and imaging studies revealed the pivotal role of persistent activity within parietal and frontal regions as the neural foundations underpinning WM capacity. The best candidate molecules determining persistent activity are the brain's major excitatory and inhibitory neurotransmitters, glutamate and gamma-aminobutyric acid (GABA), respectively. ⋯ Individual variation in parieto-cingulate connectivity was explained by glutamatergic concentration in the IPS. Moreover, we found that parieto-cingulate connectivity mediated the relationship between interparietal sulcus glutamate and WM capacity. This set of findings reveals a novel mechanistic insight by which glutamatergic concentration within the IPS shapes WM capacity via parieto-cingulate connectivity.
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We used a finger force matching task to explore the role of efferent signals in force perception. Healthy, young participants performed accurate force production tasks at different force levels with the index and middle fingers of one hand (task-hand). They received visual feedback during an early part of each trial only. ⋯ In particular, using distorted copies of the RC for the antagonist muscle group could account for the differences between the task-hand and match-hand. We conclude that efferent signals may be distorted before their participation in the perceptual process. Such distortions emerge spontaneously and may be amplified by the response of sensory endings to muscle vibration combined over both agonist and antagonist muscle groups.
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Alpha-synuclein (αS) is an intrinsically disordered protein (IDP) that is abundantly present in the brain and is associated with Parkinson's disease (PD). In spite of its abundance and its contribution to PD pathogenesis, the exact cellular function of αS remains largely unknown. The ability of αS to remodel phospholipid model membranes combined with biochemical and cellular studies suggests that αS is involved in endocytosis. ⋯ We find no structural colocalization between αS and clathrin and Rab11 positive vesicles. We conclude that in a physiological context, αS is structurally associated with caveolin dependent membrane vesiculation and is found further along the endocytic pathway, in decreasing amounts, on early and late endosomes. Our results not only shed new light on the function of αS, they also provide a possible link between αS function and vesicle trafficking malfunction in PD.
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Exposure to stress activates glucocorticoid receptors in the brain and facilitates the onset of multitude psychiatric disorders. It has been shown that FK506 binding protein 51 (FKBP5) expression increases during glucocorticoid receptor (GR) activation in various brain regions including the medial prefrontal cortex (mPFC). FKBP5 knockout (KO) mice are reported to be resilient to stress, however, it remains uninvestigated whether FKBP5 loss affects neurotransmission and if so, what the functional consequences are. ⋯ We found that GR activation significantly decreased excitatory neurotransmission in the mPFC, which was completely abolished upon FKBP5 deletion, in consistent with behavioral resilience observed in FKBP5 KO mice. Even though FKBP5 loss has minimal impact on neural excitability, we found that FKBP5 deletion distorts the excitatory/inhibitory balance in the mPFC. Our study suggests that FKBP5 deficiency leads to the mPFC insensitive to GR activation and provides a neurophysiological explanation for how FKBP5 deficiency may mediate stress resilience.