Neuroscience
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Homeostatic plasticity is a mechanism that stabilizes cortical excitability within a physiological range. Most homeostatic plasticity protocols have primed and tested the homeostatic response of the primary motor cortex (M1). This study investigated if a homeostatic response could be recorded from the primary sensory cortex (S1) after inducing homeostatic plasticity in M1. ⋯ Anodal M1 homeostatic plasticity induction significantly facilitated the N20-P25, P45 peak, and N33-P45 early SEP components up to 20-min post-induction, without any indication of a homeostatic response (i.e., reduced SEP). Cathodal homeostatic induction did not induce any significant effect on early or middle latency SEPs. M1 homeostatic plasticity induction by anodal stimulation protocol to the primary motor cortex did not induce a homeostatic response in SEPs.
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Stress resilience has been largely regarded as a process in which individuals actively cope with and recover from stress. Over the past decade, the emergence of large-scale brain networks has provided a new perspective for the study of the neural mechanisms of stress. However, the role of inter-network functional-connectivity (FC) and its temporal fluctuations in stress resilience is still unclear. ⋯ For the temporal dynamics index, FC among the dorsal-attention-network (DAN), central-executive-network (CEN) and visual-network (VN) decreased significantly during repeated stress induction. Moreover, the decline of FC positively signaled stress resilience, and this relationship only exist in people with high BAS. The current research elucidates the intricate neural underpinnings of stress resilience, offering insights into the adaptive mechanisms underlying effective stress responses.
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The ventrolateral prefrontal cortex (VLPFC) and dorsolateral prefrontal cortex (DLPFC) have been found to play important roles in negative emotion processing. However, the specific time window of their involvement remains unknown. This study addressed this issue in three experiments using single-pulse transcranial magnetic stimulation (TMS). ⋯ Furthermore, TMS applied over the DLPFC at both 0 ms and 600 ms after negative emotional exposure also resulted in deteriorated negative feelings. These findings provide potential evidence for the VLPFC-dependent semantic processing (∼400 ms) and the DLPFC-dependent attentional and cognitive control (∼0/600 ms) in negative emotion processing. The asynchronous involvement of these frontal cortices not only deepens our understanding of the neural mechanisms underlying negative emotion processing but also provides valuable temporal parameters for neurostimulation therapy targeting patients with mood disorders.
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Prism adaptation (PA) induces the after-effects of adapted tasks and transfers after-effects of non-adapted tasks, in which PA with pointing movements transfers to postural displacement during eyes-closed standing. However, the neural mechanisms underlying the transfer of PA after-effects on standing postural displacement remain unclear. The present study investigated the region-specific effects of transcranial direct current stimulation (tDCS) over the posterior parietal cortex (PPC) and cerebellum during prism exposure (PE) on standing postural displacement in healthy adults. ⋯ The PPC group only exhibited significant rightward center-of-pressure displacement during eyes-closed standing with feet-closed after leftward PE. The perception of longitudinal body axis rotation, as an indicator of the subjective body vertical axis, did not differ significantly between the pre- and post-evaluations in all groups. These results show that the PPC during PE could make an important neural contribution to inducing transfer of PA after-effect on standing postural displacement.
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It is increasingly evident that blood biomarkers have potential to improve the diagnosis and management of both acute and chronic neurological conditions. The most well-studied candidates, and arguably those with the broadest utility, are proteins that are highly enriched in neural tissues and released into circulation upon cellular damage. It is currently unknown how the brain expression levels of these proteins is influenced by demographic factors such as sex, race, and age. ⋯ Existing mass spectrometry data originating from 26 additional normal brain specimens harvested from 26 separate human donors was subsequently used to tentatively assess whether observed transcriptional variance was likely to produce corresponding variance in terms of protein abundance. Genes associated with several well-studied or emerging candidate biomarkers including neurofilament light chain (NfL), ubiquitin carboxyl-terminal hydrolase isozyme L1 (UCH-L1), neuron-specific enolase (NSE), and synaptosomal-associated protein 25 (SNAP-25) exhibited significant differences in expression with respect to sex, race, and age. In many instances, these differences in brain expression align well with and provide a mechanistic explanation for previously reported differences in blood levels.