Neuroscience
-
The current evidence suggests that aerobic fitness is associated with inhibitory control of executive functioning in children and older adults. However, the relative contributions of different neurophysiological mechanisms to this relation remain unclear and have not yet been examined in young adults. The present study aimed to compare inhibitory control between high and low-fit young adult men, and to investigate a possible mediation of fitness effects by conflict monitoring (N450 component of event-related potentials) and lateralized oxygenation difference (LOD) in the DLPFC. ⋯ In contrast, LOD was inversely correlated with Stroop interference, but did not explain the relation of aerobic fitness with behavioral performance. The present findings indicate that greater inhibitory control in high- compared to low-fit young men can be explained by more effective conflict monitoring. Moreover, young adults with left-lateralizedDLPFC oxygenation also show higher inhibitory control, but this oxygenation pattern is not influenced by aerobic fitness.
-
The activation of inflammatory cytokines following stroke leads to neuron apoptosis and microglial activation, both of which are involved in ischemic brain damages. The ubiquitin-specific protease 18 (USP18) negatively regulated the expression of inflammatory cytokines and suppresses microglial activation. This study aims to determine whether USP18 expression protects against brain damage in ischemic models of stroke. ⋯ Additionally, microglial activation was inhibited, including the suppression of the JAK/STAT pathway and the proinflammatory cytokines expression. In vitro experiments demonstrated that USP18 inhibited BV2 microglial activity and reduced the mRNA and protein levels of NF-κB, JAK1, p-JAK1, STAT1, and p-STAT1 in BV2 microglial cells. USP18 overexpression decreased ischemic brain injury through the suppression of microglial activation by negatively regulating the release of proinflammatory cytokines.
-
Previous studies reported that long-term nociceptive stimulation could result in neurovascular coupling (NVC) dysfunction in brain, but these studies were based mainly on unimodal imaging biomarkers, thus could not comprehensively reflect NVC dysfunction. We investigated the potential NVC dysfunction in chronic migraine by exploring the relationship between neuronal activity and cerebral perfusion maps. The Pearson correlation coefficients between these 2 maps were defined as the NVC biomarkers. ⋯ These brain regions were located mainly in parietal or occipital lobes and were related to visual or sensory information processing. ALFF-CBF in right SPG was positively correlated with disease history and that in right precuneus was negatively correlated with migraine persisting time. fALFF-CBF in left SMG and AG were negatively related to headache frequency and positively related to health condition and disease history. In conclusion, multi-modal MRI could be used to detect NVC dysfunction in chronic migraine patients, which is a new method to assess the impact of chronic pain on the brain.
-
Hydrocephalus is especially prevalent in countries with limited resources, where its treatment is still a challenge. However, long-term neuropathological changes in untreated hydrocephalus remain largely unexplored. The present study looks at cortical parenchyma and neuroinflammation in acquired, chronic hydrocephalus. ⋯ IL-1β expression also peaked at 4weeks and was then down-regulated. Overall the findings indicate that neuroinflammatory features build up in the first month after hydrocephalus induction implicating marked IL-1β upregulation. The data also show that astrocytes are the main source of IL-1β in this disorder.
-
Agrin is a multi-domain protein best known for its essential function during formation of the neuromuscular junction. Alternative mRNA splicing at sites named y and z in the C-terminal part of agrin regulates its interaction with a receptor complex consisting of the agrin-binding low-density lipoprotein receptor-related protein 4 (Lrp4) and the muscle-specific kinase (MuSK). Isoforms with inserts at both splice sites bind to Lrp4, activate MuSK and are synaptogenic at the neuromuscular junction. ⋯ This effect was independent of splice site z. The reduction of the gephyrin puncta density was independent of the entire extracellular part of TM-agrin but required a highly conserved serine residue in the intracellular domain of TM-agrin. These results provide further evidence for a function of TM-agrin during CNS synaptogenesis and demonstrate that different domains and alternative splicing of TM-agrin differentially affect excitatory and inhibitory synapse formation in cultured embryonic CNS neurons.