Neuroscience
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Recent evidence raised the importance of the cerebellum in emotional processes, with specific regard to negative emotions. However, its role in the processing of face emotional expressions is still unknown. This study was aimed at assessing whether face emotional expressions influence the cerebellar learning processes, using the delay eyeblink classical conditioning (EBCC) as a model. ⋯ The present study provides first evidence that the passive viewing of faces displaying emotional expressions, are processed by the cerebellum, with no apparent involvement of the brainstem and the cerebello-cortical connection. In particular, the view of sad faces, reduces the excitability of the cerebellar circuit underlying the learning phase of the EBCC. Differently, the extinction phase was shortened by both happy and sad faces, suggesting that different neural bases underlie learning and extinction of emotions expressed by faces.
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Arousal is a potent mechanism that provides the brain with functional flexibility and adaptability to external conditions. Within the wake state, arousal levels driven by activity in the neuromodulatory systems are related to specific signatures of neural activation and brain synchrony. However, direct evidence is still lacking on the varying effects of arousal on macroscopic brain characteristics and across a variety of cognitive states in humans. ⋯ Increased integration in the salience network was also related to faster pupil dilation in the two attentional tasks. Furthermore, task performance was related to arousal level, with lower accuracy at higher level of arousal. Taken together, our study provides evidence in humans for pupil size as an index of brain network state, and supports the role of arousal as a switch that drives brain coordination in specific brain regions according to the cognitive state.
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Voltage-gated Ca2+ (CaV) channels regulate multiple cell processes, including neurotransmitter release, and have been associated with several pathological conditions, such as neuropathic pain. Cdk5, a neuron-specific kinase, may phosphorylate CaV channels, altering their functional expression. During peripheral nerve injury, upregulation of CaV channels and Cdk5 in the dorsal root ganglia (DRG) and the spinal cord, has been correlated with allodynia. ⋯ Likewise, the Cdk5 inhibitor olomoucine affected the rapid and the slow C components of the cAP recorded in the dorsal roots. Patch-clamp recordings revealed an increase in T- and N-type currents recorded in the soma of acute isolated L3-4 sensory neurons after L5-6 SNL, which was prevented by olomoucine. These findings suggest changes in CaV channels location and function in L3-4 afferent fibers associated with Cdk5-mediated phosphorylation after L5-6 SNL, which may contribute to nerve injury-induced allodynia.
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Sleep deprivation critically affects vigilant attention. Previous neuroimaging studies have revealed altered inter-regional functional connectivity after sleep deprivation, which may disrupt topological properties of brain functional networks. However, little is known about alterations in the topology of intrinsic connectivity and its involvement in attention performance after sleep deprivation. ⋯ At the nodal level, the altered regions were selectively distributed in frontoparietal networks, sensorimotor networks, temporal regions, and salience networks. More specifically, the altered clustering coefficient in the posterior superior temporal sulcus (pSTS) and insula, and altered local efficiency in pSTS were further associated with PVT performance after TSD. Our results suggest that the topological properties of brain functional networks are disrupted, and aberrant topology of temporal networks and salience networks may act as neural signatures underlying the vigilant attention impairments after TSD.