Neuroscience
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Neurophysiological and neuroimaging evidence suggests a significant contribution of several brain areas, including subdivisions of the parietal and the premotor cortex, during the processing of different components of hand and arm movements. Many investigations improved our knowledge about the neural processes underlying the execution of reaching and grasping actions, while few studies have directly investigated object manipulation. Most studies on the latter topic concern the use of tools to achieve specific goals. ⋯ Then, we have described the main structures recruited during object manipulation. We have also reported the contribution of recent structural connectivity techniques whereby the cortico-cortical and cortico-subcortical connections of grasping-related and manipulation-related areas in the human brain can be determined. Based on our review, we have concluded that studies on cortical and subcortical circuits involved in grasping and manipulation might be promising to provide new insights about motor learning and brain plasticity in patients with motor disorders.
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Brain-derived neurotrophic factor (BDNF) plays an important role in processes associated with neuroplasticity and neuroprotection. Evidence suggests that decreased BDNF levels in the central nervous system (CNS) represent a mechanism underlying the development of mood disorders. We hypothesize that both congenital and traumatic brain injury (mTBI)-induced blood-brain barrier (BBB) breakdown are responsible for brain BDNF depletion that contributes to the development of depressive-like symptoms. ⋯ No alterations in BDNF levels were observed in mTBI and CMS-exposed HA mice. Moreover, CMS did not induce BBB damage or affect depressive-like behaviours in HA mice despite downregulating Bdnf gene expression. To conclude, BDNF efflux through the mTBI-disrupted BBB is strongly linked to the development of depressive-like behaviours, while the depressive phenotype in mice with congenital BBB dysfunction is independent of BDNF leakage.
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Nociception is the neuronal process of encoding noxious stimuli and could be modulated at peripheral, spinal, brainstem, and cortical levels. At cortical levels, several areas including the anterior cingulate cortex (ACC), prefrontal cortex (PFC), ventrolateral orbital cortex (VLO), insular cortex (IC), motor cortex (MC), and somatosensory cortices are involved in nociception modulation through two main mechanisms: (i) a descending modulatory effect at spinal level by direct corticospinal projections or mostly by activation of brainstem structures (i.e. periaqueductal grey matter (PAG), locus coeruleus (LC), the nucleus of raphe (RM) and rostroventral medulla (RVM)); and by (ii) cortico-cortical or cortico-subcortical interactions. ⋯ Besides, we point out the importance of considering intracortical neuronal populations and receptors expression, as well as, nociception-induced cortical changes, both functional and connectional, to better understand this modulatory effect. Finally, we discuss the possible mechanisms that could potentiate the use of cortical stimulation as a promising procedure in pain alleviation.
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The N170 is a large deflection of the human electroencephalogram (EEG), peaking at about 170 milliseconds over the occipito-temporal cortex after the sudden onset of a face stimulus. The N170 reflects perceptual awareness of a face and its onset corresponds to the emergence of reliable face-selectivity in the human brain. However, whether sensitivity to the long-term familiarity of a face identity emerges already at this early time-point remains debated. ⋯ This effect is especially present for personally familiar faces, learned in natural conditions. In the human brain, effects linked to familiarity with specific facial identities therefore appear to emerge between 150 and 200 ms in occipito-temporal brain regions, i.e., shortly after the onset of face-selectivity but at the same time as the earliest high-level effects of immediate unfamiliar face identity repetition. This observation challenges standard neurocognitive models with a clear-cut distinction between perceptual and memory stages in human face recognition.
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Cerebellar Purkinje cells develop the most elaborate dendritic trees among neurons in the brain. To examine the role of Ca2+/calmodulin-dependent protein kinase (CaMK) IIα, IIβ and IV in the dendritic differentiation of Purkinje cells, we introduced siRNA against these CaMKs into Purkinje cells in cerebellar cell cultures using a single-cell electroporation technique. Single-cell electroporation enables us to transfer siRNA into specific cells within a heterogeneous cell population. ⋯ However, the combination of all three siRNA against these CaMKs (triple knockdown) inhibited the branching of Purkinje cell dendrites. Furthermore, the triple knockdown reduced the phosphorylation of CREB in Purkinje cells. These findings suggest the promotion of dendritic differentiation of Purkinje cells by CaMKIIα, IIβ and IV and the possible involvement of phosphorylation of CREB as a common substrate of these CaMKs.