Neuroscience
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Deficits in the anticipation and experience of affective events represent a key risky factor for a variety of mental disorders, such as anxiety and depression. Here, we examined temporal dynamics underlying the modulations of the aversive mood state on neural responses of anticipating and perceiving affective pictures. Participants were asked to perform an affective cueing paradigm in both threat and safe contexts. ⋯ Our findings revealed that threat context compared with the safe context attenuated the contingent negative variation (CNV) responses to the cues of positive expressions, and decreased differential late positive potential (LPP) responses to the perception of negative and positive events. These findings suggest that aversive mood dampens the anticipation of positive events and inhibits the elaboration of negative events. The current findings do not only advance our understanding on the temporal characteristics of affective anticipation and experience but also have implications on the emotional deficits across various mental disorders characterized by chronic mood disturbances.
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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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Auto-regulation mechanisms in serotonergic neurons regulate their electrical activity and secretion. Since these neurons release serotonin from different structural compartments - including presynaptic terminals, soma, axons and dendrites - through different mechanisms, autoregulation mechanisms are also likely to be different at each compartment. Here we show that a chloride-mediated auto-inhibitory mechanism is exclusively localized at presynaptic terminals, but not at extrasynaptic release sites, in serotonergic Retzius neurons of the leech. ⋯ This shows that the auto-inhibition effects are unique to nerve terminals. We further determined that serotonin released from peri-synaptic dense-core vesicles contributes to auto-inhibition in the terminals, since blockade of L-type calcium channels, which are required to stimulate extrasynaptic but not synaptic release, decreased the amplitude of the auto-inhibition response. Our results show that the auto-regulation mechanism at presynaptic terminals is unique and different from that described in the soma of these neurons, further highlighting the differences in the mechanisms regulating serotonin release from different neuronal compartments, which expand the possibilities of a single neuron to perform multiple functions in the nervous system.
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Increasing evidence has indicated that long non-coding RNAs (lncRNAs) play a vital role for adjusting RNA transcripts as competing endogenous RNAs (ceRNAs) for microRNAs (miRNAs). The present study was intended to explore the probable regulation of lncRNA TALNEC2 in ischemic stroke. In this study, we measured the up-regulation of TALNEC2 and down-regulation of miR-650 in mice brains after cerebral ischemia/reperfusion (I/R) operation and in cultured neuroblastoma cells of neuro-2A (N2a) treated with oxygen glucose deprivation/reoxygenation (OGD/R). ⋯ In result, overexpression of TALNEC2 antagonized the inhibition impact of miR-650 on APAF1 expression and N2a cell apoptosis induced by OGD/R, while TALNEC2 knockdown aggravated the impact. Furthermore, TALNEC2 knockdown reversed brain injury and neurological deficits induced by I/R in vivo. In conclusion, we verified a TALNEC2/miR-650/APAF1 signaling pathway as a key mechanism monitoring cerebral I/R injury.
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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.