Neuroscience
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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 human nervous system is one of the most complicated systems in nature. Complex nonlinear behaviours have been shown from the single neuron level to the system level. For decades, linear connectivity analysis methods, such as correlation, coherence and Granger causality, have been extensively used to assess the neural connectivities and input-output interconnections in neural systems. ⋯ We argue that nonlinear modelling and analysis are necessary to study neuronal processing and signal transfer in neural systems quantitatively. These approaches can hopefully provide new insights to advance our understanding of neurophysiological mechanisms underlying neural functions. These nonlinear approaches also have the potential to produce sensitive biomarkers to facilitate the development of precision diagnostic tools for evaluating neurological disorders and the effects of targeted intervention.
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Crucial to an animal's movement through their environment and to the maintenance of their homeostatic physiology is the integration of sensory information. This is achieved by axons communicating from organs, muscle spindles and skin that connect to the sensory ganglia composing the peripheral nervous system (PNS), enabling organisms to collect an ever-constant flow of sensations and relay it to the spinal cord. ⋯ This review covers the origins and development of the DRG and the cells that populate it, and focuses on how sensory connectivity to the spinal cord is achieved by the diverse developmental and molecular processes that control axon guidance in the trunk sensory system. We also describe convergences and differences in sensory neuron formation among different vertebrate species to gain insight into underlying developmental mechanisms.
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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.