Neuroscience
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Cortical microcircuitry plays a pivotal role in encoding sensory information reaching the cortex. However, the fundamental knowledge concerning the mechanisms that govern feature-encoding by these sub-networks is still sparse. Here, we show through multi-electrode recordings in V1 of conventionally prepared anesthetized cats, that an avalanche of synergistic neural activity occurs between functionally connected neurons in a cell-assembly in response to the presented stimulus. ⋯ The added excitation (facilitation) of connected neurons is almost four times the responsiveness of unconnected neurons. This suggests that connectedness confers the added excitability to neurons; consequently leading to feature-encoding within the emergent 50-ms-period. Furthermore, the facilitation significantly decreases as a function of orientation selectivity spread.
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Nuclear distribution factor E homolog like 1 (NDEL1) plays an important role in mitosis, neuronal migration, and microtubule organization during brain development by binding to disrupted-in-schizophrenia-1 (DISC1) or lissencephaly (LIS1). Although some evidence has suggested that DISC1 expression is altered in epilepsy, few studies have reported the relationship between NDEL1 and the etiology of epilepsy. In present study, we first investigated the expression of NDEL1 and its binding protein DISC1 after pilocarpine-induced epilepsy in male C57BL/6 mice. ⋯ Moreover, SE also increased the number of blood vessels that fed the CA3 and DG regions of the hippocampus and increased the incidence of abnormalities in capillary network formation where NDEL1 protein was expressed positively. Meanwhile, the expression of phosphorylated ERK (p-ERK) was also increased during the spontaneous seizure period, with a similar expression pattern as NDEL1 and DISC1. Based on these results, we hypothesize that NDEL1 might interact with DISC1 to activate ERK signaling and function as a potential protective factor during the spontaneous seizure period after pilocarpine-induced SE.
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The pre-Bötzinger complex (preBötC) of the ventrolateral medulla is the kernel for inspiratory rhythm generation. However, it is not fully understood how inspiratory neural activity is generated in the preBötC and propagates to other medullary regions. We analyzed the detailed anatomical connectivity to and from the preBötC and functional aspects of the inspiratory information propagation from the preBötC on the transverse plane of the medulla oblongata. ⋯ Intra-preBötC imaging with high spatiotemporal resolution during a single spontaneous inspiratory cycle unveiled deterministic nonlinearities, i.e., chaos, in the population recruitment. Collectively, we comprehensively elucidated the anatomical pathways to and from the preBötC and dynamics of inspiratory neural information propagation: (1) From the preBötC in one side to the contralateral preBötC, which would synchronize the bilateral rhythmogenic kernels, (2) from the preBötC directly to the bilateral hypoglossal premotor and motor areas as well as to the nuclei tractus solitarius, and (3) from the hypoglossal premotor areas toward the hypoglossal motor nuclei. The coincidence of identified anatomical and functional connectivity between the preBötC and other regions in adult and neonatal rats, respectively, indicates that this fundamental connectivity is already well developed at the time of birth.
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Manganese (Mn) is an essential trace element that is required for normal brain functioning. However, excessive intake of Mn has been known to lead to neuronal loss and clinical symptoms resembling idiopathic Parkinson's disease (IPD), whose precise molecular mechanism remains largely elusive. In the study, we established a Mn-exposed rat model and identified a mitochondrial protease, the mature form of high temperature requirement A2 (HtrA2/Omi), which was significantly upregulated in rat brain striatum after Mn exposure. ⋯ In addition, blockage of HtrA2 activity with UCF-101 restored Mn-induced reduction in XIAP expression. Finally, we observed that UCF-101 treatment ameliorated Mn-induced apoptosis in PC12 cells. Collectively, these findings suggested that upregulated HtrA2 played a role in Mn-induced neuronal death in brain striatum.
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Interactions between the prelimbic cortex and the basolateral amygdala underlie fear memory processing, mostly through acquiring and consolidating the learning of a conditioned fear. More recently, studies highlighted the role of the dorsal periaqueductal gray (DPAG) in the modulation of learning fear responses. In addition, extensive data in the literature have signaled the importance of serotonin (5-HT) on fear and anxiety. ⋯ In these regions LA but not HA rats were susceptible to the anxiolytic-like effect of 5-HT1A receptor activation. It is thought that the expression of conditioned fear in HA subjects may be dependent on other 5-HT receptors, as the 5-HT1B subtype, and/or changes in other systems such as the GABA and glutamate neurotransmitters. These results increase our understanding of the rostrocaudal influence of 5-HT on the unconditioned and conditioned fear responses in LA and HA subjects and, to some extent, are in disagreement with the theoretical current that emphasizes the role of 5-HT on anxiety, mainly at the subcortical and midbrain levels.