Neuroscience
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Glycosyltransferases are enzymes that catalyze the formation of a variety of glycoconjugates. Glycoconjugates play important roles in the nervous system. β-1,3-Galactosyltransferase 2 (B3galt2) belongs to the family of β-1,3-galactosyltransferase, which is one of the major types of glycosyltransferases. Dental pulp inflammation may cause neurophysiological alterations in the trigeminal ganglion (TG), and serve as a good model for investigating the peripheral inflammation and trigeminal neuronal sensitization. ⋯ The expression of TLR4 and NFκB in the TG was activated during the inflammation, but B3galt2 gene knockdown inhibited the expression of TLR4 and NFκB. These observations indicated that dental pulp inflammation could induce B3galt2 expression in TG, and that B3galt2 might play a regulatory role in TG neuronal sensitization. These findings suggest that B3galt2 may play an important role in trigeminal neuronal sensitization induced by peripheral inflammation via mediating TLR4/NFκB signaling pathway.
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This study investigated the mechanisms underlying regulation of the serotonin system in the rat brain during exercise-induced chronic fatigue. High-performance liquid chromatography-mass spectrometry (HPLC-MS) was performed to measure serum tryptophan of the fatigued rat. HPLC was conducted to measure 5-hydroxytryptamine (5-HT) and 5-hydroxyindoleacetic acid (5-HIAA) in the frontal cortex and hippocampus. ⋯ Further, 5-HTT expression was significantly increased and 5-HT1A receptor expression was significantly decreased. These results indicate that the 5-HT system plays an important role in the development of exercise-induced chronic fatigue. The 5-HT levels in different parts of the brain increased simultaneously, especially at synapses, and these alterations were associated with changes in 5-HTT and 5-HT1A mRNA expressions.
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Humans perform object recognition effortlessly and accurately. However, it is unknown how the visual system copes with variations in objects' appearance and the environmental conditions. Previous studies have suggested that affine variations such as size and position are compensated for in the feed-forward sweep of visual information processing while feedback signals are needed for precise recognition when encountering non-affine variations such as pose and lighting. ⋯ This was reflected in both the amplitude and the latency of the category separability indices obtained from the EEG signals. Using a feed-forward computational model of the ventral visual stream, we also confirmed a more dominant role for the feed-forward visual mechanisms of the brain in the compensation of affine variations. Taken together, our experimental results support the theory that non-affine variations such as pose and lighting may need top-down feedback information from higher areas such as IT and PFC for precise object recognition.
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Spontaneous epileptiform activity has previously been observed in lateral amygdala (LA) slices derived from patients with intractable-temporal lobe epilepsy. The present study aimed to characterize intranuclear LA synaptic connectivity and to test the hypothesis that differences in the spread of flow of neuronal activity may relate to spontaneous epileptiform activity occurrence. Electrical activity was evoked through electrical microstimulation in acute human brain slices containing the LA, signals were recorded as local field potentials combined with fast optical imaging of voltage-sensitive dye fluorescence. ⋯ No differences in spread of evoked activity were observed between spontaneously and non-spontaneously active LA slices, i.e. basic properties of evoked synaptic responses were similar in the two functional types of LA slices, including input-output relationship, and paired-pulse depression. These results indicate a directed propagation of synaptic signals within the human LA in spontaneously active epileptic slices. We suggest that the lack of differences in local and in systemic information processing has to be found in confined epileptiform circuits within the amygdala likely involving well-known "epileptic neurons".
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The metabolic pathophysiology underlying ischemic stroke remains poorly understood. To gain insight into these mechanisms, we performed a comparative metabolic and transcriptional analysis of the effects of cerebral ischemia on the metabolism of the cerebral cortex using middle cerebral artery occlusion (MCAO) rat model. Metabolic profiling by gas-chromatography/mass-spectrometry analysis showed clear separation between the ischemia and control group. ⋯ Furthermore, intracerebroventricular injection of ataxia telangiectasia mutated (ATM) kinase inhibitor (KU-55933) significantly reduced HSP27 phosphorylation and G6PD upregulation after MCAO, but that of protein kinase D inhibitor (CID755673) did not affect HSP27 phosphorylation. Consequently, G6PD activation via ischemia-induced HSP27 phosphorylation by ATM kinase may be part of an endogenous antioxidant defense neuroprotection mechanism during the earliest stages of ischemia. These findings have important therapeutic implications for the treatment of stroke.