Neuroscience
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Leucine-rich α2-glycoprotein1 (LRG1), a pleiotropic protein, plays a pathogenic role in multiple human diseases. However, its pathophysiological function in ischemia/reperfusion injury remains unclear. In this study, we discussed the function and mechanism of LRG1 in acute ischemic stroke from both basic and clinical research points of view. ⋯ We also showed that patients with acute cerebral infarction had lower serum levels of LRG1 compared to healthy controls. In addition, LRG1 levels were associated with infarction volume, stroke severity, and prognosis in patients with supratentorial infarction. Taken together, the data from this study revealed that LRG1 promoted apoptosis and autophagy through the TGFβ-smad1/5 signaling pathway by up-regulating ALK1, which exacerbates ischemia/reperfusion injury.
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People commonly synchronize taps to rhythmic sounds and can continue tapping after the sounds stop, indicating that time intervals between sounds can be internalized. Here, we investigate what happens in the brain after simply listening to auditory beats in order to understand more about the automatic internalization of temporal intervals without tapping. Electroencephalograms were recorded while musicians attended to accelerating, decelerating, or steady click sequences. ⋯ In contrast, physical beats elicited P2 responses and early beta suppressions, likely reflecting a combination of stimulus-related processing and temporal prediction. These results suggest that the activities observed after the silent beat were not produced via sustained entrainment after the physical beats, but via automatically-formed expectation for an additional beat. Therefore, beta modulations may be generated endogenously by expectation violation, while P3a amplitudes may relate to strength of expectation, with acceleration endings causing the strongest expectations for sequence continuation.
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Radial glial maintenance is essential for the proper development of the cortex. It is known that the evolutionarily conserved Notch signaling pathway is required for maintaining the pool of radial glial stem cells although the mechanisms involved are not entirely understood. Here, we study the Notch ligand, Jagged1, in the mouse ventricular zone at a late stage of embryonic development. ⋯ Using in vitro approaches, we found that depletion of Jagged1 reduced the size of primary neurospheres and their capacity to self-renewal. Finally, Jagged1 mutants also showed precocious neuronal differentiation and cortical defects. Together, these data support a role for Jagged1 in radial glia maintenance in the neocortex.
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Orofacial and somatic disgust reactions are observed in rats following intraoral infusion of not only bitter quinine (innate disgust) but also sweet saccharin previously paired with illness (learned disgust). It remains unclear, however, whether these innate and learned disgust reactions share a common neural basis and which brain regions, if any, host it. In addition, there is no established method to genetically access neurons whose firing is associated with disgust (disgust-associated neurons). ⋯ In addition, TRAP following quinine infusion (Quinine-TRAP) resulted in significantly more YFP-positive neurons in the IPAC, compared to TRAP following water infusion. A significant number of the YFP-positive neurons following Quinine-TRAP were co-labeled with Arc following the second quinine infusion, confirming that Quinine-TRAP preferentially labeled quinine-activated neurons in the IPAC. Our results suggest that the IPAC activity is associated with both innate and learned disgust and that disgust-associated neurons in the IPAC are genetically accessible by TRAP.
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Epilepsy is one of the most common chronic neurological diseases. It is characterized by recurrent epileptic seizures, where one-third of patients are refractory to existing treatments. Evidence revealed the association between neuroinflammation and increased susceptibility to seizures since there is a pronounced increase in the expression of key inflammatory mediators, such as prostaglandin E2 (PGE2), during seizures. ⋯ Indeed, galangin prevented behavioral and electroencephalographic seizures, reactive species production, decreased microglial and astrocytic immunocontent, as well as decreased VCAM-1 immunocontent and p-PKA/PKA ratio induced by PGE2/PTZ. Therefore, this study suggests galangin may have an antagonizing role on PGE2-induced effects, reducing cerebral inflammation and protecting from excitatory effects evidenced by administrating PGE2 and PTZ. However, further studies are needed to investigate the clinical implications of the findings and their underlying mechanisms.