Neural oscillations after acute large artery atherosclerotic cerebral infarction during resting state and sleep spindles.

Electroencephalogram-microstate analysis was conducted using low-resolution electromagnetic tomography (LORETA)-KEY to evaluate dynamic brain network changes in patients with acute large artery atherosclerotic cerebral infarction (LAACI) during the rest and sleep stages. This study included 35 age- and sex-matched healthy controls and 34 patients with acute LAACI. Each participant performed a 3-h, 19-channel video electroencephalogram test. Subsequently, 20 epochs of 2-s sleep spindles during stage N2 sleep and five epochs of 10-s electroencephalogram data in the resting state for each participant were obtained. In both the resting state and sleep spindles, patients with LAACI displayed altered neural oscillations. The parameters of microstate A (coverage, occurrence, and duration) increased during the resting state in the patients with LAACI compared with healthy controls. The coverage and occurrence of microstate B and D were reduced in the LAACI group compared with the healthy controls (p < 0.05). Moreover, during sleep spindles, the duration of microstate A and the transition probability from microstate A and B to C decreased, but the coverage of microstate B and the transition rate from microstate B to D increased (p < 0.05) in the LAACI group compared with the healthy controls. These results enable better understanding of how neural oscillations are modified in patients with LAACI during the resting state and sleep spindles. Following LAACI, the dynamic brain network undergoes changes during sleep spindles and the resting state. Continued long-term investigations are required to determine how well these changes in brain dynamics reflect the clinical characteristics of patients with LAACI.

LncRNA embryonic stem cells expressed 1 (Lncenc1) is identified as a novel regulator in neuropathic pain by interacting with EZH2 and downregulating the expression of Bai1 in mouse microglia.

LncRNA embryonic stem cells expressed 1 (Lncenc1), named after its high expression in naïve embryonic stem cells (nESCs), has been rarely studied in almost all pathological processes. Evidences suggest that Lncenc1 is likely to work in the form of RNA-protein complex. Here, we found that Lncenc1 in dorsal root ganglion (DRG) was significantly upregulated in response to mouse nerve injury caused by partial sciatic nerve ligation (pSNL). Overexpression of Lncenc1 mediated by adenoviral expression vector promoted the activation of microglia and the production of inflammatory cytokines including TNF-α, IL-1ß and MCP-1. In contrast, knockdown of Lncenc1 suppressed activation of microglia and production of inflammatory cytokines. In the mechanism exploration, we found that Lncenc1 could bind with the RNA binding protein (RBP) enhancer of zeste homologue 2 (EZH2), an identified contributor in microglial activation and neuropathic pain. Lncenc1 interacted with EZH2 and downregulated the expression of brain-specific angiogenesis inhibitor 1 (BAI1). Either inhibition of EZH2 or overexpression of BAI1 could reverse the effects of Lncenc1 overexpression on microglial activation and neuroinflammation. Finally, the Lncenc1-siRNA was intrathecally injected into pSNL mice, and its effects on neuropathic pain were evaluated. Knockdown of Lncenc1 attenuated the development and maintenance of mechanical and thermal hyperalgesia of pSNL mice, accompanied by an increase in BAI1 expression and decrease in inflammatory cytokines. In conclusion, Lncenc1 contributes to neuropathic pain by interacting with EZH2 and downregulating the BAI1 gene in mouse microglia.