HMGB1-RAGE Pathway Contributes to the Abnormal Migration of Endogenous Subventricular Zone Neural Progenitors in an Experimental Model of Focal Microgyria.

Abnormal migration of subventricular zone (SVZ)-derived neural progenitor cells (SDNPs) is involved in the pathological and epileptic processes of focal cortical dysplasias (FCDs), but the underlying mechanisms are not clear. Recent studies indicated that high mobility group box 1 (HMGB1)/receptor for advanced glycation end products (RAGE) are widely expressed in epileptic specimens of FCDs, which suggests that the HMGB1-RAGE pathway is involved in the pathological and/or epileptic processes of FCDs. The present study used Nestin-GFPtg/+ transgenic mice, and we established a model of freezing lesion (FL), as described in our previous report. A "migrating stream" composed of GFP-Nestin+ SDNPs was derived from the SVZ region and migrated to the cortical FL area. We found that translocated HMGB1 and RAGE were expressed in cortical lesion in a clustered distribution pattern, which was especially obvious in the early stage of FL compared to the sham group. Notably, the number of GFP-Nestin+ SDNPs within the "migrating stream" was significantly decreased when the HMGB1-RAGE pathway was blocked by a RAGE antagonist or deletion of the RAGE gene. The absence of RAGE also decreased the activity of pentylenetetrazol-induced cortical epileptiform discharge. In summary, this study provided experimental evidence that the levels of extranuclear HMGB1 and its receptor RAGE were increased in cortical lesion in the early stage of the FL model. Activation of the HMGB1-RAGE pathway may contribute to the abnormal migration of SDNPs and the hyperexcitability of cortical lesion in the FL model.

Chronic stress increases pain sensitivity via activation of the rACC-BLA pathway in rats.

Exposure to chronic stress can produce maladaptive neurobiological changes in pathways associated with pain processing, which may cause stress-induced hyperalgesia (SIH). However, the underlying mechanisms still remain largely unknown. In previous studies, we have reported that the amygdala is involved in chronic forced swim (FS) stress-induced depressive-like behaviors and the exacerbation of neuropathic pain in rats, of which, the basolateral amygdala (BLA) and the central nucleus of the amygdala (CeA) are shown to play important roles in the integration of affective and sensory information including nociception. Here, using in vivo multichannel recording from rostal anterior cingulate cortex (rACC) and BLA, we found that chronic FS stress (CFSS) could increase the pain sensitivity of rats in response to low intensity innoxious stimuli (LIS) and high intensity noxious stimuli (HNS) imposed upon the hindpaw, validating the occurrence of SIH in stressed rats. Moreover, we discovered that CFSS not only induced an increased activity of rACC neuronal population but also produced an augmented field potential power (FPP) of rACC local field potential (LFP), especially in low frequency theta band as well as in high frequency low gamma band ranges, both at the baseline state and under LIS and HNS conditions. In addition, by using a cross-correlation method and a partial directed coherence (PDC) algorithm to analyze the LFP oscillating activity in rACC and BLA, we demonstrated that CFSS could substantially promote the synchronization between rACC and BLA regions, and also enhanced the neural information flow from rACC to BLA. We conclude that exposure of chronic FS stress to rats could result in an increased activity of rACC neuronal population and promote the functional connectivity and the synchronization between rACC and BLA regions, and also enhance the pain-related neural information flow from rACC to BLA, which likely underlie the pathogenesis of SIH.

Mitochondrial genome of the Siberian sturgeon Acipenser baerii.

The complete mitochondrial genome of Siberian sturgeon Acipenser baerii had been determined. The total length of the mitogenome was 16,763 bp and had 13 protein-coding, 22 tRNA, and 2 rRNA genes. Except for the eight tRNA and Nd6 genes, all other mitochondrial genes are encoded on the heavy strand. The overall base composition of the heavy strand is 30.3% A, 24.3% T, 29.1% C, 16.3% G, with an AT content of 54.6%. The DNA sequence of A. baerii shared 97.8, 97.6, 93.5, 91.6, 93.6, and 87.1% sequence homology with that of Acipenser sinensis, Acipenser gueldenstaedtii, Acipenser transmontanus, Acipenser dabryanus, Acipenser stellatus, and Polyodon spathula. Molecular data presented here provide a useful tool for evolutionary as well as population genetics studied.