Objective: To localize the neuroanatomical substrate of rapid eye movement sleep behavior disorder (RBD) and to investigate the neuroanatomical locational relationship between RBD and α-synucleinopathy neurodegenerative diseases. Materials and Methods: Using a systematic PubMed search, we identified 19 patients with lesions in different brain regions that caused RBD. First, lesion network mapping was applied to confirm whether the lesion locations causing RBD corresponded to a common brain network. Second, the literature-based RBD lesion network map was validated using neuroimaging findings and locations of brain pathologies at post-mortem in patients with idiopathic RBD (iRBD) who were identified by independent systematic literature search using PubMed. Finally, we assessed the locational relationship between the sites of pathological alterations at the preclinical stage in α-synucleinopathy neurodegenerative diseases and the brain network for RBD. Results: The lesion network mapping showed lesions causing RBD to be localized to a common brain network defined by connectivity to the pons (including the locus coeruleus, dorsal raphe nucleus, central superior nucleus, and ventrolateral periaqueductal gray), regardless of the lesion location. The positive regions in the pons were replicated by the neuroimaging findings in an independent group of patients with iRBD and it coincided with the reported pathological alterations at postmortem in patients with iRBD. Furthermore, all brain pathological sites at preclinical stages (Braak stages 1–2) in Parkinson’s disease (PD) and at brainstem Lewy body disease in dementia with Lewy bodies (DLB) were involved in the brain network identified for RBD. Conclusion The brain network defined by connectivity to positive pons regions might be the regulatory network loop inducing RBD in humans. In addition, our results suggested that the underlying cause of high phenoconversion rate from iRBD to neurodegenerative α-synucleinopathy might be pathological changes in the preclinical stage of α-synucleinopathy located at the regulatory network loop of RBD.

Objective To study the prevention effects of AduoLa Fuzhenglin(ADL)Oll the brain injury induced by microwave radiation in rats.Methods A total of 140 male Wismr rats were divided randomly into 5 groups,including control group,microwave exposed group,low dosage(0.75 g·kg-1·d-1)group.middle dosage(1.5 g·kg-1·d-1)group and high dosage(3 g·kg-1·d-1)group.Rats in three ADL groups were lavaged with ADL per day for 2 weeks before radiation.After administration,rats were exposed to microwave at 30 mW/cm2 for 15 min.The abilities of learning and memory were detected by Morris water maze,and the contents of amino acids neurotransmitter of hippocampus were detected by HPLC, then the histology and uhrastrncture of hippocampus were observed with light and electron microscope at 6 h,7 and 14 d after exposure.Results The abilities of learning and memory were declined(F=0.000-0.043,P<0.05)from 6 h to 7 d after exposure,and the contents of four kinds of amino acid neurotransmitter in hippocampus were decreased,of which GLU,GLY and GABA were decreased significantly(F=0.000-0.007,P<0.01)at 6h after exposure,then tissue edema,neuronal degeneration,neuron mitoehondria swelling and cavitation,endocytoplasmie rotieulum broaden,synaptic cleft blurred,and perivascular space widen were found in the hippocampus at 6 h and 7 d after exposure.The changes in low dosage group were similar to those of the radiation group.However,in middle and high dosage groups,the abilities of learning and memory were normal to some extent with the significant differences compared to the radiation group from 6 h to 7 d after exposure(F=0.015-0.028.P<0.05).The contents of four kinds of amino acid neurotransmitter were not decreased,especially GLU contents close tO normal level.There were significant differences between middle and high dosage groups and radiation group at 6 h after exposure(F=0.000-0.042,P<0.05).Moreover,no obvious injury in the hippocampus was observed in middle and high dosage groups at 6 h and 7 d after exposure.Conclusions Exposure to 30 mW/cm2 microwave radiation could decrease the abilities of learning and memory,induce amino acid neurotransmitter turbulence,and injure the histology and uhrastructure of hippocampus.ADL at the dosages of 1.5 and 3 g·kg-1·d-1 would have preventive effects on the injury induced by microwave exposure.The concentration of 1.5 g·kg-1 ·d-1 of ADL might be the effective dosage to prevent the brain damage after microwave exposure.

Objective To explore the changes of SOX9 and WT1 expressions in rat Sertoli cells irradiated by EMP ( electromagnetic pulse),S-HPM ( S-band high power microwave) and X-HPM ( Xband high power microwave).Methods Primary Sertoli cells were isolated from 3-week-old Wistar rats and its purity was immunocytochemistrically indentified with WT1.After exposure to 6 × 104 V/m EMP,100 mW/cm2 S-HPM and X-HPM for 4 min respectively,SOX9 and WT1 expressions in Sertoli cells were determined with real-time PCR and Western blot,respectively.Results SOX9 mRNA expression was decreased at 6 and 12 h post-irradiation of three different bands of electromagnetic microwave ( F =15.20and 4.84,P ＜ 0.05 ).SOX9 protein expression was also decreased at 6 and 24 h after irradiation ( F =8.46 and 7.47,P＜0.05).WT1 mRNA expression was decreased at6 and 12 h (F=13.46 and 5.08,P ＜ 0.05 ),but its protein expression was decreased only at 24 h post-irradiation ( F =10.26,P ＜ 0.05 ).Conclusions Three bands of electromagnetic radiation reduce the expressions of SOX9 and WT1 in rat Sertoli cells,which may provide molecular foundation for genital system hazards induced by microwave radiation.

Brain decoding based on functional magnetic resonance imaging has recently enabled the identification of visual perception and mental states. However, due to the limitations of sample size and the lack of an effective reconstruction model, accurate reconstruction of natural images is still a major challenge. The current, rapid development of deep learning models provides the possibility of overcoming these obstacles. Here, we propose a deep learning-based framework that includes a latent feature extractor, a latent feature decoder, and a natural image generator, to achieve the accurate reconstruction of natural images from brain activity. The latent feature extractor is used to extract the latent features of natural images. The latent feature decoder predicts the latent features of natural images based on the response signals from the higher visual cortex. The natural image generator is applied to generate reconstructed images from the predicted latent features of natural images and the response signals from the visual cortex. Quantitative and qualitative evaluations were conducted with test images. The results showed that the reconstructed image achieved comparable, accurate reproduction of the presented image in both high-level semantic category information and low-level pixel information. The framework we propose shows promise for decoding the brain activity.

Vision formation is classically based on projections from retinal ganglion cells (RGC) to the lateral geniculate nucleus (LGN) and the primary visual cortex (V1). Neurons in the mouse V1 are tuned to light stimuli. Although the cellular information of the retina and the LGN has been widely studied, the transcriptome profiles of single light-stimulated neuron in V1 remain unknown. In our study, in vivo calcium imaging and whole-cell electrophysiological patch-clamp recording were utilized to identify 53 individual cells from layer 2/3 of V1 as light-sensitive (LS) or non-light-sensitive (NS) by single-cell light-evoked calcium evaluation and action potential spiking. The contents of each cell after functional tests were aspirated in vivo through a patch-clamp pipette for mRNA sequencing. Moreover, the three-dimensional (3-D) morphological characterizations of the neurons were reconstructed in a live mouse after the whole-cell recordings. Our sequencing results indicated that V1 neurons with a high expression of genes related to transmission regulation, such as Rtn4r and Rgs7, and genes involved in membrane transport, such as Na/K ATPase and NMDA-type glutamatergic receptors, preferentially responded to light stimulation. Furthermore, an antagonist that blocks Rtn4r signals could inactivate the neuronal responses to light stimulation in live mice. In conclusion, our findings of the vivo-seq analysis indicate the key role of the strength of synaptic transmission possesses neurons in V1 of light sensory.