Eye opening, a natural and timed event during animal development, influences cortical circuit assembly and maturation; yet, little is known about its precise effect on inhibitory synaptic connections. Here, we show that coinciding with eye opening, the strength of unitary inhibitory postsynaptic currents (uIPSCs) from somatostatin-expressing interneurons (Sst-INs) to nearby excitatory neurons, but not interneurons, sharply decreases in layer 2/3 of the mouse visual cortex. In contrast, the strength of uIPSCs from fast-spiking interneurons (FS-INs) to excitatory neurons significantly increases during eye opening. More importantly, these developmental changes can be prevented by dark rearing or binocular lid suture, and reproduced by the artificial opening of sutured lids. Mechanistically, this differential maturation of synaptic transmission is accompanied by a significant change in the postsynaptic quantal size. Together, our study reveals a differential regulation in GABAergic circuits in the cortex driven by eye opening may be crucial for cortical maturation and function.

Aim: Pyroptosis and inflamm-aging have been newly identified to be involved in diabetic periodontitis. This study aimed to elucidate whether macrophage pyroptosis plays a role in periodontal inflamm-aging by impacting the senescence of fibroblasts, as well as the potential mechanism via NLR family CARD domain-containing protein 4 (NLRC4) phosphorylation.Materials and methods: Diabetes was induced in mice using streptozotocin. Periodontal pyroptosis and senescence were detected using immunohistochemical analysis. Prior to evaluating senescence in human gingival fibroblasts cultured with conditioned medium derived from macrophages, RAW 264.7 macrophages were confirmed to undergo pyroptosis by scanning electron microscopy and gasdermin D (GSDMD) detection. The NLRC4-related pathway was examined under hyperglycaemic conditions.Results: Our data showed that macrophage pyroptosis induced the expression of senescent markers in vivo and in vitro. Importantly, clearance of pyroptotic macrophages rescued senescence in fibroblasts. Furthermore, GSDMD activation and pyroptosis in hyperglycaemia were found to be mediated by NLRC4 phosphorylation.Conclusions: Hyperglycaemia could initially induce macrophage pyroptosis and lead to cellular senescence, thereby critically contributing to periodontal pathogenesis in diabetes. In particular, NLRC4 phosphorylation could be a potential therapeutic target for the inhibition of this process.

Background Heat treatment is widely used to break dormancy for seed germination and phytohormones could be deeply involved. However, effect of heat treatment on phytohormone related genes/proteins/metabolites and possible relationship with dormancy release remains unclear in oil palm. In this study, oil palm seeds were heat-treated at 39 °C for 60 days according to the method for commercial production. The embryos of seeds during heat treatment (0 d, 15 d, 30 d, 45 d and 60 d) and of germinated seeds (70 d and 75 d) were selected to discover the mechanisms involved in oil palm seed germination. RNA-seq and iTRAQ were applied to investigate DEGs and DEPs related to seed germination; qPCR and western blot were used as validation accordingly; endogenous phytohormones were determined by LC-MS/MS and exogenous phytohormones were also applied to validate their effects on seed germination. Results RNA-seq results showed that plant hormone signal transduction was one of the most important pathways and eight phytohormones involved, while six of them (ABA, GA, ET, CTK, IAA and JA) were also identified by iTRAQ. Both RNA-seq and iTRAQ results showed that the expression of ABA decreased after heat treatment, which was further validated by qPCR and western blot. Furthermore, changes in endogenous phytohormones showed that ABA decreased rapidly to about 9% of the control at 30 d and then stayed at very low levels until germination; GA and CTK increased while IAA was not affected by heat treatment. Besides, exogenous ABA treatments (10, 100, 1000 mg/L) showed that the germination rate decreased to 63, 42 and 16% of the control, respectively, suggesting that ABA suppress seed germination and the inhibition effect increase with higher concentration; while the germination rates of exogenous GA and IAA treatments barely changed among different concentrations. Conclusions Phytohormones are deeply involved in oil palm seed germination and ABA acts as an inhibitor. Heat treatment can eliminate endogenous ABA and break dormancy, while GA and CTK may also involve in dormancy release. At least 30 days of heat treatment might be necessary. This study provided informative perspectives on oil palm seed germination, which could be also applicable in other palm species. Electronic supplementary material The online version of this article (10.1186/s12870-019-1970-0) contains supplementary material, which is available to authorized users.

10Eye opening, a natural and timed event during animal development, influences 11 cortical circuit assembly and maturation; yet, little is known about its precise effect on 12 inhibitory synaptic connections. Here we show that coinciding with eye opening, the