Munc18 and Munc13 regulate early neurite outgrowth

Background information. During development, growth cones of outgrowing neurons express proteins involved in vesicular secretion, such as SNARE (soluble N‐ethylmaleimide‐sensitive fusion protein‐attachment protein receptor) proteins, Munc13 and Munc18. Vesicles are known to fuse in growth cones prior to synapse formation, which may contribute to outgrowth. Results. We tested this possibility in dissociated cell cultures and organotypic slice cultures of two release‐deficient mice (Munc18‐1 null and Munc13‐1/2 double null). Both types of release‐deficient neurons have a decreased outgrowth speed and therefore have a smaller total neurite length during early development [DIV1–4 (day in vitro 1–4)]. In addition, more filopodia per growth cone were observed in Munc18‐1 null, but not WT (wild‐type) or Munc13‐1/2 double null neurons. The smaller total neurite length during early development was no longer observed after synaptogenesis (DIV14–23). Conclusion. These data suggest that the inability of vesicle fusion in the growth cone affects outgrowth during the initial phases when outgrowth speed is high, but not during/after synaptogenesis. Overall, the outgrowth speed is probably not rate‐limiting during neuronal network formation, at least in vitro. In addition, Munc18, but not Munc13, regulates growth cone filopodia, potentially via its previously observed effect on filamentous actin.     

杉木和米槠细根混合分解及其养分释放

在福建省建瓯万木林自然保护区,选取针叶树种杉木(Cunninghamia lanceolata,CUL)细根和常绿阔叶树种米槠(Castanopsis carlesii,CAC)细根,采用网袋法进行了为期720d细根(分0-1mm、1-2mm两个径级)单独分解(在各自细根的起源林分)和混合分解(分别在杉木林和米槠林)干重损失及其养分释放动态的研究。结果表明:杉木和米槠细根混合分解前期(0-270d)曾对干重损失起促进作用,而之后(270-720d),细根混合起了抑制作用。分解过程中的养分释放与干重损失有所不同,混合分解前期(0-360d)出现过促进作用,分解后期(360-720d),除1-2mm径级混合细根P的释放既没有促进也没有抑制作用外,均表现为养分释放的抑制作用。细根混合分解过程中干重损失和养分释放速率变化与分解者生物群落有很大关系。     

岱海表层沉积物中内源磷的释放

以北方半干旱地区典型内陆封闭湖泊岱海为研究对象,开展了上覆水质及多种环境因子(温度,pH,溶解氧,扰动,光照)对湖泊沉积物内源磷释放的影响研究。结果表明:(1)温度升高有利于内源磷的释放,湖泊水体在温度较高的夏季更易呈现富营养化状态;(2)碱性条件有利于磷的释放,岱海水体属微碱性环境(pH8.8),若水体pH进一步升高,将会造成沉积物内源磷的大量释放;(3)厌氧条件(ρDO0.8mg/L)有利于磷的释放,岱海湖心区水深较深,易形成厌氧环境,因此湖心区内源磷释放强度较浅水区大;(4)强烈扰动有利于磷的释放,这会对浅水区的底质产生较大影响;(5)照度通过底栖藻类的生物作用,间接地限制了沉积物释磷对上覆水中磷浓度的影响。     

施用控释氮肥对稻田土壤微生物生物量碳、氮的影响

借助农业部望城红壤水稻土生态环境野外观测试验站的控释氮肥试验,研究了施用控释氮肥对水稻不同生育期间稻田土壤微生物生物量碳、氮动态变化的影响。试验共设5个处理:①CK,(不施氮肥);②Urea(施用尿素);③CRNF(施用与处理②等氮量的控释氮肥);④70%CRNF(施用控释氮肥,用氮量为处理②的70%);⑤50%CRNF+M(施用控释氮肥和猪粪,总氮量为处理②的70%,其中控释氮肥用量为处理②的50%,猪粪含氮量为处理②的20%)。结果表明,施肥后10 d,施氮处理土壤微生物生物量碳和氮均达最高,随生育进程推进逐渐下降,成熟期有一定的回升;施肥初期,施用等氮量的控释氮肥处理(CRNF)土壤微生物量碳、氮含量较尿素处理(Urea)分别增加5.4%和22.5%,而水稻生育中后期,控释氮肥处理(CRNF)土壤微生物量碳、氮含量较尿素处理(Urea)下降幅度大,该处理向地上部提供氮素营养较尿素处理高;施氮量较高的CRNF处理,土壤微生物生物量碳低于控释氮肥节氮处理(70%CRNF),但在大多数取样时期,土壤微生物量氮高于控释氮肥节氮处理(70%CRNF);控释氮肥配施有机肥的节氮处理较其他单施化肥处理显著增加土壤微生物生物量碳、氮含量。控释氮肥与有机肥配施,不仅能节约氮肥用量,而且能明显地提高土壤微生物生物量碳、氮的含量。     

0710合生元结肠靶向微生态调节剂体外释放及定位作用研究

目的将益生菌双歧杆菌与枸杞多糖提取物设计为口服结肠定位给药系统(OCDDS),制备0710合生元结肠靶向微生态调节剂,考查其体外释放行为及体内定位作用。方法以枸杞中多糖为指标,对制剂进行体外溶出实验,并利用X-射线跟踪技术验证0710合生元结肠靶向微生态调节剂在人体内的靶向性。结果该制剂在人工胃液2 h、人工小肠液4 h,几乎不释药,而在人工结肠液中6 h释药达到100%,符合中国药典2005年版对缓释制剂的规定,且体内实验在结肠中黏附性较好。结论0710合生元结肠靶向微生态调节剂在体外结肠液中释放良好,在体内结肠具有靶向性,达到制剂设计要求。     

Intracellular Ca2+ release through ryanodine receptors contributes to AMPA receptor-mediated mitochondrial dysfunction and ER stress in oligodendrocytes

Overactivation of ionotropic glutamate receptors in oligodendrocytes induces cytosolic Ca²⁺ overload and excitotoxic death, a process that contributes to demyelination and multiple sclerosis. Excitotoxic insults cause well-characterized mitochondrial alterations and endoplasmic reticulum (ER) dysfunction, which is not fully understood. In this study, we analyzed the contribution of ER-Ca²⁺ release through ryanodine receptors (RyRs) and inositol triphosphate receptors (IP₃Rs) to excitotoxicity in oligodendrocytes in vitro. First, we observed that oligodendrocytes express all previously characterized RyRs and IP₃Rs. Blockade of Ca²⁺-induced Ca²⁺ release by TMB-8 following α-amino-3-hydroxyl-5-methyl-4-isoxazole-propionate (AMPA) receptor-mediated insults attenuated both oligodendrocyte death and cytosolic Ca²⁺ overload. In turn, RyR inhibition by ryanodine reduced as well the Ca²⁺ overload whereas IP₃R inhibition was ineffective. Furthermore, AMPA-triggered mitochondrial membrane depolarization, oxidative stress and activation of caspase-3, which in all instances was diminished by RyR inhibition. In addition, we observed that AMPA induced an ER stress response as revealed by α subunit of the eukaryotic initiation factor 2α phosphorylation, overexpression of GRP chaperones and RyR-dependent cleavage of caspase-12. Finally, attenuating ER stress with salubrinal protected oligodendrocytes from AMPA excitotoxicity. Together, these results show that Ca²⁺ release through RyRs contributes to cytosolic Ca²⁺ overload, mitochondrial dysfunction, ER stress and cell death following AMPA receptor-mediated excitotoxicity in oligodendrocytes.