腹侧CA1到外侧隔核的神经元投射参与调控小鼠的社交记忆

目的:探讨参与调控小鼠同类个体识别及社交记忆行为的神经环路。方法:通过在腹侧CA1(vCA1)脑区注射腺相关病毒AAV5-hsyn-GFP,进行同性别陌生个体及熟悉个体社交行为,检测即早基因c-fos全脑表达情况,明晰小鼠在识别同类陌生个体及熟悉个体时各脑区神经元被激活情况。通过外侧隔核区(LS)逆向腺病毒注射及Fos表达,以确定参与调控小鼠同类个体识别及社交记忆的神经环路。通过药理学遗传的方法检测选择性抑制vCA1到LS的神经投射对小鼠同类个体识别的影响。结果:小鼠前额叶皮层(PFC)、海马齿状回(DG)、伏隔核(NAc)在识别熟悉及陌生个体时均存在较多神经元激活; vCA1及LS在识别陌生个体时存在更多神经元激活; vCA1脑区到LS脑区有直接的神经投射。药理学遗传手段抑制vCA1到LS的神经投射后,在三箱室社交行为实验中,不会影响小鼠辨别同类和无生命物体的能力,但是损害了小鼠识别陌生小鼠的能力。结论:vCA1、PFC、DG、NAc及LS等多个脑区参与小鼠同类社交行为,而vCA1及其到LS的神经投射则参与调控了小鼠对同类个体的社交记忆行为。     

鼻内镜下行鼻腔泪囊吻合手术配合及手术室管理技巧

[目的]探讨鼻内镜下行鼻腔泪囊吻合术围术期护理、手术配合及仪器管理的技巧。[方法]选取我院进行鼻内镜下行鼻腔泪囊吻合手术的病人142例142只眼,由同一主刀医生完成手术,回顾性分析其临床资料,总结本组病人的手术室护理方法。[结果]术后冲洗泪道通畅,无溢脓溢泪现象,无并发症发生,全部病人治愈出院,对手术室护理工作满意。[结论]鼻内窥镜下行鼻腔泪囊吻合手术是当前比较先进的微创手术,手术效果好,相比传统鼻腔泪囊吻合手术环节,需要周全的用物准备,护士的积极配合,掌握内窥镜仪器使用,优化手术流程,与医生共同完成,提高病人满意度。     

Inhibition of histamine H3 receptor alleviates ischemia/reperfusion injury through targeted autophagy but not histamine

OBJECTIVE Histamine H3 receptor(H3R) was reported important in regulation of central nervous system diseases.But less study was carried on cerebral ischemia.Here we demonstrated that inhibition of H3R was protective against ischemia reperfusion injury through reinforcement of protective autophagy.METHODS Transient focal cerebral ischemia model(MCAO) in mice and OGD /reperfusion injury on cultured rat cortical neurons were carried out.RESULTS Histamine H3R was upregulated after ischemia reperfusion injury,and eitherinhibition of H3R by three antagonists(thioperamide,clobenpropit and A331440) or H3R knock out attenuated ischemia reperfusion induced injury in mice,evidenced by lower cell injury and anti-apoptosis in vivo and in vitro,which was reversed by H3R agonist immepip in WT mice.Given that autophagy may inhibit cell apoptosis,we surprisingly found that autophagy was further activated by both H3R knock out and inhibition after ischemia,and the neuroprotective effects were significantly reversed by administration of 3-MA which is an autophagy inhibitor.Both siRNA of Atg7 gene on neurons and knock out of Atg5 gene on MEF cell lines were carried out to make sure again the importance of autophagy in protection of H3R inhibition.To explore the mechanism of regulation of H3R induced neuroprotection,interestingly,we found that histamine was not involved in H3R action.Further studies indicated that CLIC4 which was reported that lower expression led to up-regulated autophagy level interacted with H3R C-terminal tail consisting of amino acid 414-436(H3RCT) was involved in the protection of H3R inhibition through suppressing Akt/GSK3/mTOR signaling.Because inhibiting of H3R and CLIC4 interaction presented neuroprotection in cultured neurons against OGD reperfusion injury.CONCLUSION Taken together,the study demonstrated that upregulated H3R expression during ischemia reperfusion was autophagy inhibitory through activating Akt/GSK3/mTOR signaling.Inhibiting H3R inactivated the signaling by suppressing H3R and CLIC4 interaction,and then led to autophagy upregulated to protect cells against ischemia reperfusion injury,suggesting that H3R may be an attractive clinical therapeutic target.