NMDA受体与中枢神经系统发育

中枢神经系统兴奋性氨基酸离子型受体－ＮＭＤＡ受体,是由ＮＭＤＡＲ１和ＮＭＤＡＲ２两个亚单位共同构成的受体通道复合体。ＮＭＤＡ受本激活后可引起神经元细胞对Ｎａ＾＋,Ｋ＾＋和Ｃａ＾２＋通透性增强,产生兴奋性突触后电位,在中枢神经发育的过程中,ＮＭＤＡ受体通过不同亚型的选择性表达,改变自身的结构和功能,进而影响ＮＭＤＡ受体介导的Ｃａ＾２＋内流,调节神经元内Ｃａ＾２＋依赖的第二信使系统,最终实现对中枢神经     

NMDA受体与中枢神经系统的发育

离子型谷氨酸受体分为NMDA型和非NMDA型两类,其中NMDA型受体与中枢神经系统发育关系密切。本文综述了NMDA受体的分子特性及NMDA受体五种亚单位NR1、NR2A、NR2B、NR2C和NR2D在动物出生后脑内的时空表达;NMDA受体亚单位在发育中的作用以及NMDA受体活性的胞内调节机制。     

中枢神经系统去甲肾上腺素分泌的实时检测

为了探讨与中枢神经系统单胺类递质分泌失调有关疾病的中枢机制,人们对单胺类递质分泌动力学的研究越来越有兴趣。去甲肾上腺素是中枢神经系统重要的递质和调质,本文介绍了我们实验室最近发展的实时检测中枢神经系统去甲肾上腺素分泌的一些技术方法,并比较了电化学微碳纤电极（carbon fiber electrode,CFE）测量与电生理、荧光显微测量技术优缺点,阐述了CFE技术在神经科学研究中的一个基本应用。     

去甲肾上腺素引起的α1肾上腺素受体三种亚型脱敏过程的差异

将含有α１肾上腺素受体三种亚型的全长ｃＤＮＡ质粒分别转染到人胚肾脏细胞（ＨＥＫ２９３）,α１Ａ－,α１Ｂ－和α１Ｄ－ＡＲ在ＨＥＫ２９３细胞株上得到高水平稳定表达,用＾３Ｈ－ｉｎｏｓｉｔｏｌ标记和柱层析法测定细胞磷酸肌醇积。观察在去甲肾上腺素长期作用下α１三种受体亚型介导磷酸肌醇蓄积敏感性降低的差别。     

去甲肾上腺素对蟾蜍背根神经节细胞α-肾上腺素能受体的作用

在蟾蜍离体灌流背根神经节(DRG)标本上,用微电极进行细胞内记录。在51个细胞中A型神经元为46个,C型5个。此两类细胞的静息膜电位为60.06±1.34mV(x±SE)。当灌流液中滴加10~(-4)-10~(-3)mol/L去甲肾上腺素(NA)引起如下的膜电位改变:(1)超极化:幅值8.38±1.12mV(x±SE)(20/48);(2)去极化:幅值9.39±1.24mV(x±SE)(23/48);(3)无反应(5/48)。上述膜电位改变既不能由灌流液中滴加异丙基肾上腺素所拟似,也不能为心得安所阻断,因而排除了β-肾上腺能受体介导的可能性。加苯肾上腺素及可乐宁于灌流液,分别产生膜的去极化和超极化,而应用哌唑唪及育亨宾灌流,则分别阻断NA引起的膜去极化和超极化。因此认为:NA引起的DRG神经元的去极化和超极化反应分别是由胞体膜上之α_1-及α_2-肾上腺素能受体所介导的。     

孤束核内的去甲肾上腺素在阿片奖赏效应中的作用

长期药物滥用使吸毒者的中枢神经系统内出现一系列的神经生物化学的变化,包括脑内儿茶酚胺类的去甲肾上腺素（NE）和多巴胺（DA）的变化。在近几十年有关的研究中,脑内多巴胺的作用受到很大关注。相比之下,虽然已知去甲肾上腺素广泛参与阿片的戒断过程,但是在阿片引发的运动和奖赏效应中的作用所知甚少。     

毒蕈碱乙酰胆碱受体在中枢神经系统中的作用

毒蕈碱乙酰胆碱受体（muscarinic acetylcholine receptor, mAChR）作为胆碱能受体家族的一员,广泛存在于副交感神经节后纤维支配的效应器细胞上。因其在中枢和外周神经系统中作用广泛而成为一直以来的研究热点。mAChR分为五种亚型（M₁R～M₅R）,各亚型在脑内均有分布。得益于研究技术的不断发展,五种亚型在大脑内的分布情况日趋明朗。因此,近些年来在中枢神经系统方面,对于mAChR的研究越来越丰富。本文简要介绍了mAChR的主要类型、生理功能、在中枢神经系统中的分布及其与中枢神经系统疾病的关系。     

小鼠子宫平滑肌肾上腺素β受体亚型的研究

本实验分析小鼠子宫平滑肌的肾上腺素β受体亚型,以去甲肾上腺素(NA)、异丙肾上腺(ISO)及舒喘灵(SAL)为激动剂,其pD_2值分别为7.34,8.43与7.30。其中ISO的pD_2值显著大于NA及SAL(P<0.01);NA与SAL的pD_2值无显著性差别(P>0.05),提示小鼠子宫平滑肌具有β_1与β_2受体,且β_1与β_2的数量与/或活性不会相差过大。以心得安为竞争性拮抗剂,NA,ISO及SAL为激动剂,用Schild作图法得出三条不重合且几乎平行的直线,横轴上截距分别为9.01,9.17及9.68,pA_2值按激动剂顺序为SAL>ISO>NA,此结果进一步提示小鼠子宫平滑肌具有β_1与β_2受体,且β_2的数量略大于β_1     

α_1肾上腺素能受体介导去甲肾上腺素促大鼠培养心肌细胞蛋白质合成效应

在无血清和含１．０％、５．０％血清培养的新生大鼠心肌细胞标本上,去甲肾上腺素（ＮＥ,２．０μｍｏｌ／Ｌ）使细胞蛋白质含量（Ｌｏｗｒｙ法）分别比相应对照组增加４０％、２６％、１９％（Ｐ均＜０．０１）;细胞３Ｈ－亮氨酸参入量与ＮＥ浓度呈正性剂量依赖性,最大效应浓度为２０．０μｍｏｌ／Ｌ;无血清培养体系中,０．２、２．０、２０μｍｏｌ／Ｌ的ＮＥ使参入量分别比对照增加１７．８％、３５３％、３７．７％;１．０％血清培养体系中分别比对照增加１６．２％、２７．９％、３１．６％（Ｐ均＜０．０５）;哌唑嗪（２．０μｍｏｌ／Ｌ）可阻断ＮＥ的促蛋白质合成作用,心得安（２．０μｍｏｌ／Ｌ）则无此效应。提示在无血清或低浓度血清培养体系中,ＮＥ可促进心肌细胞蛋白质合成,增加细胞蛋白质含量,该作用可能是通过α１肾上腺素能受体介导。     

α肾上腺素能受体介导去甲肾上腺素促大鼠培养心肌细胞蛋白…

在无血清和含１．０％、５．０％血清培养的新生大鼠心肌细胞标本上,去甲肾上腺素（ＮＥ,２．０μｍｏ１／Ｌ）使细胞蛋白质含量（Ｌｏｗｒｙ法）分别比相应对照组增加４０％、２６％、１９％（Ｐ均＜０．０１）;细胞＾３Ｈ－亮氨酸参入量与ＮＥ浓度呈正性剂量依赖性,最大效应浓度为２０．０μｍｏ１／Ｌ;无血清培养体系中,０．２．２．０、２０μｍｏ１／Ｌ的ＮＥＷ使参入量分别比对照增加１７．８％、３５．３％、３７．７％     

中枢神经系统发育的不对称细胞分裂机制

无论在无脊椎动物还是脊椎动物中,组成中枢神经系统（CNS）的大多数细胞都是由极性神经祖细胞不对称分裂而来。通过简要综述果蝇（Drosophila melanogaste）成神经母细胞（NB）不对称分裂机制,并与近年来在脊椎动物不对称细胞分裂上取得的研究成果相比较,尝试找出两个系统的相似性和相异性。     

Neuropeptide messenger plasticity in the CNS neurons following axotomy

Neuronal peptides exert neurohormonal and neurotransmitter (neuromodulator) functions in the central nervous system (CNS). Besides these functions, a group of neuropeptides may have a capacity to create cell proliferation, growth, and survival. Axotomy induces transient (1–21 d) upregulation of synthesis and gene expression of neuropeptides, such as galanin, corticotropin releasing factor, dynorphin, calcitonin gene-related peptide, vasoactive intestinal polypeptide, cholecystokinin, angiotensin II, and neuropeptide Y. These neuropeptides are colocalized with “classic” neurotransmitters (acetylcholine, aspartate, glutamate) or neurohormones (vasopressin, oxytocin) that are downregulated by axotomy in the same neuronal cells. It is more likely that neuronal cells, in response to axotomy, increase expression of neuropeptides that promote their survival and regeneration, and may downregulate substances related to their transmitter or secretory activities.     

Histamine in brain development

J. Neurochem. (2012) 122, 872-882. ABSTRACT: The function of histamine in the adult central nervous system has been extensively studied, but data on its actions upon the developing nervous system are still scarce. Herein, we review the available information regarding the possible role for histamine in brain development. Some relevant findings are the existence of a transient histaminergic neuronal system during brain development, which includes serotonergic neurons in the midbrain and the rhombencephalon that coexpress histamine; the high levels of histamine found in several areas of the embryo nervous system at the neurogenic stage; the presence of histaminergic fibers and the expression of histamine receptors in various areas of the developing brain; and the neurogenic and proliferative effects on neural stem cells following histamine H(1) - and H(2) -receptor activation, respectively. Altogether, the reviewed information supports a significant role for histamine in brain development and the need for further research in this field.     

The effect of chronic stress on prenatal development of the central nervous system

Abstract

The survival of developing embryos depends on the control and maintenance of homeostasis. Stress caused by chronic immobilization during pregnancy in rats may alter the normal development of the nervous system and increase susceptibility to psychiatric disorders. We investigated the effects of chronic stress on cell proliferation in the forebrains of embryos at 12 days of gestation, and in the hippocampus, dentate gyrus and cortex in embryos at 17 and 21 days of gestation. We examined serial sections of the embryonic brains of control and stressed rats at days 12, 17 and 21 of gestation. Brain sections were immunolabeled with anti-PCNA and stereological analysis was performed on 540 images. The results showed no statistical differences on days 12 and 17 of gestation in the proliferation area of the structures studied, whereas on day 21 of gestation, proliferation decreased in the cortex and dentate gyrus of embryos of the stressed group. These changes were related to decreased prolactin and increased corticosterone concentrations in the plasma.     

Acetylcholinesterase activity in the rat brain after pneumococcal meningitis

Pneumococcal meningitis is a life-threatening disease characterized by acute purulent infection of the meninges causing neuronal injury, cortical necrosis and hippocampal apoptosis. Cholinergic neurons and their projections are extensively distributed throughout the central nervous system. The aim of this study was to assess acetylcholinesterase activity in the rat brain after pneumococcal meningitis. In the hippocampus, frontal cortex and cerebrospinal fluid, acetylcholinesterase activity was found to be increased at 6, 12, 24, 48 and 96 hr without antibiotic treatment, and at 48 and 96 hr with antibiotic treatment. Our data suggest that acetylcholinesterase activity could be related to neuronal damage induced by pneumococcal meningitis.     

Effects of extremely-low-frequency electric fields on neuronal activity in rat brain

The effects of 50-, 30-, and 15-Hz electric field exposure on the activity of spontaneously firing neurons in the brain of anaesthetized rats were studied. Exposure to fields of 100 V/m (peak-to-peak, in air) produced no effect on the overall rate of neuronal firing, but some synchronicity with the period of the exposure waveform was seen with 15- and 30-Hz electric fields.     

Influence of protein or cystein deficiency on hepatic subcellular distribution of methyl mercury in two rat strains

The influence of protein deprivation and cystein deficiency on the distribution of methyl mercury between 4 subcellular fractions of liver was studied in 2 rat strains (Wistar, strain R and Sprague-Dawley). Kept on a standard diet, the 2 strains showed a similar distribution pattern, with the highest mercury level found in the cytosol, followed by the mitochondrial, microsomal and nuclei fractions. The protein free diet caused on increase in the total amount of bound mercury in both strains, the greatest increase, being found in livers from strain R rats. The cystein deficient diet, on the other hand, gave rise to diverging results. Whereas the level of mercury bound to the subcellular fractions was increased in livers from strain R rats, it was markedly reduced in livers from Sprague-Dawley rats.     

The CNS renin-angiotensin system

The renin-angiotensin system (RAS) is one of the best-studied enzyme-neuropeptide systems in the brain and can serve as a model for the action of peptides on neuronal function in general. It is now well established that the brain has its own intrinsic RAS with all its components present in the central nervous system. The RAS generates a family of bioactive angiotensin peptides with variable biological and neurobiological activities. These include angiotensin-(1–8) [Ang II], angiotensin-(3–8) [Ang IV], and angiotensin-(1–7) [Ang-(1–7)]. These neuroactive forms of angiotensin act through specific receptors. Only Ang II acts through two different high-specific receptors, termed AT1 and AT2. Neuronal AT1 receptors mediate the stimulatory actions of Ang II on blood pressure, water and salt intake, and the secretion of vasopressin. In contrast, neuronal AT2 receptors have been implicated in the stimulation of apoptosis and as being antagonistic to AT1 receptors. Among the many potential effects mediated by stimulation of AT2 are neuronal regeneration after injury and the inhibition of pathological growth. Ang-(1–7) mediates its antihypertensive effects by stimulating the synthesis and release of vasodilator prostaglandins and nitric oxide and by potentiating the hypotensive effects of bradykinin. New data concerning the roles of Ang IV and Ang-(1–7) in cognition also support the existence of complex site-specific interactions between multiple angiotensins and multiple receptors in the mediation of important central functions of the RAS. Thus, the RAS of the brain is involved not only in the regulation of blood pressure, but also in the modulation of multiple additional functions in the brain, including processes of sensory information, learning, and memory, and the regulation of emotional responses.