突触体素与中枢神经系统突触发育

突触体素 (synaptophysin ,SYN)是一种分布很广的突触小泡膜蛋白 ,它在中枢神经系统的发育进程反映了一种时间与空间上的特殊表达模式。作为突触的标记物和突触密度的检测物 ,SYN对突触发育的研究具有实用价值。SYN与轴突及某些神经递质系统的发育关系密切 ,至于胆碱能纤维的发育与SYN表达的关系 ,有待深入研究     

一氧化氮神经毒性作用的分子机制

一氧化氮(N0)的形成有赖于一氧化氮合酶(NOS)对L-arginine的分解而生成,在中枢神经系统有许多神经无含有NOS,称为NOS神经元,近来对此研究颇多。 在中枢神经系统NO的释放多为突触后的.这与NMDA受体有关。一般认为,在突触前释放谷氨酸(glu)作用于NMDA受体,促使钙通道开放,Ca~(2+)与ealmodulin联合,促使NOS发挥作用而产生NO。     

极性蛋白与中枢神经系统发育

哺乳动物大脑神经元的形态多样性和突触连接的复杂性是极性细胞的典型例子,形成和维持神经元极性依赖多种极性蛋白的调节.从线虫受精卵发育到哺乳动物神经细胞的极性化通路中,许多极性蛋白存在进化保守机制.中枢神经系统发育的整个过程(包括神经元发生与移行、神经突生长以及突触联系的形成等)都有极性蛋白的直接或间接参与,是各种极性蛋白...     

转录因子Npas4影响抑制性突触发育的功能依赖性调节

哺乳动物大脑神经元的活性可以调节兴奋性突触和抑制性突触的发育和成熟。神经元活性的诸多作用都是通过兴奋性突触谷氨酸盐的释放以及突触后神经元钙流入来介导的,中枢神经系统的神经元接收来自谷氨酸能神经元的兴奋性突触的输入信号和来自释放GABA的中间神经元抑制性的输入信号。兴奋性突触和抑制性突触之间适当的平衡对感觉信息的表达、命令信号的执行以及更高级的认知功能起着关键作用。     

发育脑内的小胶质细胞及其突触修剪功能

正小胶质细胞(microglia,MC)是脑内最重要的免疫细胞,在中枢神经系统(central nervous system,CNS)的免疫反应中起着重要作用。大量研究证实MC在生理和病理情况下可呈现出不同形态,拥有不同形态的MC其功能也存在一定的差异。生理情况下,MC的突触修剪功能可清除发育脑内较少接受信号刺激的突触,即"较弱"的突触,而保留经常接受信号刺激的突触,即"较强"的突触,在发育     

腺苷及其A1受体在呼吸节律产生及传导中的作用

腺苷是中枢神经系统内突触传递和神经元活动的重要抑制性调节因子之一.正常生理情况下,腺苷能调节多种神经递质(如单胺类递质、兴奋性氨基酸、一氧化氮、乙酰胆碱等)的释放.腺苷受体遍布于整个脑和脊髓,其中腺苷A1受体对于呼吸节律的产生和传导发挥着十分重要的作用.     

中枢神经系统microRNA的研究进展

神经系统通过精密的神经网络连接以及突触间准确的识别接收外界的传入信号并作出反应,完成记忆、学习等过程[1].神经系统各阶段发育的异常都有可能引起一系列不明原因的神经精神疾病,对此知之甚少.MicroRNA是一种大小21～23nt的单链小分子RNA,在神经系统中存在一组特有的microRNA参与中枢发育、神经元分化和突触塑形的过程,与神经系统疾病的发生有关[2],这使microRNA成为研究神经系统的又一新焦点,现就microRNA在中枢神经系统研究中的进展及前景进行综述.     

神经和肌肉共同作用——神经肌肉接头形成及其分子机制的研究进展

哺乳动物的神经肌肉接头(NMJ)，作为运动神经末端和肌肉相连接的部位，是目前研究最多、了解最清楚的突触结构。NMJ乃至整个神经系统突触的发育过程就是突触前后膜特化性改变的过程：轴突末梢释放神经递质被突触后细胞接收，经过电-化学-电的转换，完成有效和准确的信息传递。20世纪70年代，大量有关NMJ发育的实验使人们认识到运动系统突触的形成与神经和肌肉之间精确的信号传导有关，之后Hall等0分离出若干参与NMJ发育的信号分子并且证实了其生物活性。20世纪90年代以来，     

小胶质细胞生物学特性及对神经元调控作用

小胶质细胞是常驻脑实质内免疫细胞,在生理状态下是高度动态的,表达多种免疫受体与神经递质受体,严格监控着中枢神经系统(CNS)微环境。近来大量研究揭示这类免疫细胞具有积极地调控神经元作用,其潜在的影响了神经元发生、突触修剪,调节突触可塑性,阻止神经毒性。小胶质细胞功能性变化对CNS的发育、成熟及退化有重要作用。     

中枢神经系统中星形胶质细胞作用的研究进展

星形胶质细胞是中枢神经系统中维持生理动态平衡的关键细胞，具有广泛功能，在正常生理和疾病状态中发挥多样的调节作用，包括提供信息传递和代谢支持、调控血脑屏障功能、调控突触形成、建立和维持适当的突触连接、调节神经保护及神经毒性作用等功能，在中枢神经系统的生长，各种生理、病理环境下均发挥重要作用。该文旨在阐明星形胶质细胞在中枢神经系统中的作用，总结其具体的调节过程和相关机制，为神经系统相关疾病的诊断和治疗提供新思路和方向。     

逆行信使NO在突触长时程增强过程中的作用

NO作为一种重要的生物信使分子,广泛存在于外周和中枢神经系统(CNS).近年来,有关NO在CNS中的作用研究已取得一定进展,尤其在神经突触可塑性方面,它参与了长时程增强(LTP)过程的诱导和维持.作为一种逆行信使,通过一系列信号通路或分子,如:NO-cGMP-PKG、激发内源性ADP核糖苷化及影响C-FOS的表达,最终参与LTP的产生和维持.     

Changes in NADPH diaphorase expression in the fish visual system during optic nerve regeneration and retinal development

The various functions of nitric oxide (NO) in the nervous system are not fully understood, including its role in neuronal regeneration. The goldfish can regenerate its optic nerve after transection, making it a useful model for studying central nervous regeneration in response to injury. Therefore, we have studied the pattern of NO expression in the retina and optic tectum after optic nerve transection, using NADPH diaphorase histochemistry. NO synthesis was transiently up-regulated in the ganglion cell bodies, peaking during the period when retinal axons reach the tectum, between 20–45 days after optic nerve transection. Enzyme activity in the tectum was transiently down-regulated and then returned to control levels at 60 days after optic nerve transection, during synaptic refinement. To compare NO expression in the developing and regenerating retina, we have looked at NO expression in the developing zebrafish retina. In the developing zebrafish retina the pattern of staining roughly followed the pattern of development with the inner plexiform layer and horizontal cells having the strongest pattern of staining. These results suggest that NO may be involved in the survival of ganglion cells in the regenerating retina, and that it plays a different role in the developing retina. In the tectum, NO may be involved in synaptic refinement.     

Nitric oxide neurons and neurotransmission

Nitric oxide was identified as a biological intercellular messenger just over 20 years ago, and its presence and potential importance in the nervous system was immediately noted. With the cloning of NO synthase and the physiological NO receptor soluble guanylyl cyclase, a variety of histochemical methods quickly led to a rather complete picture of where NO is produced and acts in the nervous system. However, the details regarding the subcellular localization of NO synthase and the identity of its molecular binding partners require further clarification. Although the hypothesis that calcium influx via activation of NMDA receptors is a key trigger for NO production has proven very popular and led to suggested roles for NO in synaptic plasticity, there is little direct evidence to support this notion. Instead, studies from the peripheral nervous system indicate a key role for voltage-sensitive calcium channels in regulating NO synthase activity. A similar mechanism may also be important in central neurons, and it remains an important task to identify the precise sources of calcium regulating NO production in specific NO neurons. Also, although cGMP production appears to mediate the physiological signaling by NO, the specific roles of cGMP-dependent ion channels, protein kinases and phosphodiesterases in mediating NO action remain to be determined.     

The role of nitric oxide in the neural control of breathing

The control of breathing has been a long examined enigma. Despite the critical biological significance of respiratory control, the framework of the molecular interactions which generate and regulate these incredible phenomena are only beginning to be delineated. Recent advances in the understanding the role of nitric oxide (NO) as a signaling molecule have facilitated our understanding of the high level complexities and multiple interacting pathways in many biological systems including those underlying neural control of ventilation. In this review, we will examine the current understanding of the contribution of NO and NO-related compounds to the neural control of breathing. We will focus our attention on the role played by NO in peripheral chemoreceptor control of ventilation and also explore the contribution of NO-mediated systems in central nervous system pathways underlying the control of ventilation. Additionally, the importance of NO and NO derivatives in synaptic plasticity and adaptive mechanisms to long-term perturbations during development will also be addressed.     

Expression of synaptic vesicle two-related protein SVOP in the developing nervous system of Xenopus laevis.

Synaptic vesicle-associated proteins are important regulators of neurotransmitter release at synaptic terminals in mature animals. Some synaptic vesicle-associated proteins are also expressed during development, although their contribution to development is not as clear. Here, we describe the cloning and developmental expression pattern of the Xenopus laevis synaptic vesicle-associated protein SVOP, a gene first identified as an immediate target for proneural basic helix-loop-helix factors. Alignment analysis revealed a high level of identity between the SVOP protein sequences from Xenopus and other vertebrates. In developing Xenopus embryos, SVOP expression is restricted to the nervous system and is first detectable at the mid-neurula stage. As development progresses SVOP becomes broadly expressed throughout the central nervous system. Our observation that SVOP is expressed in the developing Xenopus nervous system suggests that it may be involved in neuron formation, maturation, or neuronal function.     

Involvement of nitric oxide in synaptic plasticity and learning

Nitric oxide (NO) is a recently appreciated, short-lived diffusible messenger which serves as an important signaling molecule in both the central and peripheral nervous system. The enzyme that synthesizes nitric oxide, nitric oxide synthase (NOS), is broadly distributed in the brain in several distinct neuronal populations. The distribution of the NOS, as well as the short half-life and diffusible nature of NO, has prompted several studies exploring the potential role of NO in various forms of animal learning and synaptic plasticity. In this review, we discuss the evidence that NO is involved in two major forms of long-lasting neuronal plasticity: hippocampal long-term potentiation and cerebellar long-term depression. In addition, the possibility that NO is involved in several different forms of animal learning, including water maze performance, passive avoidance conditioning and associatively conditioned eyeblink responses, is also examined.     

Central release of nitric oxide mediates antinociception induced by aerobic exercise

Nitric oxide (NO) is a soluble gas that participates in important functions of the central nervous system, such as cognitive function, maintenance of synaptic plasticity for the control of sleep, appetite, body temperature, neurosecretion, and antinociception. Furthermore, during exercise large amounts of NO are released that contribute to maintaining body homeostasis. Besides NO production, physical exercise has been shown to induce antinociception. Thus, the present study aimed to investigate the central involvement of NO in exercise-induced antinociception. In both mechanical and thermal nociceptive tests, central [intrathecal (it) and intracerebroventricular (icv)] pretreatment with inhibitors of the NO/cGMP/K_ATP pathway (L-NOArg, ODQ, and glybenclamide) prevented the antinociceptive effect induced by aerobic exercise (AE). Furthermore, pretreatment (it, icv) with specific NO synthase inhibitors (L-NIO, aminoguanidine, and L-NPA) also prevented this effect. Supporting the hypothesis of the central involvement of NO in exercise-induced antinociception, nitrite levels in the cerebrospinal fluid increased immediately after AE. Therefore, the present study suggests that, during exercise, the NO released centrally induced antinociception.     

Agrin在神经系统损伤后修复中的作用

正神经系统主要由中枢神经系统(central nervous system,CNS)和周围神经系统(peripheral nervous systems,PNS)两大部分组成。CNS损伤包括脊髓损伤和脑神经损伤,主要以后者为主,具有发病率高、致残率高和死亡率高的特点。此外,CNS损伤后会引起包括DNA降解和细胞膜磷脂酰丝氨酸残基早期暴露在内的一系列程序性细胞死亡的病理过程,进     

Brain-derived neurotrophic factor

Since the purification of BDNF in 1982, a great deal of evidence has mounted for its central roles in brain development, physiology, and pathology. Aside from its importance in neural development and cell survival, BDNF appears essential to molecular mechanisms of synaptic plasticity. Basic activity-related changes in the central nervous system are thought to depend on BDNF modification of synaptic transmission, especially in the hippocampus and neocortex. Pathologic levels of BDNF-dependent synaptic plasticity may contribute to conditions such as epilepsy and chronic pain sensitization, whereas application of the trophic properties of BDNF may lead to novel therapeutic options in neurodegenerative diseases and perhaps even in neuropsychiatric disorders.     

Synaptogenesis in the CNS: An Odyssey from Wiring Together to Firing Together

To acquire a better comprehension of nervous system function, it is imperative to understand how synapses are assembled during development and subsequently altered throughout life. Despite recent advances in the fields of neurodevelopment and synaptic plasticity, relatively little is known about the mechanisms that guide synapse formation in the central nervous system (CNS). Although many structural components of the synaptic machinery are pre-assembled prior to the arrival of growth cones at the site of their potential targets, innumerable changes, central to the proper wiring of the brain, must subsequently take place through contact-mediated cell-cell communications. Identification of such signalling molecules and a characterization of various events underlying synaptogenesis are pivotal to our understanding of how a brain cell completes its odyssey from 'wiring together to firing together'. Here we attempt to provide a comprehensive overview that pertains directly to the cellular and molecular mechanisms of selection, formation and refinement of synapses during the development of the CNS in both vertebrates and invertebrates.