共查询到19条相似文献,搜索用时 109 毫秒
1.
短时程突触可塑性的功能意义 总被引:5,自引:0,他引:5
短时程的突触可塑性是突触可塑性的一种重要表现形式,对实现神经系统的正常功能起着重要作用.突触的短时程可塑性能够加强突触传递的确定性,调节大脑皮层兴奋和抑制之间的平衡,形成神经活动的时间、空间特性,形成并调节皮层丘脑网络的同步振荡.突触的短时程可塑性可能也参与了注意、启动效应、睡眠节律和学习记忆等神经系统高级功能的实现. 相似文献
2.
3.
代谢型谷氨酸受体在突触可塑性中的作用 总被引:2,自引:0,他引:2
突触可塑性是近几年神经科学研究的热点之一,因为它对于理解神经系统的学习、学习和记忆、多咱神经疾病等许多过程有着重要的意义。除了离子型谷氨酸受体外,代谢型谷氨酸受体也参与了一些脑区中不同形式的突触可塑性变化。本文就代谢型谷氨酸受体选择性激动剂和拮抗剂对长时程增强和长时程抑制的作用进行了综述,以助于人们进一步理解突触可塑性的细胞和分子机制。 相似文献
4.
5.
转录激活因子4(ATF4)属于碱性亮氨酸拉链结构域蛋白中的ATF/CREB转录因子家族,ATF4在脑内广泛表达,在应激、痛觉、突触可塑性和神经退行性变等中发挥重要作用。学习与记忆是脑的高级功能之一,学习是获取新信息的过程,记忆是将信息进行编码、储存及提取的过程,二者被认为是认知活动的基础。突触可塑性是突触在形态、结构和功能上的可变性和可修饰性,与神经系统的发育和学习记忆等脑的高级功能密切相关。突触可塑性的长时程增强和长时程抑制是学习和记忆形成的基础。近年来研究发现, ATF4与突触可塑性和学习记忆密切相关,其在神经退行性变、脑损伤和药物成瘾等疾病中扮演重要角色,有必要深入理解ATF4在学习记忆障碍相关疾病中发挥的作用,为相关疾病的治疗提供新靶点。 相似文献
6.
7.
8.
大鼠丘脑侧后核(lateral posterior thalamic nucleus,LP nucleus)到初级视皮层的突触连接是膝体外视觉通路的重要组成部分.运用场电位记录和电泳的方法在位研究了该视觉回路突触传递的短时程可塑性.结果表明,无论是运用双脉冲刺激还是串刺激都能观察到明显的短时程抑制特性.电泳荷包牡丹碱(bicuculline)和2-hydroxy-saclofen使该抑制作用减弱,电泳钙离子使抑制加强,电泳APV对抑制作用没有明显影响.所以突触前递质释放水平的改变,和γ-氨基丁酸(GABA)能受体(尤其是GABAB受体)的活动都会影响该回路突触传递的短时程可塑性,而N-甲基-D-天冬氨酸(NMDA)受体则几乎没有作用.该回路很强的短时程抑制特性可能与LP核在视觉注意中的作用有关. 相似文献
9.
Eph受体酪氨酸激酶及其配体ephrin广泛参与神经系统的发育,如轴突导向、细胞迁移、体节形成和血管生成。最近研究显示的Ephephrin在突触的定位提示其与突触可塑性有关。Ephephrin对成年神经系统的可塑性、学习和记忆,以及神经损伤后的再生可能具有重要的调节作用。 相似文献
10.
神经元的突触可塑性与学习和记忆 总被引:7,自引:0,他引:7
陈燕 《生物化学与生物物理进展》2008,35(6):610-619
大量研究表明,神经元的突触可塑性包括功能可塑性和结构可塑性,与学习和记忆密切相关.最近,在经过训练的动物海马区,记录到了学习诱导的长时程增强(long term potentiation,LTP),如果用激酶抑制剂阻断晚期LTP,就会使大鼠丧失训练形成的记忆.这些结果指出,LTP可能是形成记忆的分子基础.因此,进一步研究哺乳动物脑内突触可塑性的分子机制,对揭示学习和记忆的神经基础有重要意义.此外,在精神迟滞性疾病和神经退行性疾病患者脑内记录到异常的LTP,并发现神经元的树突棘数量减少,形态上产生畸变或萎缩,同时发现,产生突变的基因大多编码调节突触可塑性的信号通路蛋白,故突触可塑性研究也将促进精神和神经疾病的预防和治疗.综述了突触可塑性研究的最新进展,并展望了其发展前景. 相似文献
11.
Dominique Debanne Gaël Daoudal Valrie Sourdet Michaël Russier 《Journal of Physiology》2003,97(4-6):403-414
It is generally believed that spatio-temporal configurations of distributed activity in the brain contribute to the coding of neuronal information and that synaptic contacts between nerve cells could play a central role in the formation of privileged pathways of activity. Synaptic plasticity is not the only mode of regulation of information processing in the brain and persistent regulations of ionic conductances in some specialized neuronal areas such as the dendrites, the cell body and the axon could also modulate, in the short- and the long-term, the propagation of information in the brain. Persistent changes in intrinsic excitability have been reported in several brain areas in which activity is modified during a classical conditioning. The role of synaptic activity seems to be determinant in the induction but the learning rules and the underlying mechanisms remain to be defined. This review discusses the role of neuronal activity in the induction of intrinsic plasticity in cortical, hippocampal and cerebellar neurons. Activation and inactivation properties of ionic channels in the axon determine the short-term dynamics of axonal propagation and synaptic transmission. Activation of glutamate receptors initiates a long-term modification in neuronal excitability that may represent the substrate for the mnesic engram and for the stabilization of the epileptic state. Similarly to synaptic plasticity, long-lasting intrinsic plasticity appears to be reversible and to express a certain level of input or cellular specificity. These non-synaptic forms of plasticity affect the signal propagation in the axon, the dendrites and the soma. They not only share common learning rules and induction pathways with the better known synaptic plasticity such as NMDA receptor-dependent LTP and LTD but also contribute in synergy with these synaptic changes to the formation of a coherent mnesic engram. 相似文献
12.
Synaptic plasticity is considered to be the biological substrate of learning and memory. In this document we review phenomenological models of short-term and long-term synaptic plasticity, in particular spike-timing dependent plasticity (STDP). The aim of the document is to provide a framework for classifying and evaluating different models of plasticity. We focus on phenomenological synaptic models that are compatible with integrate-and-fire type neuron models where each neuron is described by a small number of variables. This implies that synaptic update rules for short-term or long-term plasticity can only depend on spike timing and, potentially, on membrane potential, as well as on the value of the synaptic weight, or on low-pass filtered (temporally averaged) versions of the above variables. We examine the ability of the models to account for experimental data and to fulfill expectations derived from theoretical considerations. We further discuss their relations to teacher-based rules (supervised learning) and reward-based rules (reinforcement learning). All models discussed in this paper are suitable for large-scale network simulations. 相似文献
13.
记忆的形成阶段包含着神经元突触的可塑性变化过程.近年来的研究表明,神经细胞粘附分子可同时增进突触的可塑性和维持突触结构的稳定性.许多研究证实神经细胞粘附分子对与学习和记忆相关的过程起着一定的调节作用. 相似文献
14.
15.
神经元突触前可塑性的结构及分子基础 总被引:1,自引:0,他引:1
突触可塑性是神经元间信息传递的重要生理调控机制,它包括突触前可塑性和突触后可塑性.突触前可塑性是指通过对神经递质释放过程的干预、修饰,调节突触强度的过程.突触强度的变化,是通过影响量子的大小,活动区的个数和囊泡释放概率来实现的.而突触前囊泡活动尤为重要:从转运、搭靠、融合至内吞进入下一轮循环,每一步都是由一群互相作用的蛋白质共同完成的. 相似文献
16.
Shaokai Zhao Yingchun Shang Ze Yang Xi Xiao Jianhai Zhang Tao Zhang 《Cognitive neurodynamics》2021,15(2):253
The indexes of synaptic plasticity, including long-term potentiation (LTP) and long-term depression (LTD), can usually be measured by evaluating the slope and/or magnitude of field excitatory postsynaptic potentials (fEPSPs). So far, the process depends on manually labeling the linear portion of fEPSPs one by one, which is not only a subjective procedure but also a time-consuming job. In the present study, a novel approach has been developed in order to objectively and effectively evaluate the index of synaptic plasticity. Firstly, we introduced an expert system applying symbolic rules to discard the contaminated waveform in an interpretable way, and further generate supervisory signals for subsequent seq 2seq model based on neural networks. For the propose of enhancing the system generalization ability to deal with the contaminated data of fEPSPs, we employed long short-term memory (LSTM) networks. Finally, the comparison was performed between the automatically labeling system and manually labeling system. These results show that the expert system achieves an accuracy of 96.22% on Type-I labels, and the LSTM supervised by the expert system obtains an accuracy of 96.73% on Type-II labels. Compared to the manually labeling system, the hybrids system is able to measure the index of synaptic plasticity more objectively and efficiently. The new system can reach the level of the human expert ability, and accurately produce the index of synaptic plasticity in a fast way. 相似文献
17.
18.
Synaptic plasticity plays a central role in the study of neural mechanisms of learning and memory. Plasticity rules are not invariant over time but are under neuromodulatory control, enabling behavioral states to influence memory formation. Neuromodulation controls synaptic plasticity at network level by directing information flow, at circuit level through changes in excitation/inhibition balance, and at synaptic level through modulation of intracellular signaling cascades. Although most research has focused on modulation of principal neurons, recent progress has uncovered important roles for interneurons in not only routing information, but also setting conditions for synaptic plasticity. Moreover, astrocytes have been shown to both gate and mediate plasticity. These additional mechanisms must be considered for a comprehensive mechanistic understanding of learning and memory. 相似文献
19.
多巴胺是脑内重要的信息传递物质,不仅可以作为递质释放到前额叶、伏隔核等脑区,直接进行信息传递,也可以作为调质调节其它突触递质的传递,并影响神经元可塑性。海马参与构成边缘系统,受多巴胺能神经支配,执行着有关学习记忆以及空间定位的功能。海马神经元的可塑性是学习记忆的细胞分子基础。研究表明,多巴胺对海马神经元的突触可塑性和兴奋性可塑性都具有重要的调节作用。本文扼要综述多巴胺对海马神经元突触可塑性和兴奋性可塑性的调节机制的研究进展,以期为DA系统参与海马区学习记忆功能的研究提供新思路,更深入地了解学习记忆的神经机制。 相似文献