神经元电信号的传播

神经元电信号的传播 Neuronal signal transmission 随着经济的高速发展,人们生活水平的不断提高,随着而来的是各种疾病的增多,其中癫痫就是很好的例子。癫痫的存在给患者带来了很大的痛苦,所以很多患者都想早日摆脱癫痫疾病,但由于对癫痫知识的匮乏,很多癫痫患者的治疗错过了最佳时期,为了丰富患者的癫痫知识,下面给大家介绍一下与癫痫相关的知识--神经元电信号的传播。 With the rapid development of economy, people's living standards continue to improve, with and various diseases increase, in which epilepsy is a good example. The presence of epilepsy patients caused great pain, so many patients want to get rid of seizure disorders, but due to the lack of knowledge of epilepsy, many patients with epilepsy treatment missed the best time, in order to enrich the knowledge of epilepsy patients, here to introduce the knowledge associated with epilepsy -- neuron electrical signal transmission. 中枢神经系统内神经元间的信息传递是通过化学递质来进行的。在静息电位基础。上神经元兴奋时产生的一种可以传播的短暂电位叫动作电位,细胞间兴奋性信息的传递开始于动作电位的扩布并传播到下位轴突。当动作电位到达突触前膜时引起局部前膜除极,开放膜上密度才良大的电压门控钙通道,钙离子内流,启动神经递质释放程序。突触囊泡膜蛋白是突触囊泡神经递质释放过程中重要的钙离子感受器,其上有多个钙离子结合位点,参与了突触传递的启动。钙离子内流是化学突触而不是电突触传递信息的关键因素。钙离子进人突触前膜,随之就有化学级联反应发生,这种化学级联反应可引起含有兴奋或抑制性神经递质的小囊泡与突触前膜的某些特殊部位融合,经出胞作用将递质释放到突触间隙。 Central nervous system neurons in the transmission of information between is carried out through chemical transmitters. The resting potential in foundation. On the neuronal excitability of a can propagate transient potentials called action potentials, cell excitability information transmission began on action potential of spreading and spread to the axon. When an action potential at the presynaptic membrane caused by the local membrane depolarization, opening film density was good in large voltage gated calcium channels, calcium influx, start the neurotransmitter release procedure. Synaptic vesicle membrane protein is a synaptic vesicle neurotransmitter release during important calcium sensor, which comprises a plurality of calcium binding sites, involved in synaptic transmission start. Calcium influx is chemical synapses rather than electrical synaptic transmission information. Calcium ion into the presynaptic membrane, then there will be a chemical cascade reaction, the chemical reaction cascade can cause containing excitatory or inhibitory neurotransmitter vesicles with the presynaptic membrane of some special parts by fusion, exocytosis of neurotransmitter release into the synaptic gap will. 递质释放后,囊泡膜与突触前膜融为一体,由网格蛋白在胞质适应蛋白的协同下,在膜的胞质侧形成网格蛋白包被,被包被的囊泡膜逐渐弯曲、内陷,并最终经剪切成为游离囊泡,游离囊泡再经去包被,重新摄取神经递质后,进行新一轮递质释放。当这些神经递质通过弥散作用跨过突触间隙与突触后膜上特殊位点结合后,非NMDA离子通道快速开放,使树突末端的棘突迅速除极,随着由镁离子介导的电压依赖型抑制作用的消除,依赖除极电压的NMDA受体缓慢激活,开始传导电流,最后。特殊的KA受体通道开放,在兴奋性突触后电流的形成中发挥重要作用。 Neurotransmitter release, membrane vesicles with the presynaptic membrane com., by clathrin in cytoplasm of adaptation to protein collaborative, on the cytoplasmic side of the membrane formation of clathrin coated, enclosed by the vesicle membrane gradually bending, invagination, and finally by cutting into free vesicles, free vesicles then to pack to be, to uptake of neurotransmitters, a new round of neurotransmitter release. When these neurotransmitters by diffusion across the synaptic cleft and postsynaptic membrane specific binding sites, the NMDA ion channel fast opening, the dendrites at the end of the spinous process rapid depolarization, as by magnesium ion mediated voltage dependent inhibition of elimination, dependent depolarization voltage NMDA slow receptor activation, start conduction current, finally. Special KA receptor channel opening, excitatory postsynaptic currents in the formation play an important role in. 递质作用方式主要有两种。一种是直接与受体离子通道复合物结合引起通透性改变,另一种是通过几种第二信号系统之一来改变神经元的通透性。目前至少发现了3种第二信号系统与神经递质有关:腺嗦岭环化酶系统、鸟嗦岭环化酶系统及磷酸肌醉和二酷酞甘浪系统。每一系统都能激活特异的蛋白激酶,后者磷酸化离子通道蛋白。这种反应较直接作用于受体离子通道复合机制慢。 There are two main ways of neurotransmitter function. One is direct and receptor ion channel complex binding induced permeability changes, another is by several second signal system to changes in neuronal permeability. Currently found at least 3 second signal system and neurotransmitter related: gland with ridge cyclase system, bird with ridge cyclase system and phosphoric acid creatinine and two cool phthalein Gan wave system. Every system can activate specific protein kinase phosphorylation of ion channel proteins, the latter. This reaction is directly on the receptor ion channel complex mechanism for slow. 兴奋性神经递质经突触间隙与突触后膜上特异性受体结合后,可增加膜对钾、氯离子,尤其是钠离子的通透性,使原有的膜电位降低,产生局部的除极化,用适当的仪器可记录到一个局部的去极化电位,这种电位就称为兴奋性突触后电位。兴奋性突触后电位的振幅取决于突触前神经元点燃的频率、点燃的模式、突触的可塑性或突触的调节。 Excitatory neurotransmitter in the synaptic cleft and postsynaptic membrane specific binding to its receptor, can increase the membrane to potassium, chloride ion, especially sodium ion permeability, so that the original membrane potential decrease, produce partial depolarization, with appropriate instrument can record to a partial depolarization potentials, this potential is called the excitatory postsynaptic potentials. Excitatory postsynaptic potential amplitude depends on the presynaptic neuron light frequency, light patterns, synaptic plasticity or synaptic regulation. 突触可塑性最简单的形式就是发生在周围或中枢的易化。易化能够随与单个突触前电位有关的突触后电位振幅增加,迅速产生或消失,可在首次动作电位的数十毫秒内产生,并在几乎相同的时间内消失。目前用剩余钙理论来解释这种现象:随着最初的动作电位,大量钙离子进人突触前末端,虽然细胞能有效地迅速清除钙离子,但在释放点附近的膜内仍有钙离子浓度的升高如果第二次动作电位在这些剩余钙离子消除前到达,随之而来的兴奋性突触后电位就会因为细胞内有大量的钙离子而比第一个大。 Synaptic plasticity in the simplest form is occurring in the peripheral or central facilitation. Easy to with single presynaptic potential related to postsynaptic potential amplitude increased rapidly, appearance or disappearance, the first action potentials generated within tens of milliseconds, and at nearly the same time. The use of residual calcium theory to explain the phenomenon: as the first action potential, a lot of calcium into the presynaptic terminal, although the cell can effectively prompt removal of calcium ions, but in the release point near the membrane are calcium ion concentration if the second action potentials in these residual calcium elimination before arrival, attendant excitatory postsynaptic potentials will because the cell contains a lot of calcium ion and greater than the first one. 最近对突触可塑性研究的另一个成果是对长时程电位的认识。长时程电位表现为高频反复激活 后几秒出现兴奋性突触后电位振幅的稳步、持续性增高,持续时间可从几小时到几天,考虑与学习 和记忆有关。突触后膜NMDA受体的激活和突触后膜内钙离子浓度的增加可能在长时程电位中起着关 键性作用,但有争论。 Recently on synaptic plasticity in another study of the result of long term potential awareness. Long term potential for high frequency activation after a few seconds to appear excitatory postsynaptic potential amplitude of the steady, persistent hypertension, duration can be from several hours to several days, consider and related to learning and memory. The postsynaptic membrane of NMDA receptor activation and the postsynaptic membrane of intracellular calcium ion concentration may increase in long term potential plays a key role, but there is controversy. 另一个突触可塑性的研究来自对海马CAL区突触的研究。1~2Hz,持续2--5分钟的刺激可引起长 时程抑制电位,提示兴奋性突触后电位的振幅在刺激的某些时间段降低了,其原因与NMDA受体反复 多次的激活有关,经离子通道进人的钙离子在建立长时程抑制中也起着关键性作用。与长时程电位 一样,存在NMDA受体拮抗剂的情况下不出现长时程抑制。 Another studies of synaptic plasticity of hippocampal CAL synapses from research. 1~2Hz, lasted 2--5 min of stimulation can cause long term inhibitory potential, prompting excitatory postsynaptic potential amplitude in the stimulation of certain period is reduced, its reason and NMDA receptor activation on repeatedly, the ion channels into the calcium ion in the establishment of long-term depression also plays a key role. And long term potential, the presence of NMDA receptor antagonists of the case does not appear long-term depression. 高频刺激可引起稳定的长时程电位,甚至在长时程抑制的初期就出现。长时程电位也可被1~2Hz 的刺激所逆转,而出现长时程的抑制,由于突触前状态不同、刺激的类型和持续时间不同,钙离子 内流的水平不同,突触可能产生动作电位或抑制。 High frequency stimulation can induce stable long term potential, even in long-term depression at early stages of emergence. Long term potential can also be 1~2Hz stimuli are reversed, and long term inhibition of presynaptic condition, due to different stimulus types, and different duration, different levels of calcium influx, may generate action potentials or synaptic inhibition. 突触前神经元的活动强或参加活动的突触数量大,兴奋性突触后电位的变化可以总合起来,当 兴奋性突触后电位增加到一定程度时,可引起突触后神经元兴奋,产生扩布性动作电位,并沿神经 纤维传播,将信息传递给下一位神经元,继续神经冲动的传导。 Presynaptic neuronal activity is strong, or to participate in the activities of the synapse number, excitatory postsynaptic potential changes can be together, when excitatory postsynaptic potentials increase to a certain extent, can induce postsynaptic neurons generate action potentials, spreading, and along the nerve fiber communication, will pass the information on to the next neurons, to continue the transmission of nerve impulses. 突触间隙谷氨酸浓度维持在1mmol/L对除极是必要的。除极1毫秒以后,谷氨酸迅速弥散,离开突触,同时,神经胶质,也包括部分神经元附近的谷氨酸主动再摄取开始。用选择性氨基酸阻滞法进行研究发现谷氨酸的再摄取在兴奋性突触后电流的衰减中所起的作用很小,而对谷氨酸在细胞外的扩散以激活突触前代谢性氮基酸受体的作用则要大得多。酶水解、失活、突触前膜或后膜重摄取、部分进入血液循环等多种机制的共同作用使突触间隙内的兴奋性递质浓度迅速下降,兴奋性突触后电流逐渐衰减、在谷氨酸存在的情况下,非NMDA受体通道迅速失活。 Synaptic cleft glutamate concentration is maintained at 1mmol/L on depolarization is necessary. Depolarization of 1 ms later, glutamate rapid diffusion, leaving the synapses, at the same time, glial, also includes parts of nearby neurons glutamate reuptake began active. Selective amino acid block method to study found that glutamate re-uptake in excitatory postsynaptic current attenuation in the role played by the very small, but on glutamate in the extracellular diffusion to the activation of presynaptic metabotropic amino acid receptor role is much greater. Enzymatic hydrolysis, inactivation, the presynaptic membrane or membrane uptake, partially into the blood circulation and other mechanisms of synaptic gap within the excitatory neurotransmitter concentrations decreased rapidly, excitatory postsynaptic currents gradually decay, in the presence of glutamate, a NMDA receptor channel rapidly inactivated. 递质与突触后膜上的特异性受体结合后并非都产生兴奋性突触后电位,当抑制性神经递质与突触后膜上的特异性受体结合后,提高了对氯离子的通透性,使膜电位增大,出现后膜的超极化,就会产生抑制性突触后电位。抑制性突触后电位是由GABA介导的突触后电位,GABA受体激活可引起抓离子通道开放,使神经元过度去极化。在新皮质和海马,GABA受体位于锥体细胞的树突上,B受体激活可产生比A受体激活更慢的抑制性突触后电位,受钾离子而不是抓离子的调节。 Neurotransmitters and synaptic membrane on the specificity of the receptor binding after not have excitatory postsynaptic potentials, when the inhibitory neurotransmitter and postsynaptic membrane by binding to specific receptor, improves on chloride ion permeability, so that the membrane potential increases, appear after membrane hyperpolarization, will produce inhibitory postsynaptic potential. Inhibitory postsynaptic potentials are mediated by GABA postsynaptic potentials, GABA receptor activation can cause catch ion channels open, allowing neurons to excessive depolarization. In the cortex and hippocampus, GABA receptors located in the dendrites of pyramidal cells, activation of B receptors can produce more slowly than A receptor activation of inhibitory postsynaptic potentials, by potassium ions rather than catching ionic regulation. 神经递质引起电流的大小或突触电位的振幅是突触递质强度的参考指标。一般来说,大多数突触中突触递质的强度不是固定的,前一个突触的活动不同,递质强度也可能有不同的变化,这种改变可以是短时间的增加(易化)或减少(抑制),也可能是长时间的增加(长时程电位)或减少(长时程抑制)。除在抑制性突触中所见到的原发性使用依赖性抑制性突触强度的减少,如反复点燃引起的海马抑制强度的减少外,这种在抑制性突触中所见到的使用依赖性抑制的机制尚不清楚,但可能是多因素的,其主要机制是突触后GAGA受体敏感性降低,抓离子再分布困难.,以及抓离子梯度的丧失和由突触前自身受体介导释放性反馈性抑制丧失有关。 Neurotransmitter induced currents or synaptic potentials amplitude is synaptic transmitter strength index. In general, most synapses synaptic transmitter strength is not fixed, the previous synaptic activity of different intensity, neurotransmitters may also have different changes, this change can be a short time increases ( facilitation ) or decrease ( inhibition), or it may be a long time ( long term potential increase or decrease ) ( Ltd ). In addition to the inhibitory synapse seen in primary use dependent inhibitory synaptic strength reduction, such as repeated kindling induced inhibition of hippocampal strength reduction, the inhibitory synapses in see use-dependent inhibition mechanism is unknown, but is likely to be multifactorial, its main mechanism postsynaptic GAGA- receptors decreased sensitivity to, catch ion distribution difficulties, and catch the ion gradient and the loss of a presynaptic autoreceptor mediated release of feedback inhibition of the loss of the relevant. 用偶联刺激法证实能抑制的主要机制是由以自身受体介导的ABA释放性反馈性抑制,但并不是唯一的解释,因为并非所有区域都有GAB。自身受体分布。由以自身受体激活所引起的快速偶联抑制持续不到1秒,而非此机制可持续儿秒。自身受体激活所引起的快速偶联抑制需要几个突触前抑制性神经元的激活。受体不依赖快速偶联抑制的出现是单个抑制突触。虽然CABA能抑制在保持突触环路兴 奋性中是必要的,但GA4H能突触力度可因受体依赖或非依赖机制产生的频率依赖性抑制而减少。这 种现象在引起癫痈发作的急性去抑制中可能有重要意义。 By using coupling stimulation confirmed to inhibit is the main mechanism by its receptor mediated release of ABA feedback inhibition, but not the only explanation, because not all regions have GAB. Its own receptor distribution. By its receptor activation caused by the quick coupling inhibition lasts less than a second, rather than the second mechanism sustainable. Autoimmune receptor activation is caused by the rapid coupling inhibition requires several presynaptic inhibitory neuron activation. Receptor dependent fast coupling inhibition appears to be a single inhibitory synapses. Although CABA can inhibit excitatory synaptic loop in keeping is necessary, but GA4H synaptic strength by receptor dependent or independent mechanism generates a frequency dependent inhibition and reduction. This phenomenon in the induced epilepsy acute inhibition may play an important role in. 神经系统的信息传递有两个特征:特异性和多相性。特异性是指突触后膜只能与突触间隙内的某种或几种递质特异性结合。多相性指突触前膜能够释放多种神经递质,而突触后膜上有多种不同的 受体离子通道复合物能与这些递质进行特异性地结合。 The nervous system of information transmission has two characteristics: specificity and heterogeneity. Specificity refers to the postsynaptic membrane and synaptic gap within only one or several neurotransmitter binding specificity. Multi phase refers to the presynaptic membrane to release neurotransmitters, and postsynaptic membrane has a variety of different receptor ion channel complex can interact with these neurotransmitters were specifically bound. 随着人们对癫痫知识的不断积累,对治疗癫痫会有很大的帮助,但是前提是患者一定要想方设 法的去了解更多的癫痫知识,希望上面的介绍能够对大家癫痫知识的积累带来一定的帮助。 For people with epilepsy knowledge accumulation on epilepsy treatment, there will be a great help, but patients must try various devices to get to know more knowledge of epilepsy, hope the introduction above that for all epilepsy knowledge accumulation of some help. 本文转载自: