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第10行： − + − + − − = = 早期研究 = = 对神经网络的早期研究见于赫伯特 · 斯宾塞的《心理学原理》第三版(1872)、西奥多 · 梅纳特的《精神病学》(1884)、威廉 · 詹姆斯的《心理学原理》(1890)和西格蒙德 · 弗洛伊德的《科学心理学计划》(1895)。1949年，赫布在其理论（即赫布理论）中提出了神经元学习的第一定律。赫布理论认为，配对中突触前神经元和突触后神经元的活动可以充分改变突触连接的动态特性，即要么促进，要么抑制信号传递。1959年，神经科学家，沃伦·麦卡洛克和 Walter Pitts 发表了关于神经网络处理的第一部著作。他们从理论上证明了人工神经元网络可以实现逻辑、算术和符号功能。生物神经元的简化模型由此建立起来，现在通常被称为感知器或人工神经元。这些简单的模型解释了神经加成作用(即突触后膜上的电位将在细胞体中加成)。后来的模型也提供了兴奋性和抑制性突触传递。 第26行：
第24行： − + − − − 动作语言理解的运动语义神经回路的组织。灰点代表语言理解的区域，创造了一个理解所有语言的网络。当理解与腿相关的词语时，运动系统的语义回路，特别是腿的运动表征(黄点)被纳入其中。改编自 Shebani 等人。(2013)+ − The establishment of synapses enables the connection of neurons into millions of overlapping, and interlinking neural circuits. Presynaptic proteins called neurexins are central to this process.+ − − − One principle by which neurons work is neural summation – potentials at the postsynaptic membrane will sum up in the cell body. If the depolarization of the neuron at the axon hillock goes above threshold an action potential will occur that travels down the axon to the terminal endings to transmit a signal to other neurons. Excitatory and inhibitory synaptic transmission is realized mostly by excitatory postsynaptic potentials (EPSPs), and inhibitory postsynaptic potentials (IPSPs).+ − − 神经元工作的一个原理是在突触后膜上的神经求和电位将在细胞体内得到总结。如果轴突柄处的神经元去极化超过阈值，就会产生动作电位，沿轴突向下传递到末端末梢，将信号传递给其他神经元。兴奋性和抑制性突触传递主要通过兴奋性突触后电位(epsp)和抑制性突触后电位(ipsp)实现。 − − 神经元工作的一个原理是神经汇总——突触后膜上的电位将在细胞体中进行汇总。如果神经元在轴突丘处的去极化超过阈值，就会发生动作电位，动作电位沿着轴突向下传递到末端，将信号传递给其他神经元。兴奋性和抑制性突触传递主要通过兴奋性突触后电位(EPSPs)和抑制性突触后电位(IPSPs)实现。 − On the electrophysiological level, there are various phenomena which alter the response characteristics of individual synapses (called synaptic plasticity) and individual neurons (intrinsic plasticity). These are often divided into short-term plasticity and long-term plasticity. Long-term synaptic plasticity is often contended to be the most likely memory substrate. Usually, the term "neuroplasticity" refers to changes in the brain that are caused by activity or experience.+ − − 在电生理层面，有各种现象改变个体突触(称为突触可塑性)和个体神经元的反应特性(内在可塑性)。这些常常分为短期可塑性和长期可塑性。长期突触可塑性是最有可能的记忆基质。通常，术语“神经可塑性”指的是由活动或经验引起的大脑变化。 − − − − Connections display temporal and spatial characteristics. Temporal characteristics refers to the continuously modified activity-dependent efficacy of synaptic transmission, called [[spike-timing-dependent plasticity]]. It has been observed in several studies that the synaptic efficacy of this transmission can undergo short-term increase (called [[neural facilitation|facilitation]]) or decrease ([[Neural facilitation#Short-term depression|depression]]) according to the activity of the presynaptic neuron. The induction of long-term changes in synaptic efficacy, by [[long-term potentiation]] (LTP) or [[long-term depression|depression]] (LTD), depends strongly on the relative timing of the onset of the [[excitatory postsynaptic potential]] and the postsynaptic action potential. LTP is induced by a series of action potentials which cause a variety of biochemical responses. Eventually, the reactions cause the expression of new receptors on the cellular membranes of the postsynaptic neurons or increase the efficacy of the existing receptors through [[phosphorylation]]. − − Connections display temporal and spatial characteristics. Temporal characteristics refers to the continuously modified activity-dependent efficacy of synaptic transmission, called spike-timing-dependent plasticity. It has been observed in several studies that the synaptic efficacy of this transmission can undergo short-term increase (called facilitation) or decrease (depression) according to the activity of the presynaptic neuron. The induction of long-term changes in synaptic efficacy, by long-term potentiation (LTP) or depression (LTD), depends strongly on the relative timing of the onset of the excitatory postsynaptic potential and the postsynaptic action potential. LTP is induced by a series of action potentials which cause a variety of biochemical responses. Eventually, the reactions cause the expression of new receptors on the cellular membranes of the postsynaptic neurons or increase the efficacy of the existing receptors through phosphorylation. − − 连接具有时间和空间特征。时间特征是指不断修改的活动依赖功效的突触传递，所谓的电峰时间相关突触可塑性。一些研究已经观察到，这种传递的突触功效可以经历短期的增加(称为易化)或减少(抑郁)根据突触前神经元的活动。长时程增强作用或抑制剂诱导突触效能的长期变化，很大程度上取决于兴奋性突触后电位和突触后动作电位发生的相对时间。LTP 是由一系列动作电位引起的，动作电位引起多种生化反应。最终，这些反应导致新受体在突触后神经元的细胞膜上表达，或者通过磷酸化增加现有受体的功效。 − − − 连接表现出时间和空间特征。时间特征是指突触传递的持续修饰的活动依赖的效能，称为峰时依赖的可塑性。多项研究发现，根据突触前神经元的活动，这种传递的突触效能可以经历短期的增加(称为易化)或减少(抑制)。通过长期增强(LTP)或抑制(LTD)诱导突触效能的长期变化，在很大程度上取决于兴奋性突触后电位和突触后动作电位的相对起病时间。LTP是由一系列动作电位引起的各种生化反应引起的。最终，这些反应导致突触后神经元细胞膜上表达新的受体或通过磷酸化增加现有受体的效能。 − − Backpropagating action potentials cannot occur because after an action potential travels down a given segment of the axon, the [[Depolarizing pre-pulse#Hodgkin–Huxley model|m gate]]s on [[voltage-gated sodium channel]]s close, thus blocking any transient opening of the [[Depolarizing pre-pulse#Hodgkin–Huxley model|h gate]] from causing a change in the intracellular sodium ion (Na<sup>+</sup>) concentration, and preventing the generation of an action potential back towards the cell body. In some cells, however, [[neural backpropagation]] does occur through the [[dendrite|dendritic branching]] and may have important effects on synaptic plasticity and computation. − − Backpropagating action potentials cannot occur because after an action potential travels down a given segment of the axon, the m gates on voltage-gated sodium channels close, thus blocking any transient opening of the h gate from causing a change in the intracellular sodium ion (Na+) concentration, and preventing the generation of an action potential back towards the cell body. In some cells, however, neural backpropagation does occur through the dendritic branching and may have important effects on synaptic plasticity and computation. − − 背向传导动作电位不能发生，因为在动作电位下行到轴突的某一特定部分后，电压门控钠通道上的 m 门关闭，从而阻止 h 门的任何瞬间开启引起细胞内钠离子(Na +)浓度的变化，并阻止动作电位回到细胞体内。然而，在一些细胞中，神经反向传播通过树突的分支发生，并可能对突触可塑性和计算产生重要影响。 − − − 反向传播的动作电位是不可能发生的，因为当动作电位沿着轴突的某一特定节段传递之后，电压门控钠通道上的m门关闭，从而阻止h门的任何瞬态打开，以免引起细胞内钠离子浓度的变化。并阻止动作电位的产生回到细胞体内。然而，在某些细胞中，神经反向传播确实通过树突分支发生，并可能对突触可塑性和计算产生重要影响。 − − A neuron in the brain requires a single signal to a [[neuromuscular junction]] to stimulate contraction of the postsynaptic muscle cell. In the spinal cord, however, at least 75 [[afferent nerve|afferent]] neurons are required to produce firing. This picture is further complicated by variation in time constant between neurons, as some cells can experience their [[Excitatory postsynaptic potential|EPSPs]] over a wider period of time than others. − A neuron in the brain requires a single signal to a neuromuscular junction to stimulate contraction of the postsynaptic muscle cell. In the spinal cord, however, at least 75 afferent neurons are required to produce firing. This picture is further complicated by variation in time constant between neurons, as some cells can experience their EPSPs over a wider period of time than others.+ − 大脑中的一个神经元需要一个单一的信号到一个神经肌肉接点来刺激突触后肌肉细胞的收缩。然而，在脊髓中，至少需要75个传入神经元来产生放电。神经元之间时间常数的变化更加复杂了，因为一些细胞可以比其他细胞经历更长的时间。+ − + − 大脑中的神经元需要一个单一的信号到神经肌肉连接刺激突触后肌肉细胞的收缩。然而，在脊髓中，产生放电需要至少75个传入神经元。由于神经元之间的时间常数变化，这幅图变得更加复杂，因为一些细胞可以在比其他细胞更长的一段时间内感受到EPSPs。 − While in synapses in the developing brain synaptic depression has been particularly widely observed it has been speculated that it changes to facilitation in adult brains.+ − − 在发育中的大脑突触中，突触抑制已经被广泛观察到，有人推测它在成人大脑中会发生易化变化。 − − 虽然在发育状态的脑突触中，突触抑制已经被广泛观察到，但据推测，它在成人大脑中改变为易化。 + + +
无编辑摘要
==Early study==
==Early study==
[[Image:Cajal actx inter.jpg|thumb|300px|right|From "Texture of the [[Nervous System]] of Man and the [[Vertebrates]]" by [[Santiago Ramón y Cajal]]. The figure illustrates the diversity of neuronal morphologies in the [[auditory cortex]].|链接=Special:FilePath/Cajal_actx_inter.jpg]]
[[Image:Cajal actx inter.jpg|thumb|300px|right|From "Texture of the [[Nervous System]] of Man and the [[Vertebrates]]" by [[Santiago Ramón y Cajal]]. The figure illustrates the diversity of neuronal morphologies in the [[auditory cortex]].|链接=Special:FilePath/Cajal_actx_inter.jpg]]
Early treatments of neural [[Biological network|networks]] can be found in [[Herbert Spencer]]'s ''Principles of Psychology'', 3rd edition (1872), [[Theodor Meynert]]'s ''[[Psychiatry]]'' (1884), [[William James]]' ''Principles of [[Psychology]]'' (1890), and [[Sigmund Freud]]'s Project for a Scientific Psychology (composed 1895).<ref>{{cite web |url=http://psych.stanford.edu/~jlm/papers/ThomasMcCIPCambEncy.pdf |title=Connectionist models of cognition |author1=Michael S. C. Thomas |author2=James L. McClelland |publisher=[[Stanford University]] |access-date=2015-08-31 |archive-url=https://web.archive.org/web/20150906120214/http://psych.stanford.edu/~jlm/papers/ThomasMcCIPCambEncy.pdf |archive-date=2015-09-06 |url-status=dead }}</ref> The first rule of neuronal learning was described by [[Donald Olding Hebb|Hebb]] in 1949, in the [[Hebbian theory]]. Thus, Hebbian pairing of pre-synaptic and post-synaptic activity can substantially alter the dynamic characteristics of the synaptic connection and therefore either facilitate or inhibit [[neurotransmission|signal transmission]]. In 1959, the [[neuroscientist]]s, [[Warren Sturgis McCulloch]] and [[Walter Pitts]] published the first works on the processing of neural networks.<ref>{{citation | title = What the frog's eye tells the frog's brain. |author1=J. Y. Lettvin |author2=H. R. Maturana |author3=W. S. McCulloch |author4=W. H. Pitts | year = 1959 | work = Proc. Inst. Radio Engr. | issue = 47 | pages = 1940–1951 }}</ref> They showed theoretically that networks of artificial neurons could [[implementation|implement]] [[logic]]al, [[arithmetic]], and [[symbol]]ic functions. Simplified [[Biological neuron model|models of biological neurons]] were set up, now usually called [[perceptrons]] or [[artificial neurons]]. These simple models accounted for [[Summation (Neurophysiology)|neural summation]] (i.e., potentials at the post-synaptic membrane will summate in the [[cell body]]). Later models also provided for excitatory and inhibitory synaptic transmission.
Early treatments of neural [[Biological network|networks]] can be found in [[Herbert Spencer]]'s ''Principles of Psychology'', 3rd edition (1872), [[Theodor Meynert]]'s ''[[Psychiatry]]'' (1884), [[William James]]' ''Principles of [[Psychology]]'' (1890), and [[Sigmund Freud]]'s Project for a Scientific Psychology (composed 1895).<ref name=":0">{{cite web |url=http://psych.stanford.edu/~jlm/papers/ThomasMcCIPCambEncy.pdf |title=Connectionist models of cognition |author1=Michael S. C. Thomas |author2=James L. McClelland |publisher=[[Stanford University]] |access-date=2015-08-31 |archive-url=https://web.archive.org/web/20150906120214/http://psych.stanford.edu/~jlm/papers/ThomasMcCIPCambEncy.pdf |archive-date=2015-09-06 |url-status=dead }}</ref> The first rule of neuronal learning was described by [[Donald Olding Hebb|Hebb]] in 1949, in the [[Hebbian theory]]. Thus, Hebbian pairing of pre-synaptic and post-synaptic activity can substantially alter the dynamic characteristics of the synaptic connection and therefore either facilitate or inhibit [[neurotransmission|signal transmission]]. In 1959, the [[neuroscientist]]s, [[Warren Sturgis McCulloch]] and [[Walter Pitts]] published the first works on the processing of neural networks.<ref name=":1">{{citation | title = What the frog's eye tells the frog's brain. |author1=J. Y. Lettvin |author2=H. R. Maturana |author3=W. S. McCulloch |author4=W. H. Pitts | year = 1959 | work = Proc. Inst. Radio Engr. | issue = 47 | pages = 1940–1951 }}</ref> They showed theoretically that networks of artificial neurons could [[implementation|implement]] [[logic]]al, [[arithmetic]], and [[symbol]]ic functions. Simplified [[Biological neuron model|models of biological neurons]] were set up, now usually called [[perceptrons]] or [[artificial neurons]]. These simple models accounted for [[Summation (Neurophysiology)|neural summation]] (i.e., potentials at the post-synaptic membrane will summate in the [[cell body]]). Later models also provided for excitatory and inhibitory synaptic transmission.
Early treatments of neural networks can be found in Herbert Spencer's Principles of Psychology, 3rd edition (1872), Theodor Meynert's Psychiatry (1884), William James' Principles of Psychology (1890), and Sigmund Freud's Project for a Scientific Psychology (composed 1895). The first rule of neuronal learning was described by Hebb in 1949, in the Hebbian theory. Thus, Hebbian pairing of pre-synaptic and post-synaptic activity can substantially alter the dynamic characteristics of the synaptic connection and therefore either facilitate or inhibit signal transmission. In 1959, the neuroscientists, Warren Sturgis McCulloch and Walter Pitts published the first works on the processing of neural networks. They showed theoretically that networks of artificial neurons could implement logical, arithmetic, and symbolic functions. Simplified models of biological neurons were set up, now usually called perceptrons or artificial neurons. These simple models accounted for neural summation (i.e., potentials at the post-synaptic membrane will summate in the cell body). Later models also provided for excitatory and inhibitory synaptic transmission.
Early treatments of neural networks can be found in Herbert Spencer's Principles of Psychology, 3rd edition (1872), Theodor Meynert's Psychiatry (1884), William James' Principles of Psychology (1890), and Sigmund Freud's Project for a Scientific Psychology (composed 1895). The first rule of neuronal learning was described by Hebb in 1949, in the Hebbian theory. Thus, Hebbian pairing of pre-synaptic and post-synaptic activity can substantially alter the dynamic characteristics of the synaptic connection and therefore either facilitate or inhibit signal transmission. In 1959, the neuroscientists, Warren Sturgis McCulloch and Walter Pitts published the first works on the processing of neural networks. They showed theoretically that networks of artificial neurons could implement logical, arithmetic, and symbolic functions. Simplified models of biological neurons were set up, now usually called perceptrons or artificial neurons. These simple models accounted for neural summation (i.e., potentials at the post-synaptic membrane will summate in the cell body). Later models also provided for excitatory and inhibitory synaptic transmission.
= = 早期研究 = = 对神经网络的早期处理见于赫伯特 · 斯宾塞的《心理学原理》第三版(1872)、西奥多 · 梅纳特的《精神病学》(1884)、威廉 · 詹姆斯的《心理学原理》(1890)和西格蒙德 · 弗洛伊德的《科学心理学计划》(1895)。1949年，Hebb 在 Hebbian 理论中提出了神经元学习的第一规则。因此，Hebbian 配对突触前和突触后活动可以充分改变突触连接的动态特性，因此要么促进或抑制信号传递。1959年，神经科学家，沃伦·麦卡洛克和 Walter Pitts 发表了关于神经网络处理的第一部著作。他们从理论上证明了人工神经元网络可以实现逻辑、算术和符号功能。生物神经元的简化模型被建立起来，现在通常被称为感知器或人工神经元。这些简单的模型解释了神经的总和(即突触后膜上的电位将在细胞体中总和)。后来的模型也提供了兴奋性和抑制性突触传递。
= = 早期研究 = = 对神经网络的早期研究见于赫伯特 · 斯宾塞Herbert Spencer的《心理学原理》第三版(1872)、西奥多 · 梅纳特Theodor Meynert的《精神病学》(1884)、威廉 · 詹姆斯William James的《心理学原理》(1890)和西格蒙德 · 弗洛伊德Sigmund Freud的《科学心理学计划》(1895)。<ref name=":0" /> 1949年，赫布Hebb在其理论（即赫布理论Hebbian theory）中提出了神经元学习的第一定律。赫布理论认为，配对中突触前神经元和突触后神经元的活动可以充分改变突触连接的动态特性，即要么促进，要么抑制信号传递signal transmission。1959年，神经科学家，沃伦·麦卡洛克Warren Sturgis和 沃尔特·皮茨Walter Pitts 发表了关于神经网络处理的第一部著作。<ref name=":1" /> 他们从理论上证明了人工神经元网络可以实现逻辑、算术和符号功能。生物神经元的简化模型models of biological neurons由此建立起来，现在通常被称为感知器perceptrons或人工神经元artificial neurons。这些简单的模型解释了神经加成作用neural summation(即突触后膜上的电位将在细胞体中加成)。后来的模型也提供了兴奋性和抑制性突触传递。
==Connections between neurons==
==Connections between neurons==
The connections between neurons in the brain are much more complex than those of the [[artificial neuron]]s used in the [[connectionism|connectionist]] neural computing models of [[artificial neural network]]s. The basic kinds of connections between neurons are [[synapse]]s: both [[chemical synapse|chemical]] and [[electrical synapse]]s.
The connections between neurons in the brain are much more complex than those of the [[artificial neuron]]s used in the [[connectionism|connectionist]] neural computing models of [[artificial neural network]]s. The basic kinds of connections between neurons are [[synapse]]s: both [[chemical synapse|chemical]] and [[electrical synapse]]s.
大脑神经元之间的连接比人工神经元之间的连接要复杂得多，人工神经元常用于人工神经网络中的连接计算模型。大脑神经元之间的基本连接是突触:化学突触和电突触。
大脑神经元之间的连接比人工神经元之间的连接要复杂得多，人工神经元常用于人工神经网络中的连接计算模型。大脑神经元之间的基本连接是突触,包括：化学突触和电突触。
Proposed organization of motor-semantic neural circuits for action language comprehension. Gray dots represent areas of language comprehension, creating a network for comprehending all language. The semantic circuit of the motor system, particularly the motor representation of the legs (yellow dots), is incorporated when leg-related words are comprehended. Adapted from Shebani et al. (2013)
Proposed organization of motor-semantic neural circuits for action language comprehension. Gray dots represent areas of language comprehension, creating a network for comprehending all language. The semantic circuit of the motor system, particularly the motor representation of the legs (yellow dots), is incorporated when leg-related words are comprehended. Adapted from Shebani et al. (2013)
理解动作语言的运动语义神经回路组织。灰点代表语言理解的区域，创造了一个理解所有语言的网络。当理解与腿相关的词语时，运动系统的语义回路，特别是腿的运动表征(黄点)被纳入其中。改编自 Shebani 等人。(2013)
The establishment of synapses enables the connection of neurons into millions of overlapping, and interlinking neural circuits. Presynaptic proteins called [[neurexin]]s are central to this process.<ref name="Sudhof">{{cite journal |last1=Südhof |first1=TC |title=Synaptic Neurexin Complexes: A Molecular Code for the Logic of Neural Circuits. |journal=Cell |date=2 November 2017 |volume=171 |issue=4 |pages=745–769 |doi=10.1016/j.cell.2017.10.024 |pmid=29100073|pmc=5694349 }}</ref>
The establishment of synapses enables the connection of neurons into millions of overlapping, and interlinking neural circuits. Presynaptic proteins called [[neurexin]]s are central to this process.<ref name="Sudhof">{{cite journal |last1=Südhof |first1=TC |title=Synaptic Neurexin Complexes: A Molecular Code for the Logic of Neural Circuits. |journal=Cell |date=2 November 2017 |volume=171 |issue=4 |pages=745–769 |doi=10.1016/j.cell.2017.10.024 |pmid=29100073|pmc=5694349 }}</ref>
突触的建立使得神经元能够连接成千上万个重叠的、相互连接的神经回路。被称为神经蛋白的突触前蛋白在这一过程中起着核心作用。<ref name="Sudhof" />
突触的建立使得神经元能够连接成千上万个重叠的、相互连接的神经回路。被称为神经蛋白的突触前蛋白在这一过程中起着核心作用。
One principle by which neurons work is [[Summation (neurophysiology)|neural summation]] – [[postsynaptic potential|potentials]] at the [[Chemical synapse|postsynaptic membrane]] will sum up in the cell body. If the [[depolarization]] of the neuron at the [[axon hillock]] goes above threshold an action potential will occur that travels down the [[axon]] to the terminal endings to transmit a signal to other neurons. Excitatory and inhibitory synaptic transmission is realized mostly by [[excitatory postsynaptic potentials]] (EPSPs), and [[inhibitory postsynaptic potentials]] (IPSPs).
One principle by which neurons work is [[Summation (neurophysiology)|neural summation]] – [[postsynaptic potential|potentials]] at the [[Chemical synapse|postsynaptic membrane]] will sum up in the cell body. If the [[depolarization]] of the neuron at the [[axon hillock]] goes above threshold an action potential will occur that travels down the [[axon]] to the terminal endings to transmit a signal to other neurons. Excitatory and inhibitory synaptic transmission is realized mostly by [[excitatory postsynaptic potentials]] (EPSPs), and [[inhibitory postsynaptic potentials]] (IPSPs).
神经元工作的其中一个原理是神经加成——突触后膜上的电位将在细胞体中进行加成。如果神经元在轴突丘处的去极化超过阈值，就会发生动作电位，动作电位沿着轴突向下传递到末端，将信号传递给其他神经元。兴奋性和抑制性突触传递主要通过兴奋性突触后电位(EPSPs)和抑制性突触后电位(IPSPs)实现。
On the [[electrophysiology|electrophysiological]] level, there are various phenomena which alter the response characteristics of individual synapses (called [[synaptic plasticity]]) and individual neurons ([[intrinsic plasticity]]). These are often divided into short-term plasticity and long-term plasticity. Long-term synaptic plasticity is often contended to be the most likely [[memory]] substrate. Usually, the term "[[neuroplasticity]]" refers to changes in the brain that are caused by activity or experience.
On the [[electrophysiology|electrophysiological]] level, there are various phenomena which alter the response characteristics of individual synapses (called [[synaptic plasticity]]) and individual neurons ([[intrinsic plasticity]]). These are often divided into short-term plasticity and long-term plasticity. Long-term synaptic plasticity is often contended to be the most likely [[memory]] substrate. Usually, the term "[[neuroplasticity]]" refers to changes in the brain that are caused by activity or experience.
在电生理层面上，存在着改变个体突触(突触可塑性)和个体神经元(内禀可塑性)的反应特征的各种现象。这些可塑性通常分为短期可塑性和长期可塑性。长期突触可塑性通常被认为是最有可能的记忆底物。通常来说，“神经可塑性”指的是由活动或经历引起的大脑变化。
在电生理层面上，存在着改变个体突触(突触可塑性)和个体神经元(内禀可塑性)的反应特征的各种现象。这些可塑性通常分为短期可塑性和长期可塑性。长期突触可塑性通常被认为是最有可能的记忆底物。通常，“神经可塑性”指的是由活动或经历引起的大脑变化。
Connections display temporal and spatial characteristics. Temporal characteristics refers to the continuously modified activity-dependent efficacy of synaptic transmission, called [[spike-timing-dependent plasticity]]. It has been observed in several studies that the synaptic efficacy of this transmission can undergo short-term increase (called [[neural facilitation|facilitation]]) or decrease ([[Neural facilitation#Short-term depression|depression]]) according to the activity of the presynaptic neuron. The induction of long-term changes in synaptic efficacy, by [[long-term potentiation]] (LTP) or [[long-term depression|depression]] (LTD), depends strongly on the relative timing of the onset of the [[excitatory postsynaptic potential]] and the postsynaptic action potential. LTP is induced by a series of action potentials which cause a variety of biochemical responses. Eventually, the reactions cause the expression of new receptors on the cellular membranes of the postsynaptic neurons or increase the efficacy of the existing receptors through [[phosphorylation]].连接表现出时间和空间特征。时间特征是指突触传递的持续修饰的活动依赖的效能，称为峰时依赖的可塑性。多项研究发现，根据突触前神经元的活动，这种传递的突触效能可以经历短期的增加(称为易化)或减少(抑制)。通过长期增强(LTP)或抑制(LTD)诱导突触效能的长期变化，在很大程度上取决于兴奋性突触后电位和突触后动作电位的相对起病时间。LTP是由一系列动作电位引起的各种生化反应引起的。最终这些反应导致突触后神经元细胞膜上表达新的受体或通过磷酸化增加现有受体的效能。
Backpropagating action potentials cannot occur because after an action potential travels down a given segment of the axon, the [[Depolarizing pre-pulse#Hodgkin–Huxley model|m gate]]s on [[voltage-gated sodium channel]]s close, thus blocking any transient opening of the [[Depolarizing pre-pulse#Hodgkin–Huxley model|h gate]] from causing a change in the intracellular sodium ion (Na<sup>+</sup>) concentration, and preventing the generation of an action potential back towards the cell body. In some cells, however, [[neural backpropagation]] does occur through the [[dendrite|dendritic branching]] and may have important effects on synaptic plasticity and computation.反向传播的动作电位是不可能发生的，因为当动作电位沿着轴突的某一特定节段传递之后，电压门控钠通道上的m门关闭，从而阻止h门的任何瞬态打开，以免引起细胞内钠离子浓度的变化。并阻止动作电位的产生回到细胞体内。然而，在某些细胞中，神经反向传播确实通过树突分支发生，并可能对突触可塑性和计算产生重要影响。
A neuron in the brain requires a single signal to a [[neuromuscular junction]] to stimulate contraction of the postsynaptic muscle cell. In the spinal cord, however, at least 75 [[afferent nerve|afferent]] neurons are required to produce firing. This picture is further complicated by variation in time constant between neurons, as some cells can experience their [[Excitatory postsynaptic potential|EPSPs]] over a wider period of time than others.大脑中的某一神经元需要一个单一的信号到神经肌肉连接，刺激突触后肌肉细胞的收缩。然而，在脊髓中，产生放电需要至少75个传入神经元。由于神经元之间的时间常数变化，情形变得更加复杂，因为一些细胞会比其他细胞在更长的一段时间内感受到兴奋性突触后电位（EPSPs）。
While in synapses in the [[development of the human brain|developing brain]] synaptic depression has been particularly widely observed it has been speculated that it changes to facilitation in adult brains.
While in synapses in the [[development of the human brain|developing brain]] synaptic depression has been particularly widely observed it has been speculated that it changes to facilitation in adult brains.
虽然在发育状态的脑突触中，突触抑制已经被广泛观察到，但能够推断的是，它在成人大脑中得到完善。
==Circuitry==
==Circuitry==
[[File:Model of Cerebellar Perceptron.jpg|thumb|Model of a neural circuit in the [[cerebellum]]|链接=Special:FilePath/Model_of_Cerebellar_Perceptron.jpg]]
[[File:Model of Cerebellar Perceptron.jpg|thumb|Model of a neural circuit in the [[cerebellum]]|链接=Special:FilePath/Model_of_Cerebellar_Perceptron.jpg]]
电路
An example of a neural circuit is the [[trisynaptic circuit]] in the [[hippocampus]]. Another is the [[Papez circuit]] linking the [[hypothalamus]] to the [[limbic lobe]]. There are several neural circuits in the [[cortico-basal ganglia-thalamo-cortical loop]]. These circuits carry information between the cortex, [[basal ganglia]], thalamus, and back to the cortex. The largest structure within the basal ganglia, the [[striatum]], is seen as having its own internal microcircuitry.<ref name="Stocco">{{cite journal |last1=Stocco |first1=Andrea |last2=Lebiere |first2=Christian |last3=Anderson |first3=John R. |title=Conditional Routing of Information to the Cortex: A Model of the Basal Ganglia's Role in Cognitive Coordination |journal=Psychological Review |volume=117 |issue=2 |pages=541–74 |year=2010 |pmid=20438237 |doi=10.1037/a0019077 |pmc=3064519}}</ref>
An example of a neural circuit is the [[trisynaptic circuit]] in the [[hippocampus]]. Another is the [[Papez circuit]] linking the [[hypothalamus]] to the [[limbic lobe]]. There are several neural circuits in the [[cortico-basal ganglia-thalamo-cortical loop]]. These circuits carry information between the cortex, [[basal ganglia]], thalamus, and back to the cortex. The largest structure within the basal ganglia, the [[striatum]], is seen as having its own internal microcircuitry.<ref name="Stocco">{{cite journal |last1=Stocco |first1=Andrea |last2=Lebiere |first2=Christian |last3=Anderson |first3=John R. |title=Conditional Routing of Information to the Cortex: A Model of the Basal Ganglia's Role in Cognitive Coordination |journal=Psychological Review |volume=117 |issue=2 |pages=541–74 |year=2010 |pmid=20438237 |doi=10.1037/a0019077 |pmc=3064519}}</ref>