大脑的可塑性是指大脑的结构和功能都由制造商塑造以适应各种需求的方式来塑造大脑的结构和功能。当我们学习和应对伤害时,在神经系统的发展过程中发生脑可塑性。这种可塑性不仅由神经元(大脑的原理信息处理细胞)表现出来,而且还由包括神经胶质细胞和构成大脑血管网络的细胞在内的支持元素表现出来。
Developmental Versus Adulthood Plasticity
Greenough及其同事(1987年)提出,发展中的和成人神经系统的可塑性在形式上相似,但表达方式不同。他们在开发过程中指出,神经元和突触(神经元之间的连接)后来被经验所修剪。他们建议这种类型的可塑性可以被描述为“经验丰富的人”。也就是说,我们的基因已经对神经系统进行了编程,以在特定时间点(例如,大开眼界)在预期物种常见的经验中表现出旺盛的连接增长。例如,所有人类都可以期望出生到一个视觉上富裕的世界中。因此,我们的基因直接创建大脑的视觉中心,其中有能够处理视觉信息(形状,颜色,运动)的神经元。但是,我们的基因不知道我们将遇到哪种类型的视觉信息,因此将系统编程以说明所有可能性。一旦我们睁开眼睛并开始检查视觉世界,大脑就会修剪那些在我们特定环境中不需要的额外联系和神经元。如果我们出生于缺乏水平线的环境中,我们的神经系统将保留那些神经元和突触,这些神经元和突触处理垂直线,颜色和运动,但会去除负责编码水平线的神经元和突触。相比之下,成年后,“依赖经验”的可塑性是针对新的情况而发生的。 Plasticity in this case is manifested by smaller bursts of new synaptic growth within localized regions of the brain that is then pruned by the continuing experience. For example, an adult that learns to play the piano would add new synapses in motor regions of the brain that control finger movement. As the adult becomes more practiced, some of these new synapses would be pruned away, leaving only those that provide for coordinated movement.
经验诱导的神经元可塑性
Studies of brain plasticity indicate that characteristic changes include alterations of neuronal number, cell body (soma) size, dendritic extent and morphology, composition of the cellular membrane, and connectivity with other neurons (synapses). For example, several reports indicate that animals engaging in prolonged exercise exhibit increased neuronal proliferation (neurogenesis) and survival in the hippocampus. Other studies have consistently reported that the rearing of animals in an enriched environment produces substantial increases in brain volume (around 25%). This increase is distributed across areas of the brain (motor cortex, visual cortex, cerebellum) but is largest in visual cortex. Subsequent studies have indicated that this volume increase is accompanied by increases in the size of dendritic trees, increased numbers of synapses per neuron, and changes in the shape of presynaptic and postsynaptic elements.
A Model Of Brain Plasticity
许多神经科学家已经假设经验如何促进大脑可塑性并改变神经元输出。最有影响力的科学家之一是唐纳德·奥·赫布(Donald O.Bliss和Lomo在1970年代初发现了这一现象的生理证明,并被称为“长期增强”。
长期增强(LTP)是高频刺激爆发后细胞的兴奋性的长期增加。许多神经科学家认为,LTP是开发和对学习过程中发生的电生理和结构变化的良好模型。它最常在海马中进行研究,这是一种大脑结构,被认为是在学习和记忆中发挥作用的。在海马中,当传入途径的刺激导致神经递质谷氨酸释放时,就会发生LTP。谷氨酸与突触后神经元上的受体(蛋白质对接位点)结合。神经递质的结合打开离子通道,然后允许钠进入细胞。钠离子进入细胞的运动会导致神经元的膜电压变化。如果足够大的话,膜中的这种电压变化会促进第二种神经递质受体被称为NMDA受体的镁的离子阻断。去除镁阻塞后,神经递质谷氨酸可以自由结合NMDA受体,并以钙的开放离子通道结合。增加的细胞内钙会触发一系列事件,包括改变现有细胞蛋白的酶的激活,并触发新蛋白的合成。 Collectively, these events promote increases in neurotransmitter release from the presynaptic neuron as well as postsynaptic changes in the composition of the membrane and dendrites (e.g., exposure and/or creation of more glutamate receptors, the formation of more synapses, or larger synapses). The net effect of these events is a relatively permanent change in the excitability of the neuron. For example, hippocampal LTP induction is associated with a 100% to 200% increase in the size of extracellularly recorded field potentials in as little as 10 to 15 minutes after the application of the tetanus. This increase in field potential amplitude is long lasting.
Vascular Plasticity Of The Brain
大脑可塑性形态学研究的主要重点集中在突触连接质量或数量的变化上。然而,最近的研究观察到,现有毛细血管或血管生成的新血管的生长是响应涉及广泛体育锻炼的行为操纵而发生的。在这些研究中,对大鼠在跑步轮上进行了30天的训练,并解剖了小脑皮层和运动皮层,并确定毛细血管的密度。这些研究发现,与无活性对照相比,运动大鼠的毛细血管密度约为25%。鉴于早期的报道表明,大鼠的皮质血管生成是由成年哺乳动物大脑中的血管生成的证明尤其重要的
21天大。最新的关于放置在复杂环境中的成年大鼠脑皮质血管生成的报道,接受运动或暴露于低碱性缺氧的情况表明,皮质血管生成的能力虽然随着年龄的增长而减少,但至少持续到大鼠生命的第二年。
受伤后的可塑性
损坏大脑后的塑料变化是强大的。大多数CNS神经元试图再生但通常失败。这种失败的部分原因是神经胶质细胞的作用,该作用显示出对脑损伤的塑性反应。例如,在损伤部位,星形胶质细胞,少突胶质细胞和小胶质细胞迅速增殖。星形胶质细胞和少突胶质细胞都释放抑制轴突再生的蛋白聚糖。活化的小胶质细胞提供了一个宽松的环境。他们释放神经营养蛋白。但是,他们的作用无法克服其他细胞提供的抑制作用。
Many neuroscientists draw a parallel between mechanisms of recovery of function following injury and the plasticity associated with learning and memory. For example, a now classic study by Raisman and Field examined the synaptic contacts onto septal neurons. Septal neurons receive afferent information from the fimbria and medial forebrain bundle. These inputs make approximately equal numbers of synaptic contacts onto septal neurons. In their experiment, Raisman and Field lesioned one or the other of the inputs and counted synapses over a period of time. They found that, within 1 or 2 days of the lesion, synaptic contacts onto the septal neurons decreased by about 50% (commensurate with axon degeneration of the cut pathway). But, over the course of several weeks, the synaptic numbers once again approached normal levels. They determined that the new synaptic contacts were coming from the pathway that was not lesioned. In other words, neurons from the intact path were sprouting axonal branches and making additional synaptic contact with the septal neurons. This process is known ascollateral sprouting。这是一项具有里程碑意义的研究,因为这是第一个证明大脑的非损害区域试图弥补损害的方法。
More recently, this idea of compensation has been examined in the somatosensory cerebral cortex. Michael Merzenich and his group have carefully mapped the topography of the hand onto the somatosensory cortex. In one study, they either lesioned a sensory nerve of one of the fingers or removed the finger and recorded the neural activity from the cortex. They expected to see diminished activity in the region of the cortex that had just lost its input from the finger. Instead, they found that the cortex displayed neural responses to stimulation of parts of the hand adjacent to the damaged nerve or removed finger. This observation is consistent with the idea that adjacent portions of the body make synapses in their own area of the cortex as well as adjacent portions, but that the synapses that are formed in adjacent areas are repressed. When the finger information is removed, a short-term plastic change occurs that removes the repression associated with synapses from the adjacent parts of the cortex. In other words, the motor maps for adjacent portions of the body have expanded or taken over the functions of the denervated cortex. Further, Merzenich’s group reports that over the course of a month or two, axons in adjacent regions of the cortex sprout collaterals that will more fully innervate the denervated region. The consequence of this is that adjacent body parts become more sensitive to stimulation.
随后的研究表明,与附带发芽有关的可塑性遵循HEBBIAN规则。也就是说,突触形成和增强取决于前突触后神经元的相关活性。此外,该机制似乎取决于NMDA受体和钙流入的激活。
参考:
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