{"title":"[Acquiring new information in a neuronal network: from Hebb's concept to homeostatic plasticity].","authors":"Nicolas Le Roux, Muriel Amar, Philippe Fossier","doi":"10.1051/jbio:2008018","DOIUrl":null,"url":null,"abstract":"<p><p>Synaptic plasticity is the cellular mechanism underlying the phenomena of learning and memory. Much of the research on synaptic plasticity is based on the postulate of Hebb (1949) who proposed that, when a neuron repeatedly takes part in the activation of another neuron, the efficacy of the connections between these neurons is increased. Plasticity has been extensively studied, and often demonstrated through the processes of LTP (Long Term Potentiation) and LTD (Long Term Depression), which represent an increase and a decrease of the efficacy of long-term synaptic transmission. This review summarizes current knowledge concerning the cellular mechanisms of LTP and LTD, whether at the level of excitatory synapses, which have been the most studied, or at the level of inhibitory synapses. However, if we consider neuronal networks rather than the individual synapses, the consequences of synaptic plasticity need to be considered on a large scale to determine if the activity of networks are changed or not. Homeostatic plasticity takes into account the mechanisms which control the efficacy of synaptic transmission for all the synaptic inputs of a neuron. Consequently, this new concept deals with the coordinated activity of excitatory and inhibitory networks afferent to a neuron which maintain a controlled level of excitability during the acquisition of new information related to the potentiation or to the depression of synaptic efficacy. We propose that the protocols of stimulation used to induce plasticity at the synaptic level set up a \"homeostatic potentiation\" or a \"homeostatic depression\" of excitation and inhibition at the level of the neuronal networks. The coordination between excitatory and inhibitory circuits allows the neuronal networks to preserve a level of stable activity, thus avoiding episodes of hyper- or hypo-activity during the learning and memory phases.</p>","PeriodicalId":80018,"journal":{"name":"Journal de la Societe de biologie","volume":"202 2","pages":"143-60"},"PeriodicalIF":0.0000,"publicationDate":"2008-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1051/jbio:2008018","citationCount":"7","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal de la Societe de biologie","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1051/jbio:2008018","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2008/6/13 0:00:00","PubModel":"Epub","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 7
Abstract
Synaptic plasticity is the cellular mechanism underlying the phenomena of learning and memory. Much of the research on synaptic plasticity is based on the postulate of Hebb (1949) who proposed that, when a neuron repeatedly takes part in the activation of another neuron, the efficacy of the connections between these neurons is increased. Plasticity has been extensively studied, and often demonstrated through the processes of LTP (Long Term Potentiation) and LTD (Long Term Depression), which represent an increase and a decrease of the efficacy of long-term synaptic transmission. This review summarizes current knowledge concerning the cellular mechanisms of LTP and LTD, whether at the level of excitatory synapses, which have been the most studied, or at the level of inhibitory synapses. However, if we consider neuronal networks rather than the individual synapses, the consequences of synaptic plasticity need to be considered on a large scale to determine if the activity of networks are changed or not. Homeostatic plasticity takes into account the mechanisms which control the efficacy of synaptic transmission for all the synaptic inputs of a neuron. Consequently, this new concept deals with the coordinated activity of excitatory and inhibitory networks afferent to a neuron which maintain a controlled level of excitability during the acquisition of new information related to the potentiation or to the depression of synaptic efficacy. We propose that the protocols of stimulation used to induce plasticity at the synaptic level set up a "homeostatic potentiation" or a "homeostatic depression" of excitation and inhibition at the level of the neuronal networks. The coordination between excitatory and inhibitory circuits allows the neuronal networks to preserve a level of stable activity, thus avoiding episodes of hyper- or hypo-activity during the learning and memory phases.
突触可塑性是学习和记忆现象背后的细胞机制。许多关于突触可塑性的研究都是基于Hebb(1949)的假设,他提出,当一个神经元反复参与另一个神经元的激活时,这些神经元之间的连接的效力就会增加。可塑性已被广泛研究,并经常通过LTP (Long Term Potentiation)和LTD (Long Term Depression)的过程来证明,这两个过程代表了长期突触传递功效的增加和减少。本文综述了目前关于LTP和LTD的细胞机制,无论是在研究最多的兴奋性突触水平,还是在抑制性突触水平。然而,如果我们考虑神经元网络而不是单个突触,则需要大规模地考虑突触可塑性的后果,以确定网络的活动是否发生了变化。稳态可塑性考虑了控制神经元所有突触输入的突触传递效能的机制。因此,这一新概念涉及传入神经元的兴奋性和抑制性网络的协调活动,这些网络在获取与突触效能增强或抑制相关的新信息期间保持受控的兴奋性水平。我们提出,用于诱导突触水平可塑性的刺激方案在神经元网络水平上建立了兴奋和抑制的“稳态增强”或“稳态抑制”。兴奋性回路和抑制性回路之间的协调使神经元网络保持稳定的活动水平,从而避免在学习和记忆阶段出现过度活动或缺乏活动的情况。