突触连接定义了在特定功能任务期间参与相关活动的神经元组。这些神经元的协同群形成集合,参与的作战单位,例如,感官知觉,运动协调和记忆(然后称为全写)。传统上,集合形成被认为是通过长期增强(LTP)作为可塑性机制来加强突触连接而发生的。这种突触记忆理论源于Hebb制定的学习规则,与许多实验观察结果一致。这里,我们提议,作为替代,神经元的内在兴奋性和可塑性构成了第二个,非突触机制,这对合奏的初始形成可能很重要。的确,在行为学习之后,在多个大脑区域广泛观察到增强的神经兴奋性。在皮质结构和杏仁核中,兴奋性变化通常被报告为短暂的,即使它们可以持续几十分钟到几天。也许正是出于这个原因,它们传统上被认为是调制的,仅通过促进LTP诱导来支持集合形成,没有进一步参与记忆功能(记忆分配假设)。我们在这里建议-基于两条线的证据-除了调节LTP分配,增强的兴奋性在学习中起着更根本的作用。首先,增强的兴奋性构成了活跃合奏的标志,由于它,在没有突触可塑性的情况下,亚阈值突触连接变为超阈值(冰山模型)。第二,增强的兴奋性促进树突状电位向体细胞的传播,并允许增强EPSP振幅(LTP)与尖峰输出的耦合(从而增强整体参与)。这个许可门模型描述了永久增加兴奋性的需求,这似乎与它作为一种短暂机制的传统考虑相矛盾。我们建议通过低阈值的内在可塑性诱导,可以对兴奋性进行更长的修改。这表明兴奋性可能会在短时间间隔内进行开/关调节。与此一致,在小脑浦肯野细胞中,兴奋性持续几天到几周,这表明在某些电路中,该现象的持续时间首先不是限制因素。在我们的模型中,突触可塑性定义了神经元通过嵌入的连接网络接收的信息内容。然而,细胞自主兴奋性的可塑性可以动态调节单个神经元的集合参与以及集合的整体活动状态。
Synaptic connectivity defines groups of neurons that engage in correlated activity during specific functional tasks. These co-active groups of neurons form ensembles, the operational units involved in, for example, sensory perception, motor coordination and memory (then called an engram). Traditionally, ensemble formation has been thought to occur via strengthening of synaptic connections via long-term potentiation (LTP) as a plasticity mechanism. This synaptic theory of memory arises from the learning rules formulated by Hebb and is consistent with many experimental observations. Here, we propose, as an alternative, that the intrinsic excitability of neurons and its plasticity constitute a second, non-synaptic mechanism that could be important for the initial formation of ensembles. Indeed, enhanced neural excitability is widely observed in multiple brain areas subsequent to behavioral learning. In cortical structures and the amygdala, excitability changes are often reported as transient, even though they can last tens of minutes to a few days. Perhaps it is for this reason that they have been traditionally considered as modulatory, merely supporting ensemble formation by facilitating LTP induction, without further involvement in memory function (memory allocation hypothesis). We here suggest-based on two lines of evidence-that beyond modulating LTP allocation, enhanced excitability plays a more fundamental role in learning. First, enhanced excitability constitutes a signature of active ensembles and, due to it, subthreshold synaptic connections become suprathreshold in the absence of synaptic plasticity (iceberg model). Second, enhanced excitability promotes the propagation of dendritic potentials toward the soma and allows for enhanced coupling of EPSP amplitude (LTP) to the spike output (and thus ensemble participation). This permissive gate model describes a need for permanently increased excitability, which seems at odds with its traditional consideration as a short-lived mechanism. We propose that longer modifications in excitability are made possible by a low threshold for intrinsic plasticity induction, suggesting that excitability might be on/off-modulated at short intervals. Consistent with this, in cerebellar Purkinje cells, excitability lasts days to weeks, which shows that in some circuits the duration of the phenomenon is not a limiting factor in the first place. In our model, synaptic plasticity defines the information content received by neurons through the connectivity network that they are embedded in. However, the plasticity of cell-autonomous excitability could dynamically regulate the ensemble participation of individual neurons as well as the overall activity state of an ensemble.