Bannon Nicholas M, Chistiakova Marina, Volgushev Maxim
Department of Psychological Sciences, University of Connecticut, Storrs, CT, United States.
Front Cell Neurosci. 2020 Sep 4;14:204. doi: 10.3389/fncel.2020.00204. eCollection 2020.
Inhibitory neurons play a fundamental role in the normal operation of neuronal networks. Diverse types of inhibitory neurons serve vital functions in cortical networks, such as balancing excitation and taming excessive activity, organizing neuronal activity in spatial and temporal patterns, and shaping response selectivity. Serving these, and a multitude of other functions effectively requires fine-tuning of inhibition, mediated by synaptic plasticity. Plasticity of inhibitory systems can be mediated by changes at inhibitory synapses and/or by changes at excitatory synapses at inhibitory neurons. In this review, we consider that latter locus: plasticity at excitatory synapses to inhibitory neurons. Despite the fact that plasticity of excitatory synaptic transmission to interneurons has been studied in much less detail than in pyramids and other excitatory cells, an abundance of forms and mechanisms of plasticity have been observed in interneurons. Specific requirements and rules for induction, while exhibiting a broad diversity, could correlate with distinct sources of excitatory inputs and distinct types of inhibitory neurons. One common requirement for the induction of plasticity is the rise of intracellular calcium, which could be mediated by a variety of ligand-gated, voltage-dependent, and intrinsic mechanisms. The majority of the investigated forms of plasticity can be classified as Hebbian-type associative plasticity. Hebbian-type learning rules mediate adaptive changes of synaptic transmission. However, these rules also introduce intrinsic positive feedback on synaptic weight changes, making plastic synapses and learning networks prone to runaway dynamics. Because real inhibitory neurons do not express runaway dynamics, additional plasticity mechanisms that counteract imbalances introduced by Hebbian-type rules must exist. We argue that weight-dependent heterosynaptic plasticity has a number of characteristics that make it an ideal candidate mechanism to achieve homeostatic regulation of synaptic weight changes at excitatory synapses to inhibitory neurons.
抑制性神经元在神经网络的正常运作中发挥着基础性作用。多种类型的抑制性神经元在皮质网络中发挥着至关重要的功能，比如平衡兴奋和抑制过度活动、以空间和时间模式组织神经元活动以及塑造反应选择性。要有效地发挥这些以及众多其他功能，需要通过突触可塑性对抑制进行精细调节。抑制系统的可塑性可由抑制性突触的变化和/或抑制性神经元上兴奋性突触的变化介导。在本综述中，我们关注后一个位点：抑制性神经元兴奋性突触的可塑性。尽管与锥体神经元和其他兴奋性细胞相比，对中间神经元兴奋性突触传递可塑性的研究要少得多，但在中间神经元中已观察到丰富多样的可塑性形式和机制。可塑性诱导的特定要求和规则虽然具有广泛的多样性，但可能与兴奋性输入的不同来源以及不同类型的抑制性神经元相关。可塑性诱导的一个共同要求是细胞内钙的升高，这可由多种配体门控、电压依赖性和内在机制介导。大多数已研究的可塑性形式可归类为赫布型联合可塑性。赫布型学习规则介导突触传递的适应性变化。然而，这些规则也会在突触权重变化上引入内在的正反馈，使可塑性突触和学习网络易于出现失控动力学。由于实际的抑制性神经元不会表现出失控动力学，因此必然存在抵消赫布型规则引入的失衡的额外可塑性机制。我们认为，权重依赖性异突触可塑性具有许多特性，使其成为实现对抑制性神经元兴奋性突触突触权重变化进行稳态调节的理想候选机制。
