Department of Neurosciences, Centre for Interdisciplinary Research on Brain and Learning, Research Group on the Central Nervous System, Université de Montréal, Montreal, QC, Canada.
Front Neural Circuits. 2021 Jun 2;15:687558. doi: 10.3389/fncir.2021.687558. eCollection 2021.
A distinctive feature of the hippocampal structure is the diversity of inhibitory interneurons. These complex inhibitory interconnections largely contribute to the tight modulation of hippocampal circuitry, as well as to the formation and coordination of neuronal assemblies underlying learning and memory. Inhibitory interneurons provide more than a simple transitory inhibition of hippocampal principal cells (PCs). The synaptic plasticity of inhibitory neurons provides long-lasting changes in the hippocampal network and is a key component of memory formation. The dendrite targeting interneurons expressing the peptide somatostatin (SOM) are particularly interesting in this regard because they display unique long-lasting synaptic changes leading to metaplastic regulation of hippocampal networks. In this article, we examine the actions of the neuropeptide SOM on hippocampal cells, synaptic plasticity, learning, and memory. We address the different subtypes of hippocampal SOM interneurons. We describe the long-term synaptic plasticity that takes place at the excitatory synapses of SOM interneurons, its singular induction and expression mechanisms, as well as the consequences of these changes on the hippocampal network, learning, and memory. We also review evidence that astrocytes provide cell-specific dynamic regulation of inhibition of PC dendrites by SOM interneurons. Finally, we cover how, in mouse models of Alzheimer's disease (AD), dysfunction of plasticity of SOM interneuron excitatory synapses may also contribute to cognitive impairments in brain disorders.
海马体结构的一个显著特点是抑制性中间神经元的多样性。这些复杂的抑制性相互连接在很大程度上有助于海马回路的紧密调节,以及学习和记忆所基于的神经元集合的形成和协调。抑制性神经元提供的不仅仅是对海马体主要细胞(PC)的简单瞬时抑制。抑制性神经元的突触可塑性为海马体网络提供了持久的变化,是记忆形成的关键组成部分。在这方面,表达肽生长抑素(SOM)的树突靶向中间神经元特别有趣,因为它们显示出独特的持久突触变化,导致海马体网络的超可塑性调节。在本文中,我们研究了神经肽 SOM 对海马体细胞、突触可塑性、学习和记忆的作用。我们研究了海马体 SOM 中间神经元的不同亚型。我们描述了 SOM 中间神经元兴奋性突触发生的长期突触可塑性,及其独特的诱导和表达机制,以及这些变化对海马体网络、学习和记忆的影响。我们还回顾了证据表明,星形胶质细胞为 SOM 中间神经元对 PC 树突的抑制提供了特定于细胞的动态调节。最后,我们讨论了在阿尔茨海默病(AD)的小鼠模型中,SOM 中间神经元兴奋性突触可塑性的功能障碍也可能导致大脑疾病中的认知障碍。