Grassi S, Pettorossi V E
Dipartimento di Medicina Interna, Sezione di Fisiologia Umana, Università di Perugia, I-06100, Perugia, Italy.
Prog Neurobiol. 2001 Aug;64(6):527-53. doi: 10.1016/s0301-0082(00)00070-8.
The analysis of cellular-molecular events mediating synaptic plasticity within vestibular nuclei is an attempt to explain the mechanisms underlying vestibular plasticity phenomena. The present review is meant to illustrate the main results, obtained in vitro, on the mechanisms underlying long-term changes in synaptic strength within the medial vestibular nuclei. The synaptic plasticity phenomena taking place at the level of vestibular nuclei could be useful for adapting and consolidating the efficacy of vestibular neuron responsiveness to environmental requirements, as during visuo-vestibular recalibration and vestibular compensation. Following a general introduction on the most salient features of vestibular compensation and visuo-vestibular adaptation, which are two plastic events involving neuronal circuitry within the medial vestibular nuclei, the second and third sections describe the results from rat brainstem slice studies, demonstrating the possibility to induce long-term potentiation and depression in the medial vestibular nuclei, following high frequency stimulation of the primary vestibular afferents. In particular the mechanisms sustaining the induction and expression of vestibular long-term potentiation and depression, such as the role of various glutamate receptors and retrograde messengers have been described. The relevant role of the interaction between the platelet-activating factor, acting as a retrograde messenger, and the presynaptic metabotropic glutamate receptors, in determining the full expression of vestibular long-term potentiation is also underlined. In addition, the mechanisms involved in vestibular long-term potentiation have been compared with those leading to long-term potentiation in the hippocampus to emphasize the most significant differences emerging from vestibular studies. The fourth part, describes recent results demonstrating the essential role of nitric oxide, another retrograde messenger, in the induction of vestibular potentiation. Finally the fifth part suggests the possible functional significance of different action times of the two retrograde messengers and metabotropic glutamate receptors, which are involved in mediating the presynaptic mechanism sustaining vestibular long-term potentiation.
对介导前庭核内突触可塑性的细胞分子事件进行分析，旨在解释前庭可塑性现象背后的机制。本综述旨在阐述在体外获得的关于内侧前庭核内突触强度长期变化机制的主要研究结果。发生在前庭核水平的突触可塑性现象，可能有助于适应和巩固前庭神经元对环境需求的反应能力，比如在视前庭重新校准和前庭代偿过程中。在对前庭代偿和视前庭适应这两个涉及内侧前庭核内神经回路的可塑性事件的最显著特征进行一般性介绍之后，第二和第三部分描述了大鼠脑干切片研究的结果，这些结果表明在高频刺激初级前庭传入神经后，内侧前庭核内有可能诱导出长时程增强和长时程抑制。特别描述了维持前庭长时程增强和长时程抑制的诱导和表达的机制，例如各种谷氨酸受体和逆行信使的作用。还强调了作为逆行信使的血小板活化因子与突触前代谢型谷氨酸受体之间的相互作用在决定前庭长时程增强的充分表达中的重要作用。此外，还将前庭长时程增强所涉及的机制与导致海马体中长时程增强的机制进行了比较，以强调前庭研究中出现的最显著差异。第四部分描述了最近的研究结果，这些结果表明另一种逆行信使一氧化氮在前庭增强的诱导中起着至关重要作用。最后，第五部分提出了两种逆行信使和代谢型谷氨酸受体不同作用时间的可能功能意义，它们参与介导维持前庭长时程增强的突触前机制。
