Sadeghi Soroush G, Pyott Sonja J, Yu Zhou, Glowatzki Elisabeth
Departments of Otolaryngology, Head and Neck Surgery, and.
Department of Otorhinolaryngology, Head and Neck Surgery, University Medical Center Groningen, University of Groningen, Groningen 9700 RB, The Netherlands.
J Neurosci. 2014 Oct 29;34(44):14536-50. doi: 10.1523/JNEUROSCI.0369-13.2014.
In the vestibular periphery a unique postsynaptic terminal, the calyx, completely covers the basolateral walls of type I hair cells and receives input from multiple ribbon synapses. To date, the functional role of this specialized synapse remains elusive. There is limited data supporting glutamatergic transmission, K(+) or H(+) accumulation in the synaptic cleft as mechanisms of transmission. Here the role of glutamatergic transmission at the calyx synapse is investigated. Whole-cell patch-clamp recordings from calyx endings were performed in an in vitro whole-tissue preparation of the rat vestibular crista, the sensory organ of the semicircular canals that sense head rotation. AMPA-mediated EPSCs showed an unusually wide range of decay time constants, from <5 to >500 ms. Decay time constants of EPSCs increased (or decreased) in the presence of a glutamate transporter blocker (or a competitive glutamate receptor blocker), suggesting a role for glutamate accumulation and spillover in synaptic transmission. Glutamate accumulation caused slow depolarizations of the postsynaptic membrane potentials, and thereby substantially increased calyx firing rates. Finally, antibody labelings showed that a high percentage of presynaptic ribbon release sites and postsynaptic glutamate receptors were not juxtaposed, favoring a role for spillover. These findings suggest a prominent role for glutamate spillover in integration of inputs and synaptic transmission in the vestibular periphery. We propose that similar to other brain areas, such as the cerebellum and hippocampus, glutamate spillover may play a role in gain control of calyx afferents and contribute to their high-pass properties.
在前庭外周，一种独特的突触后终末——花萼，完全覆盖了I型毛细胞的基底外侧壁，并接收来自多个带状突触的输入。迄今为止，这种特殊突触的功能作用仍不清楚。支持谷氨酸能传递、突触间隙中钾离子或氢离子积累作为传递机制的数据有限。本文研究了花萼突触处谷氨酸能传递的作用。在大鼠前庭嵴的体外全组织标本中进行了花萼终末的全细胞膜片钳记录，前庭嵴是感受头部旋转的半规管的感觉器官。AMPA介导的兴奋性突触后电流（EPSCs）显示出异常广泛的衰减时间常数范围，从<5毫秒到>500毫秒。在谷氨酸转运体阻断剂（或竞争性谷氨酸受体阻断剂）存在的情况下，EPSCs的衰减时间常数增加（或减少），表明谷氨酸积累和溢出在突触传递中起作用。谷氨酸积累导致突触后膜电位缓慢去极化，从而显著提高花萼放电率。最后，抗体标记显示，很大比例的突触前带状释放位点和突触后谷氨酸受体并未并列，这支持了溢出的作用。这些发现表明谷氨酸溢出在前庭外周输入整合和突触传递中起重要作用。我们提出，与其他脑区，如小脑和海马体类似，谷氨酸溢出可能在花萼传入神经的增益控制中起作用，并有助于其高通特性。
