GluN2A- and GluN2B-immunoreactive type I cells attached to vesicular glutamate transporter 2-immunoreactive afferent nerve terminals of the rat carotid body
GluN2A- and GluN2B-immunoreactive type I cells attached to vesicular glutamate transporter 2-immunoreactive afferent nerve terminals of the rat carotid body
复制标题
DOI：
10.1007/s00418-021-01970-5
复制
发表时间：
2021-02
影响因子：
2.3
通讯作者：
Takuya Yokoyama;Yoshio Yamamoto;Masato Hirakawa;T. Saino
中科院分区：
文献类型：
--
作者：
Takuya Yokoyama;Yoshio Yamamoto;Masato Hirakawa;T. Saino
我们之前报道了附着在颈动脉体（CB）I型化学感受器细胞上的传入神经末梢中囊泡谷氨酸转运蛋白2（VGLUT2）的免疫反应性，表明谷氨酸从传入神经末梢释放以刺激这些细胞。在本研究中，我们检查了大鼠CB中N-甲基-D-天冬氨酸（NMDA）受体的谷氨酸结合亚基、GluN2A和GluN2B的免疫反应性，以及这些亚基与VGLUT2之间的免疫组织化学关系。 GluN2A 和 GluN2B 的免疫反应性在酪氨酸羟化酶免疫反应性 I 型细胞亚群中占主导地位，而不是在多巴胺 β-羟化酶免疫反应性细胞亚群中占主导地位。点状 VGLUT2 免疫反应产物附着在 GluN2A 和 GluN2B 免疫反应 I 型细胞上。巴松管免疫反应产物位于 VGLUT2 免疫反应性斑点和 GluN2A 和 GluN2B 免疫反应性 I 型细胞之间。这些结果表明传入神经末梢通过胞吐作用释放谷氨酸，通过含有 GluN2A 和 GluN2B 亚基的 NMDA 受体调节 I 型细胞亚群的化学感应活性。
We previously reported the immunoreactivity for the vesicular glutamate transporter 2 (VGLUT2) in afferent nerve terminals attached to chemoreceptor type I cells of the carotid body (CB), suggesting that glutamate is released from afferent terminals to stimulate these cells. In the present study, we examined the immunoreactivity for the glutamate-binding subunits ofN-methyl-D-aspartate (NMDA) receptors, GluN2A and GluN2B in the rat CB, and the immunohistochemical relationships between these subunits and VGLUT2. Immunoreactivities for GluN2A and GluN2B were predominant in a subpopulation of tyrosine hydroxylase-immunoreactive type I cells rather than those of dopamine beta-hydroxylase-immunoreactive cells. Punctate VGLUT2-immunoreactive products were attached to GluN2A- and GluN2B-immunoreactive type I cells. Bassoon-immunoreactive products were localized between VGLUT2-immunoreactive puncta and type I cells immunoreactive for GluN2A and GluN2B. These results suggest that afferent nerve terminals release glutamate by exocytosis to modulate chemosensory activity of a subpopulation of type I cells via GluN2A- and GluN2B subunits-containing NMDA receptors.