EVIDENCE FOR PRESYNAPTIC N-METHYL-D-ASPARTATE AUTORECEPTORS IN THE SPINAL-CORD DORSAL HORN
EVIDENCE FOR PRESYNAPTIC N-METHYL-D-ASPARTATE AUTORECEPTORS IN THE SPINAL-CORD DORSAL HORN
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DOI：
10.1073/pnas.91.18.8383
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发表时间：
1994-08-30
影响因子：
11.1
通讯作者：
BASBAUM, AI
中科院分区：
文献类型：
--
作者：
LIU, H;WANG, H;BASBAUM, AI
n -甲基- d -天冬氨酸（NMDA）受体与中枢神经系统的多种可塑性变化有关。我们使用电子显微镜免疫细胞化学方法，针对NMDA受体的基本功能亚基NMDAR1的C端附近的一个选择性剪接外显子的抗体，研究了NMDA受体在脊髓和海马CA1区域的分布，这两个区域已经证明了NMDA介导的长期可塑性。在CA1中，我们发现NMDA受体只在突触后结构上表达。相比之下，在脊髓中，我们发现在大约三分之一的标记突触中，受体位于突触前末端，紧邻活跃区的囊泡释放位点。结合包埋后免疫细胞化学，我们还发现，bb0 - 70%的NMDA受体免疫反应端谷氨酸阳性，这表明突触前NMDA受体是一个自身受体。神经结扎研究表明，受体分别通过背根神经和坐骨神经转运到脊髓和周围神经。这些数据表明，NMDA自身受体位于初级传入纤维的末端，它可以通过增加初级传入末端的神经递质释放来促进输入信息向脊髓的传递。
The N-methyl-D-aspartate (NMDA) receptor has been implicated in a variety of systems that undergo plastic changes in the central nervous system. We used electron microscopic immunocytochemistry with an antibody directed against an alternatively spliced exon near the C terminus of NMDAR1, the essential functional subunit of the NMDA receptor, to study the distribution of the NMDA receptor in the spinal cord and CA1 region of the hippocampus, two regions where NMDA-mediated long-term plasticity has been demonstrated, In CA1, we found that the NMDA receptor is exclusively expressed on postsynaptic structures. By contrast, in the spinal cord we found that in about one-third of labeled synapses, the receptor is located in the presynaptic terminal, immediately adjacent to the vesicle release site at the active zone. Using combined postembedding immunocytochemistry, we also showed that >70% of the NMDA receptor immunoreactive terminals are glutamate positive, which suggests that the presynaptic NMDA receptor is an autoreceptor. Nerve ligation studies demonstrated that the receptor is transported in dorsal roots and sciatic nerve to the spinal cord and periphery, respectively. These data indicate that an NMDA autoreceptor is located in terminals of primary afferent fibers, where it could facilitate the transmission of inputs to the spinal cord by increasing the release of neurotransmitter from the primary afferent terminal.