Dynorphin-immunoreactive terminals in the rat nucleus accumbens: cellular sites for modulation of target neurons and interactions with catecholamine afferents.
Dynorphin-immunoreactive terminals in the rat nucleus accumbens: cellular sites for modulation of target neurons and interactions with catecholamine afferents.
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大鼠伏隔核中的强啡肽免疫反应末端：调节靶神经元以及与儿茶酚胺传入神经相互作用的细胞位点。
DOI：
10.1002/cne.903410102
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发表时间：
1994
期刊：
影响因子：
--
通讯作者：
Pickel,VM
中科院分区：
文献类型：
--
作者：
VanBockstaele,EJ;Sesack,SR;Pickel,VM
强啡肽通过潜在地涉及直接激活靶神经元或从丘脑核中的传入神经释放儿茶酚胺的机制促进条件性位置厌恶并减少自发活动。我们研究了这些行动的超微结构基板结合免疫过氧化物酶标记强啡肽1-8和免疫金银标记的儿茶酚胺合成酶，酪氨酸羟化酶（TH）。这两种标记物在大鼠延髓核的单个冠状切片中同时可视化。通过光学显微镜，强啡肽免疫反应被看作是补丁的免疫反应性静脉曲张在所有的吻尾侧水平的延髓核。通过电子显微镜鉴定的强啡肽免疫反应性终末的横截面直径范围为0.2 - 1.5 μm，包含许多小的（30-40 nm）透明囊泡以及一个或多个大的（80-100 nm）致密核心囊泡。在单张切片中定量检查的强啡肽免疫反应终末中，74%（173/370）显示对称的突触连接，主要是大的未标记树突。在形成可识别突触的强啡肽免疫反应性终末中，约30%接触了一个以上的树突靶点。此外，单个树突经常从多个强啡肽标记的终端接收会聚输入。不考虑它们的树突状联系，强啡肽免疫反应终末也经常与其他轴突和终末紧密并列;这些包括未标记（41%），TH标记（10%）或强啡肽标记轴突（14%）。与强啡肽免疫反应终末相反，TH标记终末主要形成具有小树突和棘的对称突触，或者在分析的截面上缺乏可识别的特化。在某些情况下，单个树突与强啡肽和TH免疫反应终末突触后。我们得出结论，强啡肽免疫反应终末有效地调节，最有可能抑制，在大鼠延髓核的两个亚区的靶神经元。这种调节作用可以减弱或加强传入的儿茶酚胺信号的更远的树突的神经元。研究结果还表明，突触前调制的相互作用，涉及强啡肽和儿茶酚胺或其他递质在并列终端的潜在网站。
Dynorphin facilitates conditioned place aversion and reduces locomotor activity through mechanisms potentially involving direct activation of target neurons or release of catecholamines from afferents in the nucleus accumbens. We examined the ultrastructural substrates underlying these actions by combining immunoperoxidase labeling for dynorphin 1–8 and immunogold silver labeling for the catecholamine synthesizing enzyme, tyrosine hydroxylase (TH). The two markers were simultaneously visualized in single coronal sections through the rat nucleus accumbens. By light microscopy, dynorphin immunoreactivity was seen as patches of immunoreactive varicosities throughout all rostrocaudal levels of the nucleus accumbens. The dynorphin‐immunoreactive terminals identified by electron microscopy ranged from 0.2 to 1.5 μm in cross‐sectional diameter, contained numerous small (30–40 nm) clear vesicles, as well as one or more large (80–100 nm) dense core vesicles. From the dynorphin‐immunoreactive terminals quantitatively examined in single sections, 74% (173/370) showed symmetric synaptic junctions mainly with large unlabeled dendrites. Of the dynorphin‐immunoreactive terminals forming identifiable synapses, approximately 30% contacted more than one dendritic target. In addition, single dendrites frequently received convergent input from more than one dynorphin‐labeled terminal. Irrespective of their dendritic associations, dynorphin‐immunoreactive terminals also frequently showed close appositions with other axons and terminals; these included unlabeled (41%), TH‐labeled (10%) or dynorphin‐labeled axons (14%). In contrast to dynorphin‐immunoreactive terminals, TH‐labeled terminals formed primarily symmetric synapses with small dendrites and spines or lacked recognizable specializations in the plane of section analyzed. In some cases, single dendrites were postsynaptic to both dynorphin and TH‐immunoreactive terminals. We conclude that dynorphin‐immunoreactive terminals potently modulate, and most likely inhibit, target neurons in both subregions of the rat nucleus accumbens. This modulatory action could attenuate or potentiate incoming catecholamine signals on more distal dendrites of the accumbens neurons. The findings also suggest potential sites for presynaptic modulatory interactions involving dynorphin and catecholamine or other transmitters in apposed terminals.