Magoul R, Dubourg P, Benjelloun W, Tramu G
Laboratoire de Neurocytochimie Fonctionnelle, URA CNRS, Talence, France.
J Chem Neuroanat. 1993 Nov-Dec;6(6):419-29. doi: 10.1016/0891-0618(93)90016-w.
Anatomical connections between tachykinin-containing terminals and three neuronal populations of the arcuate nucleus, chemically defined respectively by beta-endorphin (beta-END), tyrosine-hydroxylase or neuropeptide Y (NPY) and well represented in the arcuate nucleus, were studied using electron microscope double pre-embedding immunocytochemistry involving a combination of two sensitive chromogens: diaminobenzidine and tetramethylbenzidine. Following tachykinin immunodetection by diaminobenzidine, and tyrosine-hydroxylase, beta-END or NPY immunolabelling by tetramethylbenzidine, tachykinin-immunoreactive terminals were seen presynaptic to tyrosine-hydroxylase immunopositive cells and dendrites principally in the dorsomedial portion of the arcuate nucleus. Tachykinin-immunoreactive processes were also seen in synaptic contact with ventrolaterally located beta-END immunopositive perikarya. Tachykinin-immunopositive terminals also contacted NPY-immunoreactive cells and dendritic processes ventromedially. These results demonstrate the existence of a direct tachykinergic input onto three neuronal populations expected to play a role in the control of reproductive events. Consequently, they suggest, at least, an indirect action for tachykinins in the regulation of reproduction. Especially, tachykinins may indirectly control the luteinizing hormone-releasing hormone neurons via dopamine, beta-END and NPY cells and thereby influence luteinizing hormone secretion.
利用电子显微镜双重预包埋免疫细胞化学技术,结合两种灵敏显色剂(二氨基联苯胺和四甲基联苯胺),研究了含速激肽终末与弓状核中三个神经元群体之间的解剖学联系,这三个神经元群体分别由β-内啡肽(β-END)、酪氨酸羟化酶或神经肽Y(NPY)进行化学定义,且在弓状核中均有很好的代表性。在用二氨基联苯胺进行速激肽免疫检测,并用四甲基联苯胺进行酪氨酸羟化酶、β-内啡肽或NPY免疫标记后,可见速激肽免疫反应性终末主要位于弓状核背内侧部分的酪氨酸羟化酶免疫阳性细胞和树突的突触前。速激肽免疫反应性突起也见于与位于腹外侧的β-内啡肽免疫阳性核周体的突触接触中。速激肽免疫阳性终末也与腹内侧的NPY免疫反应性细胞和树突状突起相接触。这些结果表明,存在对预期在生殖事件控制中起作用的三个神经元群体的直接速激肽能输入。因此,它们至少提示速激肽在生殖调节中具有间接作用。特别是,速激肽可能通过多巴胺、β-内啡肽和NPY细胞间接控制促黄体生成素释放激素神经元,从而影响促黄体生成素的分泌。