Involvement of medullary catecholamine cells in neuroendocrine responses to systemic cholecystokinin
Involvement of medullary catecholamine cells in neuroendocrine responses to systemic cholecystokinin
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DOI：
10.1046/j.1365-2826.1996.05252.x
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发表时间：
1996-11-01
影响因子：
3.2
通讯作者：
Day, TA
中科院分区：
文献类型：
--
作者：
Buller, KM;Day, TA
全身给予胆囊收缩素 (CCK) 可刺激下丘脑的神经分泌催产素 (OT) 和结节漏斗部促肾上腺皮质激素释放因子 (CRF) 细胞。先前研究的数据表明，背内侧髓质的 A2 去甲肾上腺素能神经元有助于 OT 细胞反应，但其他髓质儿茶酚胺细胞的作用仍不清楚。使用c-fos表达作为细胞活性的标记，我们发现CCK（100μg/kg，腹膜内）激活髓质中大量的酪氨酸羟化酶和苯基-N-甲基转移酶免疫反应性细胞群，这与腹外侧和背内侧髓质中重叠的去甲肾上腺素能和肾上腺素能细胞群的募集一致。在腹外侧延髓中，obex 水平的 C1 肾上腺素能神经元有特别显着的激活。为了直接测试 VLM 儿茶酚胺细胞对下丘脑神经内分泌细胞对 CCK 反应的贡献，为动物准备了单侧 VLM 损伤，这些损伤对应于对 CCK 显示最显着反应的那些区域。用 CCK 处理的 VLM 病变动物显示，病变同侧室旁核 (PVN) OT 细胞 c-fos 表达显着但小幅减少，但视上核 OT 细胞或内侧小细胞 PVN 细胞（其中许多是 GRF 细胞）的反应没有变化。这些发现表明，VLM 儿茶酚胺细胞对下丘脑神经内分泌细胞对 CCK 的反应几乎没有贡献，因此有助于进一步强调背内侧儿茶酚胺细胞的作用。然而，现在很明显，除了 A2 去甲肾上腺素能细胞外，CCK 治疗还招募了背内侧髓质的 C2 肾上腺素能细胞，其中许多细胞先前已被证明可以投射到 PVN。
Systemic administration of cholecystokinin (CCK) stimulates neurosecretory oxytocin (OT) and tuberoinfundibular corticotrophin releasing factor (CRF) cells of the hypothalamus. Data from previous studies suggest that A2 noradrenergic neurons of the dorsomedial medulla contribute to the OT cell response, but the role of other medullary catecholamine cells remains unclear. Using c-fos expression as a marker for cellular activity, we have found that CCK (100 mu g/kg, ip) activates substantial populations of tyrosine hydroxylase and phenyl-N-methyl-transferase immunoreactive cells in the medulla, consistent with recruitment of overlapped noradrenergic and adrenergic cell populations in both the ventrolateral and dorsomedial medulla. in the ventrolateral medulla there was a particularly prominent activation of C1 adrenergic neurons at the level of the obex. To directly test the contribution of VLM catecholamine cells to hypothalamic neuroendocrine cell responses to CCK, animals were prepared with unilateral VLM lesions corresponding to those areas that had displayed the most marked response to CCK. VLM lesioned animals treated with CCK displayed a significant although small reduction in paraventricular nucleus (PVN) OT cell c-fos expression ipsilateral to the lesion, but no change in the responses of supraoptic nucleus OT cells or in cells of the medial parvocellular PVN, many of which are GRF cells. These findings indicate that VLM catecholamine cells make little contribution to hypothalamic neuroendocrine cell responses to CCK and thus serve to further highlight the role of dorsomedial catecholamine cells. However, it is now apparent that, in addition to A2 noradrenergic cells, CCK treatment also recruits C2 adrenergic cells of the dorsomedial medulla, many of which have previously been shown to project to the PVN.