Target organ regulation of substance P in sympathetic neurons in culture.
Target organ regulation of substance P in sympathetic neurons in culture.
复制标题
培养物中交感神经元 P 物质的靶器官调节。
DOI：
10.1016/0012-1606(84)90008-3
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发表时间：
1984
影响因子：
2.7
通讯作者：
Black,IB
中科院分区：
文献类型：
--
作者：
Kessler,JA;Adler,JE;Jonakait,GM;Black,IB
在新生大鼠颈交感上级神经节（SCG）的外植体和分离的细胞培养物中，研究了假定的肽类神经递质P物质（SP）的靶器官调节。SP水平显着增加外植体，72小时后，在文化中上升超过30倍。相比之下，肽水平没有增加解离神经节文化。然而，SP增加了近10倍的细胞培养物上生长的单层细胞来自松果体或唾液腺，SCG的目标。相比之下，SP含量没有增加的培养物上的细胞来源于心脏或肠的基板上生长。通过组合的高压液相色谱（HPLC）-放射免疫测定法鉴定SCG-靶共培养物中的肽身份。此外，免疫组织化学检查定位的肽几乎完全交感神经元和神经过程。在SCG-松果体共培养中研究了介导交感神经-靶相互作用的机制。肽的增加需要与活组织的相互作用，因为杀死的靶细胞的底物不升高SP水平。目标的影响不介导的神经生长因子或吲哚胺，潜在的分泌产物的松果体在文化。藜芦定治疗防止SP的增加，在共培养物中，河豚毒素阻断藜芦定的效果，这表明钠内流和膜去极化防止SP升高。我们的观察结果表明，交感神经元与靶器官的相互作用影响肽能表达，这种相互作用可能仅限于某些适当的靶结构。
Target organ regulation of the putative, peptide neurotransmitter, substance P (SP) was examined in explants and dissociated cell cultures of the neonatal rat sympathetic superior cervical ganglion (SCG). SP levels increased dramatically in explants, rising more than 30-fold after 72 hr in culture. By contrast, peptide levels did not increase in dissociated ganglion cultures. However, SP increased almost 10-fold in cell cultures grown on a monolayer of cells derived from the pineal or salivary gland, targets of the SCG. By contrast, SP content did not increase in cultures grown on a substrate of cells derived from heart or intestine. Peptide identity in the SCG-target cocultures was authenticated by means of combined high-pressure liquid chromatography (HPLC)-radioimmunoassay. Moreover, immunohistochemical examination localized the peptide virtually exclusively to sympathetic neurons and nerve processes. Mechanisms mediating the sympathetic-target interaction were examined in SCG-pineal cocultures. The increase in peptide required interactions with living tissue, since substrates of killed target cells did not elevate SP levels. The target influences were not mediated by nerve growth factor or indoleamines, potential secretory products of pineal in culture. Veratridine treatment prevented the increase in SP in the cocultures, and tetrodotoxin blocked the veratridine effect, suggesting that sodium influx and membrane depolarization prevent SP elevation. Our observations suggest that sympathetic neuron interactions with target organs influence peptidergic expression, and that this interaction may be restricted to certain appropriate target structures.