Ethanol-induced c-Fos expression in catecholamine- and neuropeptide Y-producing neurons in rat brainstem

Ethanol-induced c-Fos expression in catecholamine- and neuropeptide Y-producing neurons in rat brainstem
复制标题

DOI:
10.1097/00000374-200006000-00009
复制
发表时间:
2000-06-01
影响因子:
3.2
通讯作者:
Bernstein, IL
Bernstein, IL
中科院分区:
医学3区
文献类型:
--
作者:
Thiele, TE;Cubero, I;Bernstein, IL

文献摘要

被引文献

相似文献

背景:之前的研究使用 c-Fos 样免疫反应性 (cFLI) 来检查响应乙醇给药而激活的细胞的神经解剖学位置。然而,单独使用 cFLI 无法揭示细胞的表型特征。在本研究中,我们使用双标记程序来鉴定在大鼠脑干中显示乙醇诱导的 cFLI 的神经元的神经化学表型。方法:各组大鼠接受腹腔注射乙醇(1.5 g/kg 或 3.5 g/kg)或等渗盐水(23 ml/kg)。为了评估乙醇诱导的 cFLI 的特异性,我们给其他大鼠注射了药物氯化锂 (LiCl;76 mg/kg)。注射后两小时,处死大鼠,并对它们的大脑进行免疫组织化学处理。结果:两种剂量的乙醇均促进了几个脑干区域的 cFLI,包括孤束核 (NTS)、脑干区域 蓝斑肌 (LC) 和腹外侧延髓 (VLM)。尽管 LiCl 在 NTS 中引起显着的 cFTI,但该药物仅促进 VLM 中最小的 cFLI,并且在 LC 中没有显着激活。我们发现,在 VLM(大约 75-85%)、NTS(大约 65-75%)和 LC(大约 30-65%)中,很大比例的酪氨酸羟化酶(TH)阳性神经元共表达乙醇诱导的 cFLI。此外,VLM 中很大一部分产生神经肽 Y (NPY) 的神经元共表达乙醇诱导的 cFLI(类似于 60-75%)。另一方面,LiCl促进VLM和NTS中TW阳性神经元的激活,但未能刺激LC中产生TH的神经元或VLM中产生NPY的神经元中的cFLI。结论:显示乙醇诱导的c-Fos表达的大鼠脑干神经元产生儿茶酚胺和NPY。这项研究证明了双标记免疫组织化学程序在识别乙醇给药后激活的神经元的神经化学特性方面的有用性。
Background: Previous studies have used c-Fos-like immunoreactivity (cFLI) to examine the neuroanatomical location of cells that are activated in response to ethanol administration. However, the use of cFLI alone fails to reveal the phenotypical identity of cells. Tn the present study we used double-labeling procedures to identify the neurochemical phenotype of neurons that showed ethanol-induced cFLI in the rat brainstem.Methods: Individual groups of rats received intraperitoneal injection of ethanol (1.5 g/kg or 3.5 g/kg) or isotonic saline (23 ml/kg). To assess the specificity of cFLI induced by ethanol, we injected other rats with the drug lithium chloride (LiCl; 76 mg/kg).Two hours after injection, rats were killed and their brains were processed for immunohistochemistry.Results: Both doses of ethanol promoted cFLI in several brainstem regions, including the nucleus of the solitary tract (NTS), the locus coeruleus (LC), and the ventrolateral medulla (VLM). Although LiCl caused significant cFTI in the NTS, this drug promoted only minimal cFLI in the VLM and no significant activation in the LC. We found that a significant proportion of tyrosine hydroxylase (TH)-positive neurons coexpressed ethanol-induced cFLI in the VLM (similar to 75-85%), the NTS (similar to 65-75%), and the LC (similar to 30-65%). Additionally, a significant proportion of neuropeptide Y (NPY)-producing neurons in the VLM coexpressed ethanol-induced cFLI (similar to 60-75%). On the other hand, LiCl promoted activation of TW-positive neurons in the VLM and the NTS but failed to stimulate cFLI in TH-producing neurons in the LC or in NPY-producing neurons of the VLMConclusions: Neurons in the rat brainstem that show ethanol-induced c-Fos expression produce catecholamines and NPY. This research demonstrates the usefulness of double-labeling immunohistochemistry procedures for identifying the neurochemical identity of neurons that are activated after ethanol administration.