首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Loss of haloperidol induced gene expression and catalepsy in protein kinase A-deficient mice
【24h】

Loss of haloperidol induced gene expression and catalepsy in protein kinase A-deficient mice

机译:缺少氟哌啶醇诱导的蛋白激酶A缺陷小鼠的基因表达和僵直

获取原文
获取原文并翻译 | 示例
           

摘要

The antipsychotic drug, haloperidol, elicits the expression of neurotensin and c-fos mRNA in the dorsal lateral region of the striatum and produces an acute cataleptic response in rodents that correlates with the motor side effects of haloperidol in humans. Mice harboring a targeted disrup- tion of the RIIβ subunit of protein kinase A have a profound deficit in cAMP-stimulated kinase activity in the striatum. When treated with haloperidol, RIIβ mutant mice fail to induce either c-fos or neurotensin mRNA and the acute cataleptic response is blocked. However, both wild-type and mutant mice become cataleptic when neurotensin peptide is directly injected into the lateral ventricle, demonstrating that the kinase deficiency does not interfere with the action of neurotensin but rather its synthesis and release.
机译:抗精神病药氟哌啶醇在纹状体背外侧区域引起神经降压素和c-fos mRNA的表达,并在啮齿类动物中产生急性毒性反应,与氟哌啶醇对人体的运动副作用有关。蛋白质激酶A的RIIβ亚基被靶向破坏的小鼠纹状体中cAMP刺激的激酶活性严重不足。当用氟哌啶醇治疗时,RIIβ突变小鼠不能诱导c-fos或神经降压素mRNA,并且急性过敏反应被阻断。但是,当将神经降压素肽直接注射到侧脑室时,野生型和突变型小鼠均具有抗感性,这表明该激酶的缺乏并不干扰神经降压素的作用,而是其合成和释放。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号