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| 延髓头端腹外侧区血管紧张素Ⅱ对脊髓投射神经元氨基酸递质释放的调节 | |
| 引用本文： | Hu L,Zhu DN,Wang JQ,Sun ZJ,Yao T. 延髓头端腹外侧区血管紧张素Ⅱ对脊髓投射神经元氨基酸递质释放的调节[J]. 生理学报, 2001, 53(5): 385-390 |
| 作者姓名： | Hu L Zhu DN Wang JQ Sun ZJ Yao T |
| 作者单位： | 1. 复旦大学基础医学院生理学教研室 2. Present address: Division of Pharmacology, School of Pharmacy, University of Missouri-Kansas City, 3. Present address: Department of Physiology, College of Medicine, University of Florida, |
| 基金项目： | The work was supported by a grant from the National Natural Science Foundation of China (No.39970267) and China Medical Board Grant. |
| 摘 要： | 用脊髓(T8)中间外侧柱(IML)微透析方法结合高效液相色谱(HPLC)技术,研究延髓头端腹外侧区(RVLM)微量注射血管紧张素Ⅱ(ANGⅡ,100pmol,n=11)后脊髓IML氨基酸递质释放的变化.在RVLM区微量注射ANGⅡ(100pmol,n=11),能显著增加(P<0.01)脊髓(T8)内天门冬氨酸(ASP,从4.75±1.01升至8.90±2.28pmol/20μl)和谷氨酸(GLU,从18.99±8.64升至73.88±29.26pmol/20μl)的释放.在同一RVLM部位注射losartan(10nmol,n=8)可以显著抑制注射ANGⅡ引起的GLU释放升高反应(P<0.05).免疫荧光双标记结合共聚焦显微镜观察到RVLM内62%～91%的谷氨酸能神经元呈AT1受体免疫阳性.此结果提示ANGⅡ诱发的脊髓内谷氨酸释放可能来源于RVLM内AT1受体免疫阳性的谷氨酸能脊髓投射神经元. |
| 关 键 词： | 延髓头端腹外侧区 脊髓中间外侧柱 血管紧张素Ⅱ 微透析 免疫荧光双标记 氨基酸递质 心血管运动神经元 |
| 修稿时间： | 2001-04-11 |
Angiotensin II in rostral ventrolateral medulla mediates amino acids release from spinally projecting nerve terminals in the spinal cord |
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| Hu L,Zhu D N,Wang J Q,Sun Z J,Yao T. Angiotensin II in rostral ventrolateral medulla mediates amino acids release from spinally projecting nerve terminals in the spinal cord[J]. Acta Physiologica Sinica, 2001, 53(5): 385-390 | |
| Authors: | Hu L Zhu D N Wang J Q Sun Z J Yao T |
| Affiliation: | Department of Physiology, Medical Center of Fudan University, National Key Laboratory for Medical Neurobiology, Shanghai 200032. |
| Abstract: | Microdialysis in the intermediolateral column (IML) was employed to examine amino acids release induced by angiotensin II (ANG II) applied into the rostral ventrolateral medulla (RVLM). Microinjection of ANG II (100 pmol, n = 11) into the RVLM significantly increased (P < 0.01) the release of aspartate (from 4.75 +/- 1.01 to 8.90 +/- 2.28 pmol/20 microliters) and glutamate (from 18.99 +/- 8.64 to 73.88 +/- 29.26 pmol/20 microliters) in the spinal cord. The increase of glutamate release was significantly attenuated (P < 0.05) by pretreatment with losartan (10 nmol, n = 8) at the same RVLM site. Immunofluorescence double labeling combined with confocal microscopic observation demonstrated that 62%-91% of the glutamatergic neurons in the RVLM were double-labeled with AT1 receptors, supporting the view that ANG II-induced glutamate release in the spinal cord may arise from the AT1 receptor-containing glutamatergic spinally projecting neurons in the RVLM. |
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