拮抗剂对培养的中脑神经元中使君子氨酸和烟碱样受体介导电流的影响。
Effects of antagonists on quisqualate and nicotinic receptor-mediated currents of midbrain neurones in culture.
作者信息
Bijak M, Jarolimek W, Misgeld U
机构信息
Department of Neurophysiology, Max-Planck-Institute for Psychiatry, Planegg-Martinsried, F.R.G.
出版信息
Br J Pharmacol. 1991 Mar;102(3):699-705. doi: 10.1111/j.1476-5381.1991.tb12236.x.
Abstract
- The action of non-N-methyl-D-aspartate (non-NMDA) and nicotinic antagonists on excitatory postsynaptic currents (e.p.s.cs) and on quisqualate (Quis)- and nicotine-gated currents was studied by use of whole-cell recording in dissociated culture of the rat midbrain. 2. 6-Cyano-7-nitroquinoxaline-2,3-dione (CNQX; 0.1 microM) and kynurenic acid (0.1 mM) attenuated network-generated and miniature e.p.s.cs while mecamylamine (100 microM) and hexamethonium (400 microM) had no effect. Acetylcholine (ACh) enhanced or suppressed e.p.s.cs. The suppressing effect of ACh was blocked by atropine (0.1-10 microM). 3. ACh (50-1000 microM) and quisqualate (Quis, 0.1-20 microM) induced inward currents with the same reversal potential as e.p.s.cs. 4. Application of Quis and alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) in a low concentration (0.5 and 5 microM, respectively) evoked a maintained current which was attenuated by CNQX (1 microM) and kynurenic acid (0.5 mM) but not by mecamylamine (100 microM). 5. Higher concentrations of Quis (5-20 microM) and AMPA (50-100 microM) evoked a transient and a maintained current component. Kynurenic acid (1 mM) reduced the transient but not the maintained component. CNQX (5-10 microM) increased the maintained component without reducing the transient one; 20 microM CNQX reduced both components. 6. ACh-induced transient current was mimicked by nicotine and reversibly and dose-dependently blocked by mecamylamine. Atropine (10 microM), hexamethonium (400 microM) as well as CNQX (100 microM) and kynurenic acid (1 mM) did not affect the current. 7. Hexamethonium (50-400 microM) voltage-dependently depressed the maintained current elicited by both Quis and ACh. 8. In conclusion, although the antagonists examined here seem to discriminate between non-NMDA and nicotinic receptor-mediated e.p.s.cs, they vary considerably in respect of their mode of action when tested on Quis, AMPA and ACh-induced currents.
摘要
- 运用全细胞记录技术，在大鼠中脑的离体培养物中，研究了非N-甲基-D-天冬氨酸（非NMDA）和烟碱拮抗剂对兴奋性突触后电流（e.p.s.cs）以及对喹啉酸（Quis）和烟碱门控电流的作用。2. 6-氰基-7-硝基喹喔啉-2,3-二酮（CNQX；0.1微摩尔）和犬尿氨酸（0.1毫摩尔）减弱了网络产生的和微小的e.p.s.cs，而美加明（100微摩尔）和六甲铵（400微摩尔）则无作用。乙酰胆碱（ACh）增强或抑制e.p.s.cs。ACh的抑制作用被阿托品（0.1 - 10微摩尔）阻断。3. ACh（50 - 1000微摩尔）和喹啉酸（Quis，0.1 - 20微摩尔）诱导出与e.p.s.cs具有相同反转电位的内向电流。4. 分别以低浓度（0.5和5微摩尔）施加喹啉酸和α-氨基-3-羟基-5-甲基异恶唑-4-丙酸（AMPA）诱发了一个持续电流，该电流被CNQX（1微摩尔）和犬尿氨酸（0.5毫摩尔）减弱，但未被美加明（100微摩尔）减弱。5. 较高浓度的喹啉酸（5 - 20微摩尔）和AMPA（50 - 100微摩尔）诱发了一个瞬态电流成分和一个持续电流成分。犬尿氨酸（1毫摩尔）减少了瞬态成分，但未减少持续成分。CNQX（5 - 10微摩尔）增加了持续成分而未减少瞬态成分；20微摩尔CNQX减少了两个成分。6. ACh诱导的瞬态电流可被烟碱模拟，并被美加明可逆性地、剂量依赖性地阻断。阿托品（10微摩尔）、六甲铵（400微摩尔）以及CNQX（100微摩尔）和犬尿氨酸（1毫摩尔）均不影响该电流。7. 六甲铵（50 - 400微摩尔）电压依赖性地抑制由喹啉酸和ACh诱发的持续电流。8. 总之，尽管此处所检测的拮抗剂似乎能够区分非NMDA和烟碱受体介导的e.p.s.cs，但当对喹啉酸、AMPA和ACh诱导的电流进行测试时，它们在作用方式上有很大差异。
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