Substance P modulates nicotinic responses of intracardiac neurons to acetylcholine in the guinea pig.

Substance P modulates nicotinic responses of intracardiac neurons to acetylcholine in the guinea pig.
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DOI:
10.1152/ajpregu.2001.281.6.r1792
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发表时间:
2001-12
期刊:
American journal of physiology. Regulatory, integrative and comparative physiology
影响因子:
--
通讯作者:
Lili Zhang;John D. Tompkins;John C. Hancock;Donald B. Hoover
Lili Zhang;John D. Tompkins;John C. Hancock;Donald B. Hoover
中科院分区:
其他
文献类型:
--
作者:
Lili Zhang;John D. Tompkins;John C. Hancock;Donald B. Hoover

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将P物质(SP)应用于豚鼠心内神经元引起缓慢的去极化和增加神经元的兴奋性。本实验观察了SP对ACh引起的心内神经元快兴奋反应的影响。用细胞内记录方法,在豚鼠心房神经节丛的整体标本上测定心内神经元的反应。局部压力喷射100 μ M SP(1秒)从玻璃微量移液管引起所有神经元(n = 38)的缓慢去极化和触发动作电位产生的47%的细胞测试。浴应用SP(0.5-100 μ M)引起心内神经元的剂量依赖性去极化,但很少诱发动作电位,即使在最高浓度。然而,这种治疗与SP增强烟碱反应诱发的局部压力喷射乙酰胆碱(10毫米,10- 100毫秒的持续时间)在77%的心内神经元研究(n = 52)。在0.5 μ M SP治疗期间,ACh诱发的快速去极化幅度显著增加(对照组为13.0 +/- 1.8 mV,SP组为17.7 +/- 1.9 mV,n = 7,P = 0.019)。在较高浓度的SP,增强ACh的反应,主要是在动作电位的产生。然而,在15%的心内神经元的研究,乙酰胆碱的反应被SP衰减。这种衰减主要发生在暴露于10和100 μ M SP的过程中,表现为烟碱快速去极化幅度的降低或ACh诱发的动作电位的抑制。这些结果支持了SP在豚鼠心内神经节中作为神经调质和神经递质的结论。
Application of substance P (SP) to intracardiac neurons of the guinea pig causes slow depolarization and increases neuronal excitability. The present study was done to determine the influence of SP on fast excitatory responses of intracardiac neurons to ACh. Intracellular recording methods were used to measure responses of intracardiac neurons in whole mount preparations of atrial ganglionated nerve plexus from guinea pig hearts. Local pressure ejection of 100 microM SP (1 s) from a glass micropipette caused slow depolarization of all neurons (n = 38) and triggered action potential generation in 47% of the cells tested. Bath application of SP (0.5-100 microM) caused a dose-dependent depolarization of intracardiac neurons but rarely evoked action potentials, even at the highest concentration. However, such treatment with SP enhanced nicotinic responses evoked by local pressure ejections of ACh (10 mM, 10- to 100-ms duration) in 77% of intracardiac neurons studied (n = 52). A significant increase in amplitude of ACh-evoked fast depolarization occurred during treatment with 0.5 microM SP (13.0 +/- 1.8 mV for control vs. 17.7 +/- 1.9 mV with SP present, n = 7, P = 0.019). At higher concentrations of SP, enhancement of the response to ACh resulted mainly in action potential generation. However, responses to ACh were attenuated by SP in 15% of the intracardiac neurons studied. This attenuation occurred primarily during exposure to 10 and 100 microM SP and was manifest as a reduction in amplitude of nicotinic fast depolarization or inhibition of ACh-evoked action potentials. These findings support the conclusion that SP could function as a neuromodulator and neurotransmitter in intracardiac ganglia of the guinea pig.