中枢毒蕈碱受体对大鼠迷走神经传出放电活性的影响

发布时间：2018-03-13 14:00

本文选题：毒蕈碱受体　切入点：迷走神经活性　出处：《广东医学》2017年S2期 　论文类型：期刊论文

【摘要】：目的探讨中枢毒蕈碱受体(M受体)对大鼠迷走神经传出放电活性的影响。方法取健康成年雄性SD大鼠,随机分为6组(每组6只):加兰他敏组、中枢M受体拮抗组、新斯的明腹腔组、新斯的明侧脑室组、M1受体激动组及M2受体拮抗组。将迷走神经放电信号引导至BL-420F生理仪持续记录,其中采样速率1k Hz/s,滤波范围100~1 000 Hz。稳定记录神经放电信号10 min(作为基础值)后,按照上述分组注射相应药物,并持续记录迷走神经传出放电活性60 min。整个放电观察周期内,每隔10 min为时间点,记录放电频率和峰值,并进行统计学处理。结果传出放电频率于加兰他敏注射后17 min开始明显增加,持续至观察期结束。期间最高值为(516±40)Hz,最低值为(249±26)Hz,与给药前相比差异均有统计学意义(P0.05)。腹腔注射加兰他敏前给予硫酸阿托品干预处理后,各时间点放电频率和峰值与给药前比较无明显改变(P0.05),放电图内仅观察到散在爆发电位。腹腔注射新斯的明前10 min内观察,迷走神经传出放电频率和峰值记录无明显变化(P0.05)。侧脑室注射新斯的明前10 min内观察,放电频率和峰值无明显变化(P0.05)。放电频率于新斯的明注射后13min开始明显增加,持续至观察期结束,与给药前相比差异均有统计学意义(P0.05)。侧脑室注射MCN-A-343前10 min内观察,放电频率和峰值记录无明显变化。放电频率于MCN-A-343注射后12 min开始明显增加,持续至观察期结束,与给药前相比差异均有统计学意义(P0.05)。侧脑室注射美索曲明前10 min内观察,迷走神经传出放电频率和峰值无明显变化,注射美索曲明后8 min左右,放电峰值显著增加,持续48 min后回落至注射药物前水平,期间各时间点,与给药前相比差异均有统计学意义(P0.05)。放电频率于美索曲明注射后17min开始明显增加,持续至观察期结束。与给药前相比差异均有统计学意义(P0.05)。结论通过抑制中枢胆碱酯酶而提高乙酰胆碱含量,可增强迷走神经的传出活性;此过程可能是由中枢M1受体介导的;而中枢M2受体则可能抑制迷走神经传出活性。
[Abstract]:Objective to investigate the effect of muscarinic muscarinic receptor (muscarinic receptor) on the efferent discharge activity of vagus nerve in rats. Methods healthy adult male SD rats were randomly divided into 6 groups (6 rats in each group: Galantamine group, central M receptor antagonistic group). In neostigmine peritoneal group, neostigmine group, M 1 receptor stimulation group and M 2 receptor antagonism group, the vagus nerve discharge signals were directed to the BL-420F physiological apparatus for continuous recording. The sampling rate was 1k Hz / s and the filtering range was 100 Hz / s. The nerve discharge signals were recorded stably for 10 mins (as the base value), then the corresponding drugs were injected according to the above groups, and the efferent discharge activity of vagus nerve was recorded continuously for 60 mins. The discharge frequency and peak value were recorded every 10 min. Results the efferent discharge frequency increased significantly at 17 min after galantamine injection. The maximum value was 516 卤40 Hz and the lowest value was 249 卤26hz.There were significant differences between before and after administration of atropine sulfate before intraperitoneal injection of galantamine. There was no significant change in the frequency and peak value of discharge at each time point compared with that before administration, but only the scattered burst potential was observed in the discharges. 10 min before intraperitoneal injection of neostigmine, the discharges were observed within 10 min after intraperitoneal injection of neostigmine. There was no significant change in the frequency and peak value of vagus nerve efferent discharge (P 0.05). The discharge frequency and peak value of neostigmine were observed 10 min before injection of neostigmine. The frequency of discharge began to increase 13 minutes after neostigmine injection. There were significant differences between the two groups until the end of the observation period (P 0.05). The discharge frequency and peak value were not significantly changed within 10 min before intracerebroventricular injection of MCN-A-343. The frequency of discharge began to increase significantly at 12 min after MCN-A-343 injection. At the end of the observation period, the differences were statistically significant compared with those before administration. The frequency and peak value of vagal nerve efferent discharge did not change significantly within 10 min before injection of misotramine, and the frequency and peak value of vagal nerve efferent discharge did not change significantly, about 8 min after injection of misotremine. The peak value of discharge increased significantly, and decreased to the pre-injection level after 48 min. There was a significant difference between the two groups at different time points (P 0.05). The discharge frequency began to increase at 17 minutes after misotromine injection. Conclusion the efferent activity of vagus nerve can be enhanced by inhibiting central cholinesterase and increasing the efferent activity of vagus nerve, which may be mediated by central M1 receptor. Central M 2 receptor may inhibit the efferent activity of vagus nerve.
【作者单位】：石河子大学医学院基础医学系;石河子大学医学院临床医学院;石河子大学医学院第一附属医院神经内科;石河子大学医学院第一附属医院心内科;新疆医科大学附属肿瘤医院影像中心CT室;
【分类号】：R338

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