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Dual activation of cardiac sympathetic and parasympathetic components during conditioned fear to context in the rat.

机译:在大鼠对周围环境的恐惧中,心脏交感神经和副交感神经的双重激活。

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摘要

1. The present study investigates the contribution of the sympathetic and vagal parasympathetic systems to the tachycardic response of long-lasting (40 min) conditioned fear responses to context. 2. The conditioned fear response evoked by re-exposure to a footshock chamber was tested 10 min after intravenous injection of the beta-adrenoceptor antagonist propranolol (2 mg/kg) or the muscarinic antagonist atropine methyl nitrate (2 mg/kg) in rats implanted with radiotelemetric probes. 3. Compared with saline controls, the drugs did not change the behavioural component of the response (freezing, 22 kHz ultrasonic vocalizations) or its pressor component (+28 mmHg). 4. Propranolol abolished the tachycardic response of fear, whereas atropine more than doubled it (from +75 to +175 b.p.m. above resting baseline). 5. The results demonstrate that both sympathetic and vagal parasympathetic outflows to the heart are strongly activated during conditioned fear. The vagal activation may act to hold back cardiac acceleration while the animal waits for the aversive stimulus to come.
机译:1.本研究调查了交感神经和迷走神经副交感神经系统对持续性(40分钟)条件性恐惧反应对背景的心动过速反应的贡献。 2.在大鼠中静脉内注射β-肾上腺素能受体拮抗剂普萘洛尔(2 mg / kg)或毒蕈碱拮抗剂阿托品硝酸甲酯(2 mg / kg)静脉注射10分钟后,测试了再次暴露于休克室引起的条件恐惧反应。植入无线电遥测探针。 3.与生理盐水对照组相比,药物没有改变反应的行为成分(冻结,22 kHz超声发声)或其加压成分(+28 mmHg)。 4.普萘洛尔消除了恐惧的心动过速反应,而阿托品将其恐惧增加了一倍以上(从高于静息基线的+75到+175 b.p.m.)。 5.结果表明,在有条件的恐惧中,交感神经和迷走神经副交感神经均被强烈激活。迷走神经的激活可能会阻止心脏的加速,而动物等待厌恶刺激的来临。

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