Hindbrain chemical mediators of reflex-induced inhibition of gastric tone produced by esophageal distension and intravenous nicotine
Hindbrain chemical mediators of reflex-induced inhibition of gastric tone produced by esophageal distension and intravenous nicotine
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DOI：
10.1152/ajpregu.00003.2005
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发表时间：
2005-11-01
影响因子：
2.8
通讯作者：
Gillis, RA
中科院分区：
文献类型：
--
作者：
Ferreira, M;Sahibzada, N;Gillis, RA
本研究的目的是通过食管扩张和尼古丁激活迷走神经反射，并测试后脑一氧化氮和去甲肾上腺素是否参与这种反射功能。我们使用双标记免疫细胞化学方法，以确定是否食管扩张（和尼古丁）激活c-Fos的表达在孤束核（NTS）的氮能和去甲肾上腺素能神经元。我们还研究了c-Fos在迷走神经背侧运动核（DMV）神经元投射到周边的表达。食管扩张引起19.7 +/- 2.3%的去甲肾上腺素能NTS神经元位于0.60 mm嘴的菖蒲（CS）被激活，但对DMV神经元的c-Fos几乎没有影响。静脉注射尼古丁导致19.7 +/- 4.2%的去甲肾上腺素能NTS神经元0.90 mm吻CS被激活，如前所述，对DMV神经元中的c-Fos表达没有影响。为了确定去甲肾上腺素和一氧化氮是否是食管扩张引起的胃内压降低的中枢介质（球囊记录），将N-G-硝基-L-精氨酸甲酯微量注射到NTS（n = 5）中，但不注射到DMV中，阻断迷走神经反射。相反，α（2）-肾上腺素能受体阻滞剂微量注射到DMV（n = 7），但不进入NTS，阻断迷走神经反射。这些数据与我们早期的尼古丁药理学微量注射数据相结合，表明食道扩张和尼古丁都会在NTS中产生一氧化氮，然后激活去甲肾上腺素能神经元，这些神经元终止并抑制DMV神经元。
The purpose of this study was to activate a vagovagal reflex by using esophageal distension and nicotine and test whether hindbrain nitric oxide and norepinephrine are involved in this reflex function. We used double-labeling immunocytochemical methods to determine whether esophageal distension (and nicotine) activates c-Fos expression in nitrergic and noradrenergic neurons in the nucleus tractus solitarii (NTS). We also studied c-Fos expression in the dorsal motor nucleus of the vagus (DMV) neurons projecting to the periphery. Esophageal distension caused 19.7 +/- 2.3% of the noradrenergic NTS neurons located 0.60 mm rostral to the calamus scriptorius (CS) to be activated but had little effect on c-Fos in DMV neurons. Intravenous administration of nicotine caused 19.7 +/- 4.2% of the noradrenergic NTS neurons 0.90 mm rostral to CS to be activated and, as reported previously, had no effect on c-Fos expression in DMV neurons. To determine whether norepinephrine and nitric oxide were central mediators of esophageal distension-induced decrease in intragastric pressure (balloon recording), N-G-nitro-L- arginine methyl ester microinjected into the NTS (n = 5), but not into the DMV, blocked the vagovagal reflex. Conversely, alpha(2)-adrenergic blockers microinjected into the DMV (n = 7), but not into the NTS, blocked the vagovagal reflex. These data, in combination with our earlier pharmacological microinjection data with nicotine, indicate that both esophageal distension and nicotine produce nitric oxide in the NTS, which then activates noradrenergic neurons that terminate on and inhibit DMV neurons.