The present study was designed to elucidate the neurotransmitters involved in activation of the noradrenergic nucleus, locus coeruleus, by distention of the distal colon. Locus coeruleus spontaneous discharge rate was recorded from halothane-anesthetized rats before, during and after distention of the colon produced by inflation of a balloon catheter with varying volumes of water. Locus coeruleus activation by colon distention was volume-dependent and reversible. Activation of cortical electroencephalographic activity was temporally correlated with locus coeruleus activation during colon distention and prolonged distention (greater than 2 min) resulted in tachyphalaxis to both locus coeruleus and cortical electroencephalographic activation. The corticotropin-releasing factor antagonist, DPheCRF(12-41), administered intracerebroventricularly (3 microg) or microinfused into the locus coeruleus (10 ng) significantly attenuated locus coeruleus activation produced by lower, but not higher magnitudes of colon distention, implicating corticotropin-releasing factor afferents to the locus coeruleus in this response. Consistent with this, prior exposure to 30 min of footshock stress, which desensitizes locus coeruleus neurons to corticotropin-releasing factor, produced a similar attenuation of locus coeruleus activation by low, but not high magnitudes of distention. Kynurenic acid, administered intracerebroventricularly (5 micromol), significantly antagonized locus coeruleus activation by all magnitudes of colon distention. However, this excitatory amino acid antagonist was ineffective when administered directly into the locus coeruleus (0.3 nmol). Together, these findings suggest that low magnitudes of colon distention activate the locus coeruleus-noradrenergic system via corticotropin-releasing factor release within the locus coeruleus and that excitatory amino acid neurotransmission at a site distal to the locus coeruleus is necessary for this response. Activation of the locus coeruleus-noradrenergic system during colon distention may serve as a cognitive limb of the peripheral parasympathetic response. This activation may also play a role in disorders characterized by comorbidity of colonic and psychiatric symptoms, such as irritable bowel syndrome.

译文

本研究旨在阐明通过远端结肠扩张而激活去甲肾上腺素能核蓝斑的神经递质。记录了氟烷麻醉大鼠的蓝斑自然放电速率,该速率是在通过气囊导管充满不同体积的水而产生的结肠扩张之前,期间和之后。结肠扩张对蓝斑的激活是体积依赖性和可逆的。在结肠扩张期间,皮质脑电图活动的激活与蓝斑轨迹的激活在时间上相关,而长时间的扩张 (大于2分钟) 导致蓝斑轨迹和皮质脑电图激活均出现心动过速。促肾上腺皮质激素释放因子拮抗剂DPheCRF(12-41) 在脑室内给药 (3 microg) 或微注入蓝斑 (10 ng) 显着减弱了由较低但不是较高程度的结肠扩张产生的蓝斑激活,在这种反应中,促肾上腺皮质激素释放因子传入蓝斑。与此一致的是,先前暴露于30分钟的脚休克应激,使蓝斑基因座神经元对促肾上腺皮质激素释放因子脱敏,通过低但不高的扩张幅度产生了类似的蓝斑基因座激活衰减。脑室内给药 (5 micromol) 的犬尿酸可通过所有程度的结肠扩张显着拮抗蓝斑的激活。然而,当直接给予蓝斑 (0.3 nmol) 时,这种兴奋性氨基酸拮抗剂是无效的。总之,这些发现表明,低程度的结肠扩张通过在蓝斑内释放促肾上腺皮质激素释放因子来激活蓝斑-去甲肾上腺素能系统,并且在蓝斑远端的兴奋性氨基酸神经传递是这种反应所必需的。结肠扩张期间蓝斑-去甲肾上腺素能系统的激活可能是周围副交感神经反应的认知肢体。这种激活也可能在以结肠和精神症状合并症为特征的疾病中发挥作用,例如肠易激综合征。

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