Lechner S M, Curtis A L, Brons R, Valentino R J
Department of Psychiatry, Allegheny University, Philadelphia, PA 19102, USA.
Brain Res. 1997 May 9;756(1-2):114-24. doi: 10.1016/s0006-8993(97)00116-9.
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.
本研究旨在阐明通过扩张远端结肠激活去甲肾上腺素能核团——蓝斑所涉及的神经递质。在通过向球囊导管内注入不同体积的水使结肠扩张之前、期间和之后,记录氟烷麻醉大鼠的蓝斑自发放电率。结肠扩张对蓝斑的激活呈体积依赖性且是可逆的。在结肠扩张期间,皮质脑电图活动的激活与蓝斑激活在时间上相关,并且长时间扩张(大于2分钟)导致对蓝斑和皮质脑电图激活均产生快速耐受。脑室内注射(3微克)促肾上腺皮质激素释放因子拮抗剂DPheCRF(12 - 41)或微量注入蓝斑(10纳克)可显著减弱较低但非较高程度结肠扩张所产生的蓝斑激活,这表明在此反应中促肾上腺皮质激素释放因子传入蓝斑参与其中。与此一致的是,预先暴露于30分钟的足部电击应激会使蓝斑神经元对促肾上腺皮质激素释放因子脱敏,导致低程度而非高程度扩张对蓝斑激活的类似减弱。脑室内注射(5微摩尔)犬尿喹啉酸可显著拮抗所有程度结肠扩张对蓝斑的激活。然而,当直接注入蓝斑(0.3纳摩尔)时,这种兴奋性氨基酸拮抗剂无效。总之,这些发现表明,低程度的结肠扩张通过蓝斑内促肾上腺皮质激素释放因子的释放激活蓝斑 - 去甲肾上腺素能系统,并且在蓝斑远端部位的兴奋性氨基酸神经传递对于此反应是必需的。结肠扩张期间蓝斑 - 去甲肾上腺素能系统的激活可能是外周副交感反应的一个认知环节。这种激活也可能在以结肠和精神症状合并为特征的疾病中起作用,如肠易激综合征。