Importance of stress receptor-mediated mechanisms in the amygdala on visceral pain perception in an intrinsically anxious rat.
Importance of stress receptor-mediated mechanisms in the amygdala on visceral pain perception in an intrinsically anxious rat.
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DOI：
10.1111/j.1365-2982.2012.01899.x
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发表时间：
2012-05
影响因子：
3.5
通讯作者：
Greenwood-Van Meerveld B
中科院分区：
文献类型：
--
作者：
Johnson AC;Tran L;Schulkin J;Greenwood-Van Meerveld B
应激是肠易激综合征（IBS）患者经历的腹痛，IBS是一种原因不明的慢性疾病，伴有焦虑症。我们以前已经证明了结肠超敏反应的Wistar-Kyoto大鼠（WKYs），一个高度焦虑的应变，模型腹痛IBS。在低焦虑大鼠，我们已经证明，中央核杏仁核（CeA）调节结肠过敏和焦虑诱导的糖皮质激素受体（GR）或盐皮质激素受体（MR）的选择性激活，这也是由促肾上腺皮质激素释放因子（CRF）1型受体介导的。本研究的目的是检验CeA通过GR、MR和/或CRF-1 R调节WKY结肠超敏反应的假设。一个系列的WKY具有GR拮抗剂、MR拮抗剂或胆固醇（对照）的微丸，其立体定位地植入到CeA上。另一系列在CeA中输注CRF-1 R拮抗剂或溶剂。结肠敏感性被测量为对分级结肠直肠扩张（CRD）的内脏反应（VMR）。在WKY中，夸大的VMR到分级CRD不受CeA中GR或MR拮抗作用的影响。与此相反，直接输注CRF-1 R拮抗剂CeA显着抑制VMR CRD在有害扩张压力。CeA中的应激激素通过应变依赖性平行途径调节大鼠结肠超敏反应。WKY的结肠超敏反应是由CeA中的CRF-1 R机制介导的，独立于GR和MR。这些互补途径表明多种病因，其中CeA中的应激激素可调节IBS患者的腹痛。
Stress worsens abdominal pain experienced by patients with irritable bowel syndrome (IBS), a chronic disorder of unknown origin with comorbid anxiety. We have previously demonstrated colonic hypersensitivity in Wistar-Kyoto rats (WKYs), a high-anxiety strain, that models abdominal pain in IBS. In low-anxiety rats, we have demonstrated that the central nucleus of the amygdala (CeA) regulates colonic hypersensitivity and anxiety induced by selective activation of either glucocorticoid receptors (GR) or mineralocorticoid receptors (MR), which is also mediated by the corticotropin releasing factor (CRF) type-1 receptor. The goal of the present study was to test the hypothesis that the CeA through GR, MR and/or CRF-1R regulates colonic hypersensitivity in WKYs. One series of WKYs had micropellets of a GR antagonist, an MR antagonist or cholesterol (control) stereotaxically implanted onto the CeA. Another series were infused in the CeA with CRF-1R antagonist or vehicle. Colonic sensitivity was measured as a visceromotor response (VMR) to graded colorectal distension (CRD). The exaggerated VMR to graded CRD in WKYs was unaffected by GR or MR antagonism in the CeA. In contrast, direct CeA infusion of CRF-1R antagonist significantly inhibited the VMR to CRD at noxious distension pressures. Stress-hormones in the CeA regulate colonic hypersensitivity in the rat through strain-dependent parallel pathways. The colonic hypersensitivity in WKYs is mediated by a CRF-1R mechanism in the CeA, independent of GR and MR. These complementary pathways suggest multiple etiologies whereby stress hormones in the CeA may regulate abdominal pain in IBS patients.
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影响因子：
3.5
作者：
Greenwood-van Meerveld, B;Johnson, AC;Myers, DA
通讯作者：
Myers, DA
影响因子：
3.3
作者：
Ji, Y.;Tang, B.;Traub, R. J.
通讯作者：
Traub, R. J.
影响因子：
2.9
作者：
Marti, J;Armario, A
通讯作者：
Armario, A
DOI：
10.1152/ajpgi.00434.2001
发表时间：
2002-05-01
影响因子：
4.5
作者：
Miampamba, M;Maillot, C;Taché, Y
通讯作者：
Taché, Y
影响因子：
2.9
作者：
Greenwood-Van Meerveld, B;Gibson, M;Myers, D
通讯作者：
Myers, D