TY - JOUR
T1 - Injection of corticotropin-releasing hormone into the amygdala aggravates visceral nociception and induces noradrenaline release in rats
AU - Su, J.
AU - Tanaka, Y.
AU - Muratsubaki, T.
AU - Kano, M.
AU - Kanazawa, M.
AU - Fukudo, S.
N1 - Publisher Copyright:
© 2014 John Wiley & Sons Ltd.
PY - 2015/1/1
Y1 - 2015/1/1
N2 - Background: Corticotropin-releasing hormone (CRH) and its receptor 1 (CRH-R1) play an important role in the colonic response to stress. The central nucleus of the amygdala (CeA) is a major extrahypothalamic site that contains a large number of neurons expressing both CRH and CRH-R1. Here, we verified the hypothesis that CRH in the CeA sensitizes visceral nociception via CRH-R1 with release of noradrenaline, dopamine, and serotonin (5-HT) in the CeA. Methods: In male Wistar rats, visceral sensitivity was quantified by recording the visceromotor response to colorectal distension (CRD) with administration of vehicle, CRH, or the CRH-R1 antagonist CP-154526+ CRH or CRH-R1 antagonist CP-154526 alone into the CeA. Simultaneously, extracellular levels of noradrenaline, dopamine, and 5-HT were measured in the CeA using microdialysis. All data were obtained under restraint conditions. Key Results: Administration of CRH into the CeA significantly increased the number of abdominal muscle contractions in response to CRD. CP-154526 significantly blocked the number of abdominal muscle contractions in response to CRD with the administration of CRH into the CeA. Noradrenaline in the CeA was increased by CRD, further increased by CRH, and inhibited by CRH-R1 antagonist. Dopamine in the CeA was also exaggerated by CRH but was not inhibited by CRH-R1 antagonist. 5-HT in the CeA was unchanged. Conclusions & Inferences: These results suggest that CRH in the CeA sensitizes visceral nociception via CRH-R1 with release of noradrenaline.
AB - Background: Corticotropin-releasing hormone (CRH) and its receptor 1 (CRH-R1) play an important role in the colonic response to stress. The central nucleus of the amygdala (CeA) is a major extrahypothalamic site that contains a large number of neurons expressing both CRH and CRH-R1. Here, we verified the hypothesis that CRH in the CeA sensitizes visceral nociception via CRH-R1 with release of noradrenaline, dopamine, and serotonin (5-HT) in the CeA. Methods: In male Wistar rats, visceral sensitivity was quantified by recording the visceromotor response to colorectal distension (CRD) with administration of vehicle, CRH, or the CRH-R1 antagonist CP-154526+ CRH or CRH-R1 antagonist CP-154526 alone into the CeA. Simultaneously, extracellular levels of noradrenaline, dopamine, and 5-HT were measured in the CeA using microdialysis. All data were obtained under restraint conditions. Key Results: Administration of CRH into the CeA significantly increased the number of abdominal muscle contractions in response to CRD. CP-154526 significantly blocked the number of abdominal muscle contractions in response to CRD with the administration of CRH into the CeA. Noradrenaline in the CeA was increased by CRD, further increased by CRH, and inhibited by CRH-R1 antagonist. Dopamine in the CeA was also exaggerated by CRH but was not inhibited by CRH-R1 antagonist. 5-HT in the CeA was unchanged. Conclusions & Inferences: These results suggest that CRH in the CeA sensitizes visceral nociception via CRH-R1 with release of noradrenaline.
KW - Brain-gut interaction
KW - CRD
KW - Central amygdaloid nucleus
KW - Dopamine
KW - Noradrenaline
KW - Serotonin
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U2 - 10.1111/nmo.12462
DO - 10.1111/nmo.12462
M3 - Article
C2 - 25359531
AN - SCOPUS:84920084069
VL - 27
SP - 30
EP - 39
JO - Neurogastroenterology and Motility
JF - Neurogastroenterology and Motility
SN - 1350-1925
IS - 1
ER -