Pavcovich L A, Valentino R J
Department of Psychiatry, Hahnemann University MS 403, Philadelphia, PA 19102-1192, USA.
Neurosci Lett. 1995 Aug 25;196(3):185-8. doi: 10.1016/0304-3940(95)11873-u.
Barrington's nucleus, a pontine nucleus implicated in micturition, contains numerous corticotropin-releasing hormone (CRH) neurons that project to the spinal parasympathetic nucleus that innervates the bladder. We now report that CRH from Barrington's nucleus may serve to inhibit micturition. Selective chemical activation of Barrington's nucleus by microinjection of glutamate evoked bladder contractions that were increased in magnitude after intrathecal administration of a CRH antagonist, D-PheCRH12-41. In contrast, intrathecally administered CRH decreased the magnitude of Barrington's stimulated bladder contractions. These results suggest that activation of Barrington's nucleus releases an excitatory neurotransmitter responsible for bladder contractions, and CRH, which inhibits this neurotransmitter. The balance between these two neuromediators may regulate bladder contractility, and thereby, urinary continence.
巴林顿核是脑桥中的一个与排尿有关的核团,含有众多促肾上腺皮质激素释放激素(CRH)神经元,这些神经元投射至支配膀胱的脊髓副交感神经核。我们现在报告,来自巴林顿核的CRH可能起到抑制排尿的作用。通过微量注射谷氨酸对巴林顿核进行选择性化学激活可诱发膀胱收缩,鞘内注射CRH拮抗剂D-PheCRH12-41后,膀胱收缩幅度增大。相反,鞘内注射CRH可减小巴林顿核刺激引起的膀胱收缩幅度。这些结果表明,巴林顿核的激活释放出一种负责膀胱收缩的兴奋性神经递质,而CRH则抑制这种神经递质。这两种神经介质之间的平衡可能调节膀胱收缩力,从而调节尿失禁。