Lack of light-induced elevation of renal sympathetic nerve activity and plasma corticosterone levels in PACAP-deficient mice
Lack of light-induced elevation of renal sympathetic nerve activity and plasma corticosterone levels in PACAP-deficient mice
复制标题
DOI：
10.1016/j.neulet.2008.08.030
复制
发表时间：
2008-10-24
影响因子：
2.5
通讯作者：
Baba, Akemichi
中科院分区：
文献类型：
--
作者：
Hatanaka, Michiyoshi;Tanida, Mamoru;Baba, Akemichi
PACAP是一种神经递质，参与视交叉上核（SCN）中光刺激的信号转导。光刺激通过SCN影响自主神经活动，在这里，我们使用PACAP缺陷（Adcyap 1（-/-））小鼠测试PACAP是否参与光诱导的交感-肾上腺活动调节。光刺激（100勒克斯，30分钟）显着升高肾交感神经活动（RSNA），这是在数字示波器上监测，和野生型小鼠的血浆皮质酮水平，但这两种反应几乎被废除在Adcyap 1（-/-）小鼠。虽然在两种基因型中观察到光诱导的SCN中的c-Fos表达，但在Adcyap 1（-/-）小鼠中c-Fos阳性细胞的数量显著减少。提示PACAP信号通路参与了光刺激RSNA和通过SCN释放皮质酮的过程。(C)2008爱思唯尔爱尔兰有限公司保留所有权利。
PACAP is a neurotransmitter involved in the signal transduction of light stimulation in the suprachiasmatic nucleus (SCN). Light stimulation affects autonomic nerve activity via the SCN, and here we tested whether PACAP participates in light-induced regulation of sympatho-adrenal activity by using PACAP-deficient (Adcyap1(-/-)) mice. Light stimulation (100 lux, 30 min) significantly elevated both renal sympathetic nerve activity (RSNA), which was monitored on a digital oscilloscope, and plasma corticosterone levels in wildtype mice, but both responses were almost abolished in Adcyap1(-/-) mice. Although light-induced c-Fos expression in the SCN was observed in both genotypes, the numbers of c-Fos positive cells were significantly decreased in Adcyap1(-/-) mice. These data suggest that PACAP signaling pathway is involved in light-induced stimulation of RSNA and plasma corticosterone release through SCN of brain. (C) 2008 Elsevier Ireland Ltd. All rights reserved.