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链脲佐菌素诱导的糖尿病大鼠孤束核心血管神经元调节功能受损。

Impaired regulation function in cardiovascular neurons of nucleus tractus solitarii in streptozotocin-induced diabetic rats.

作者信息

Chen Hsin-Yung, Wu Jin-Shang, Chen Jia-Jin Jason, Cheng Juei-Tang

机构信息

Institute of Biomedical Engineering, National Cheng Kung University, Tainan, Taiwan.

出版信息

Neurosci Lett. 2008 Jan 31;431(2):161-6. doi: 10.1016/j.neulet.2007.11.035. Epub 2007 Dec 3.

Abstract

This study characterizes neural firing activity of the nucleus tractus solitarii (NTS) and baroreflex sensitivity (BRS) in streptozotocin (STZ)-induced diabetic rats relative to control rats by implantation of multi-wire electrode into rat NTS for direct monitoring of barosensitive NTS neurons before and after baroreflex system challenge by phenylephrine (PE) injection. NTS firing data is correlated with arterial pressure for both control and diabetic rats. In control rats, NTS firing rate and systolic arterial pressure correlate significantly with both pre-PE (baseline) and post-PE (p<0.01). In STZ-induced diabetic rats, positive correlation is observed only after PE injection (p<0.05). Although NTS firing rate was not significantly different between control and diabetic rats (p=0.085) in the baseline condition, it was significantly reduced in STZ-induced diabetic rats (p=0.042) with adjustment for BRS. After PE injection, NTS firing rate is significantly lower in diabetic rats relative to control rats (p<0.01). With adjustment for BRS, multivariate analysis shows that diabetes is independently associated with NTS firing rate after PE injection (p=0.034). Prior physiological and immunofluorescent studies found differing NTS data for control and diabetic rat only after PE challenge, but our data show diabetes-induced barosensitive NTS impairment in the baseline condition for STZ-induced diabetic rats. This latter finding suggests greater sensitivity of multi-wire electrode study of NTS relative to earlier methods.

摘要

本研究通过将多线电极植入大鼠孤束核(NTS),在注射去氧肾上腺素(PE)激发压力反射系统前后直接监测压力敏感的NTS神经元,从而对链脲佐菌素(STZ)诱导的糖尿病大鼠相对于对照大鼠的孤束核神经放电活动和压力反射敏感性(BRS)进行了表征。对照大鼠和糖尿病大鼠的NTS放电数据均与动脉压相关。在对照大鼠中,NTS放电频率和收缩期动脉压在注射PE前(基线)和注射PE后均显著相关(p<0.01)。在STZ诱导的糖尿病大鼠中,仅在注射PE后观察到正相关(p<0.05)。尽管在基线条件下对照大鼠和糖尿病大鼠之间的NTS放电频率无显著差异(p=0.085),但在调整BRS后,STZ诱导的糖尿病大鼠的NTS放电频率显著降低(p=0.042)。注射PE后,糖尿病大鼠的NTS放电频率相对于对照大鼠显著降低(p<0.01)。在调整BRS后,多变量分析显示糖尿病与注射PE后的NTS放电频率独立相关(p=0.034)。先前的生理学和免疫荧光研究仅在PE激发后发现对照大鼠和糖尿病大鼠的NTS数据不同,但我们的数据显示STZ诱导的糖尿病大鼠在基线条件下存在糖尿病诱导的压力敏感NTS损伤。后一发现表明,相对于早期方法,多线电极对NTS的研究具有更高的敏感性。

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