本研究利用多點電極植入於大鼠孤立束核（nucleus tractus solitarii, NTS）中對於心血管之神經元直接記錄的方式，針對鏈脲佐菌素誘發之糖尿病大鼠在孤立束核之神經放電活動與血管感壓反射靈敏度（baroreflex sensitivity, BRS)與對照組間之特性進行探討。針對鏈脲佐菌素誘發之糖尿病大鼠與對照組間之心血管控制功能，於下列的情況進行觀察：1)注射phenylephrine (PE)前後孤立束核中心血管神經元之改變，及2)孤立束核中心血管神經元與前庭交感反射(vestibulosympathetic reflex, VSR)在非垂直軸旋轉(off-vertical axis rotation, OVAR)期間，對於動脈血壓控制之角色。
在控制組大鼠中，孤立束核之放電次數在PE注射前後與動脈血壓間有明顯具統計意義之相關。在鏈脲佐菌素誘發之糖尿病大鼠中，孤立束核之放電次數在PE注射後與動脈血壓正相關。雖然在PE注射前孤立束核之放電次數在鏈脲佐菌素誘發之糖尿病大鼠與控制組間沒有統計上的差異，但在針對血管感壓反射靈敏度調整後，鏈脲佐菌素誘發之糖尿病大鼠孤立束核之放電次數的減少具有統計上的意義。經過血管感壓反射靈敏度調整後，多變異數分析顯示在PE注射後糖尿病與孤立束核之放電次數較間呈現彼此獨立的狀態。先前的生理學及免疫染色研究發現，鏈脲佐菌素誘發之糖尿病大鼠與控制組間孤立束核之資料，僅於PE注射後出現差異。然而，本研究顯示，糖尿病誘發之孤立束核血管感壓敏感神經元之損傷，在PE注射前可以於鏈脲佐菌素誘發之糖尿病大鼠中發現。這個結果顯示，多點電極植入的方式在孤立束核的研究中比先前的研究方法要更為敏感。
研究顯示，在與重力相關之姿勢改變中，孤立束核與前庭反射之整合將對交感神經活動進行調控。為了探討孤立束核心血管神經元與前庭交感反射對於鏈脲佐菌素誘發之糖尿病大鼠在動脈壓控制上的角色，我們藉由非垂直軸旋轉對於耳石及身體重力覺沿著大鼠頭部之冠狀面軸線提供選擇刺激，並且記錄血管感壓反射靈敏度與動脈血壓作為交感神經輸出活動之資訊。所有的參數均於非垂直軸旋轉的過程中，在旋轉艙中以0.16轉/秒(60/秒)的旋轉速度中進行記錄。在本研究中控制組動脈壓訊號，由於鼻子向上的位置時所造成的向前線性加速度的作用而增加訊號，而在鼻子向下的位置產生減少的現象。然而，相較於控制組，鏈脲佐菌素誘發之糖尿病大鼠在動脈壓的活動明顯較小且具統計上的差異。相對地，鏈脲佐菌素誘發之糖尿病大鼠所造成之血管感壓反射靈敏度損傷在正向線性加速度在鼻枕軸向中為最大時，將造成心血管調控上的改變。因此，在鏈脲佐菌素誘發之糖尿病大鼠所產生之孤立束核心血管神經元的改變，將在向前線性加速度期間對於維持動脈血壓的能力造成損傷。這樣在孤立束核心血管神經元的損傷，可能是在糖尿病患者姿勢改變時，動脈血壓受到影響的早期機轉之一。本研究顯示在施以PE與重力改變後，經由孤立束核與血管感壓反射靈敏度的結果，支持孤立束核心血管神經元損傷對於鏈脲佐菌素誘發之糖尿病大鼠之心血管的控制將造成影響。

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 cardiovascular NTS neurons. The cardiovascular regulation function for both control and diabetic rats were observed under the conditions of 1) the changes of cardiovascular neurons of NTS in the conditions before and after baroreflex system challenged by phenylephrine (PE) injection and 2) the roles of cardiovascular neurons of NTS and vestibulosympathetic reflex (VSR) in controlling the arterial blood pressure during off-vertical axis rotation (OVAR).
In control rats, NTS firing rate and systolic arterial pressure correlate significantly with both pre-PE (baseline) and post-PE. In STZ-induced diabetic rats, positive correlation is observed only after PE injection. NTS firing rate was significantly reduced in STZ-induced diabetic rats with adjustment for BRS. After PE injection, NTS firing rate is significantly lower in diabetic rats relative to control rats. With adjustment for BRS, multivariate analysis shows that diabetes is independently associated with NTS firing rate after PE injection. 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.
Research has shown that the integration of NTS and vestibular reflex modulates sympathetic activity during the changes in posture with respect to gravity. To investigate the changes in the roles of NTS cardiovascular neurons and VSR in controlling the arterial blood pressure in STZ-induced diabetic rats, we selectively stimulated otolith and body graviceptors sinusoidally along the rat’s head axis in the coronal plane with OVAR and recorded sympathetic efferent activity in the BRS and blood pressure. All parameters were entrained during OVAR performed in a rotation chamber at 0.16 revolution/second (60/second) rotation speed. Our data indicated that the blood pressure increased in nose up positions during forward linear acceleration and decreased when nose down in the control groups. Compared to the control group, however, significant attenuation increase in blood pressure was observed in STZ-induced diabetic rats in the nose up position. Impairment of BRS,  coefficients, contributes to the alternations of cardiovascular modulation when positive linear acceleration was maximal along the naso-ocipital axis, on STZ-induced diabetic rats. The alternation of NTS cardiovascular neurons in STZ-induced diabetes might contribute to the impairment of blood pressure maintenance during forward linear acceleration. This impaired regulation function in cardiovascular neurons of NTS maybe one of the earliest mechanisms to affect the regulation of blood pressure during the posture change in diabetes. In conclusion, the changes observed in NTS cardiovascular neuronal activity and BRS results from PE administration and gravitational stress support the notion that there are impairments of cardiovascular regulation function in STZ-induced diabetic rats.

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