BLOOD PRESSURE CONTROL BY FOREBRAIN AND BRAINSTEM NEURON

这项研究的长期目标是确定电生理 控制交感神经放电（SND）的CNS通路， 心血管功能 PI研究了巴比妥类药物的这些途径- 麻醉猫，其中SND同步为爆发（慢波） 通过压力感受器反射锁定在心动周期上。 后 压力感受器去神经这些交感神经慢波发生在频率 主要在2和6 Hz之间变化。 其他人报告说，在一些 未麻醉-去大脑（UD）、麻醉-清醒或清醒的猫， 10赫兹的节律与2 - 6赫兹的活动共存。 的近期研究 PI的实验室证实UD的SND中存在10 Hz节律， 失去压力感受器神经的猫 这些研究的主要发现包括： 以下. 1)10-Hz活动在每一个 研究的神经（心下神经、椎神经和肾神经）。 （二） 10-Hz活动的发作通常伴随着动脉粥样硬化的增加。 压力，表明这种节奏调节血管紧张度。 3)10-Hz 而不是2 - 6-Hz的活动被消除的中线矢状切割的 髓质（在奥贝喙侧0 - 6毫米）。 这种情况发生时， SND的总功率，但血压显著降低。 这 这表明，模式（10赫兹vs 2 - 6赫兹），而不仅仅是总 SND中的功率调节血压水平。 4)的活性 在SND中，一些中缝神经元与10-Hz慢波同步。 虽然 这种10赫兹的节律是在大约25年前描述的，还没有人确定它的 起源区域，调节这种节律的中枢神经元的特性，或 将这种活动传递给交感神经的通路。 可用数据 表明10赫兹的节律是在脑干中产生的。 国家 艺术电生理技术（尖峰触发平均，逆行 映射，自谱，相干性和相位谱分析）将被 用于在UD猫的实验中解决以下目的：1） 确定这种活动的起源部位，2）识别脑干 其活动与SND中的这种节律相关的神经元，3）以确定 负责10 Hz节律的神经元的相互连接，4）评估 这种节律在调节心血管系统中的功能意义 功能，和5）评估中枢呼吸驱动对 交感神经慢波频率。 这些研究将确定， SND中2 - 6-Hz和10-Hz分量由不同的 脑干网络，或者如果这两种模式反映了不同的生理 同一个网络的国家。 这些研究将增进我们对 负责产生静息SND的中央回路的 没有麻醉的影响。

The long range goal of this research is to identify electrophysiologically CNS pathways that control sympathetic nerve discharge (SND) and cardiovascular function. The PI has studied these pathways in barbiturate- anesthetized cats in which SND is synchronized into bursts (slow waves) that are locked to the cardiac cycle via the baroreceptor reflex. After baroreceptor-denervation these sympathetic slow waves occur at frequencies varying mainly between 2 and 6 Hz. Others report that in some unanesthetized-decerebrate (UD), urethane-anesthetized, or conscious cats, a 10-Hz rhythm coexists with this 2- to 6-Hz activity. Recent studies in the PI's laboratory confirm the existence of a 10-Hz rhythm in SND of UD, baroreceptor-denervated cats. Key findings of these studies include the following. 1) 10-Hz activity coheres (correlates) strongly among each of the nerves studied (inferior cardiac, vertebral, and renal nerves). 2) Episodes of 10-Hz activity are often followed by increases in arterial pressure, suggesting that this rhythm regulates vasomotor tone. 3) 10-Hz but not 2- to 6-Hz activity is eliminated by a midline sagittal cut of the medulla (0-6 mm rostral to the obex). This occurs without a change in total power in SND, but blood pressure significantly decreases. This suggests that the pattern (10-Hz vs 2- to 6-Hz) rather than just total power in SND regulates the level of blood pressure. 4) The activity of some raphe neurons is synchronized to 10-Hz slow waves in SND. Although this 10-Hz rhythm was described ~ 25 yr ago, no one has yet established its region of origin, properties of central neurons mediating this rhythm, or pathways that relay this activity to sympathetic nerves. Data available suggest that the 10-Hz rhythm is generated in the brainstem. State-of-the- art electrophysiological techniques (spike-triggered averaging, antidromic mapping, and autospectral, coherence, and phase spectral analyses) will be used to address the following aims in experiments on UD cats: 1) to determine the site of origin of this activity, 2) to identify brainstem neurons whose activity is correlated to this rhythm in SND, 3) to determine interconnections of neurons responsible for the 10-Hz rhythm, 4) to assess the functional significance of this rhythm in regulating cardiovascular function, and 5) to assess the effects of central respiratory drive on the frequency of sympathetic nerve slow waves. These studies will determine if the 2- to 6-Hz and 10-Hz components in SND are generated by different brainstem networks, or if the two patterns reflect different physiological states of the same network. These studies will enhance our understanding of the central circuitry responsible for generating resting SND in the absence of the effects of anesthesia.