引用

外周化学感受器传入信息被发送到孤束核(nTS)，整合，并传递到其他脑区，以改变心肺功能。nTS投射到下丘脑室旁核(PVN)，但化学反射刺激期间这些投射的激活和表型尚不清楚。我们假设pvn投射的nTS神经元的激活主要发生在高强度的缺氧下。我们评估了通气和心血管参数对缺氧严重程度增加的反应。逆行示踪剂用于标记nTS pvn投射神经元，在一些大鼠中，标记口侧腹外侧髓质(RVLM)投射神经元。通过免疫组织化学鉴定缺氧后激活的nTS细胞(Fos-immunoreactive, Fos-IR)、儿茶酚胺能的和gaba能的。意识清醒的大鼠接受3小时常氧(n = 4,21% O(2))或急性缺氧(12,10,8% O(2));N = 5个)。缺氧可增加通气和Fos-IR nTS细胞数量(21%，13 2;12%， 58 4; 10%, 166 22; 8%, 186 6). Fos expression after 10% O(2) was similar whether arterial pressure was allowed to decrease (-13 1 mmHg) or was held constant. The percentage of PVN-projecting cells activated was intensity dependent, but contrary to our hypothesis, PVN-projecting nTS cells exhibiting Fos-IR were found at all hypoxic intensities. Notably, at all intensities of hypoxia, 75% of the activated PVN-projecting nTS neurons were catecholaminergic. Compared with RVLM-projecting cells, a greater percentage of PVN-projecting nTS cells was activated by 10% O(2). Data suggest that increasing hypoxic intensity activates nTS PVN-projecting cells, especially catecholaminergic, PVN-projecting neurons. The nTS to PVN catecholaminergic pathway may be critical even at lower levels of chemoreflex activation and more important to cardiorespiratory responses than previously considered.