Hypoxia activates nucleus tractus solitarii neurons projecting to the paraventricular nucleus of the hypothalamus
Hypoxia activates nucleus tractus solitarii neurons projecting to the paraventricular nucleus of the hypothalamus
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DOI：
10.1152/ajpregu.00028.2012
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发表时间：
2012-05-01
影响因子：
2.8
通讯作者：
Hasser, Eileen M.
中科院分区：
文献类型：
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作者：
King, T. Luise;Heesch, Cheryl M.;Hasser, Eileen M.
King TL、Heesch CM、Clark CG、Kline DD、Hasser EM。缺氧激活投射到下丘脑室旁核的孤束核神经元。 Am J Physiol Regul Integr Comp Physiol 302：R1219-R1232，2012。首次发表于 2012 年 3 月 7 日； doi:10.1152/ajpregu.00028.2012.-外周化学感受器传入信息被发送到孤束核 (nTS)、整合并转发到其他大脑区域以改变心肺功能。 nTS 投射到下丘脑室旁核 (PVN)，但这些投射在化学反射刺激期间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缺氧的情况下。我们评估了通气和心血管参数，以应对日益严重的缺氧情况。逆行示踪剂被用来标记 nTS PVN 投射神经元，并且在一些大鼠中，标记头端腹外侧髓质 (RVLM) 投射神经元。进行免疫组织化学鉴定缺氧后被激活（Fos 免疫反应性，Fos-IR）、儿茶酚胺能和 GABA 能的 nTS 细胞。清醒的大鼠接受 3 小时常氧（n = 4，21% O-2）或急性缺氧（12、10 或 8% O-2；n = 5 只）。缺氧增加通气量和 Fos-IR nTS 细胞数量（21%，13 +/- 2；12%，58 +/- 4；10%，166 +/- 22；8%，186 +/- 6）。无论动脉压降低 (-13 +/- 1 mmHg) 还是保持恒定，10% O2 后的 Fos 表达都相似。激活的 PVN 投射细胞的百分比与强度相关，但与我们的假设相反，在所有缺氧强度下都发现了表现出 Fos-IR 的 PVN 投射 nTS 细胞。值得注意的是，在所有缺氧强度下，75% 的激活的 PVN 投射 nTS 神经元都是儿茶酚胺能神经元。与 RVLM 投射细胞相比，10% O2 激活的 PVN 投射 nTS 细胞比例更高。数据表明，缺氧强度的增加会激活 nTS PVN 投射细胞，尤其是儿茶酚胺能 PVN 投射神经元。即使在化学反射激活水平较低的情况下，nTS 至 PVN 儿茶酚胺能途径也可能至关重要，并且对心肺反应比之前认为的更重要。
King TL, Heesch CM, Clark CG, Kline DD, Hasser EM. Hypoxia activates nucleus tractus solitarii neurons projecting to the paraventricular nucleus of the hypothalamus. Am J Physiol Regul Integr Comp Physiol 302: R1219-R1232, 2012. First published March 7, 2012; doi:10.1152/ajpregu.00028.2012.-Peripheral chemoreceptor afferent information is sent to the nucleus tractus solitarii (nTS), integrated, and relayed to other brain regions to alter cardiorespiratory function. The nTS projects to the hypothalamic paraventricular nucleus (PVN), but activation and phenotype of these projections during chemoreflex stimulation is unknown. We hypothesized that activation of PVN-projecting nTS neurons occurs primarily at high intensities of hypoxia. We assessed ventilation and cardiovascular parameters in response to increasing severities of hypoxia. Retrograde tracers were used to label nTS PVN-projecting neurons and, in some rats, rostral ventrolateral medulla (RVLM)-projecting neurons. Immunohistochemistry was performed to identify nTS cells that were activated (Fos-immunoreactive, Fos-IR), catecholaminergic, and GABAergic following hypoxia. Conscious rats underwent 3 h normoxia (n = 4, 21% O-2) or acute hypoxia (12, 10, or 8% O-2; n = 5 each). Hypoxia increased ventilation and the number of Fos-IR nTS cells (21%, 13 +/- 2; 12%, 58 +/- 4; 10%, 166 +/- 22; 8%, 186 +/- 6). Fos expression after 10% O2 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, similar to 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% O2. 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.