Angiotensin II's role in sodium lactate-induced panic-like responses in rats with repeated urocortin 1 injections into the basolateral amygdala: amygdalar angiotensin receptors and panic.
Angiotensin II's role in sodium lactate-induced panic-like responses in rats with repeated urocortin 1 injections into the basolateral amygdala: amygdalar angiotensin receptors and panic.
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血管紧张素II在乳酸钠诱导的大鼠中的恐慌样反应中的作用，反复注射泌尿肌素1对基底外侧杏仁核：杏仁核血管紧张素受体和恐慌。
DOI：
10.1016/j.pnpbp.2013.02.014
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发表时间：
2013-07-01
影响因子：
5.6
通讯作者：
Shekhar, Anantha
中科院分区：
文献类型：
--
作者：
Johnson, Philip L.;Sajdyk, Tammy J.;Fitz, Stephanie D.;Hale, Mathew W.;Lowry, Christopher A.;Hay-Schmidt, Anders;Shekhar, Anantha
每天三次将尿皮质素1（UCN）注射到基底外侧杏仁核（BLA;即，UCN/BLA-primed大鼠）发展出延长的焦虑相关行为和对恐慌样生理反应的脆弱性（即，心动过速、高血压和呼吸急促）。在这些UCN致敏的大鼠中，神经元敏感的穹窿下器官（SFO）可能是检测血浆NaLac增加并动员恐慌通路的潜在部位，因为在该模型中抑制SFO会阻断NaLac后的恐慌。此外，由于SFO神经元合成血管紧张素II（A-II），我们假设，SFO项目的BLA和释放A-II动员恐慌反应UCN/BLA引发大鼠注射NaLac。为了检验这一假设，大鼠每天接受双侧注射UCN或媒介物到BLA中，持续3天。在BLA内注射后5 - 7天，我们在NaLac激发前将非特异性A-II 1型（AT 1 r）和2型（AT 2 r）受体拮抗剂saralasin或AT 2 r选择性拮抗剂PD 123319微量注射到BLA中。预先注射saralasin而不是PD 123319或溶媒的UCN/BLA致敏大鼠具有减少的NaAc诱导的焦虑相关行为和恐慌相关的心动过速和呼吸急促反应。然后，我们证实了AT 1 rs的存在下，在BLA使用免疫组化，结合以前的数据，表明A-II的panicogenic效应在BLA是AT 1 r依赖。令人惊讶的是，SFO几乎没有直接支配BLA的神经元，这表明了一种间接的传递NaLac信号的途径。总的来说，这些结果是第一个牵连A-II和AT 1 rs作为假定的神经递质受体在NaLac诱导的恐慌样反应在UCN/BLA-致敏大鼠。
Rats treated with three daily urocortin 1 (UCN) injections into the basolateral amygdala (BLA; i.e., UCN/BLA-primed rats) develop prolonged anxiety-associated behavior and vulnerability to panic-like physiological responses (i.e., tachycardia, hypertension and tachypnea) following intravenous infusions of 0.5 M sodium lactate (NaLac, an ordinarily mild interoceptive stressor). In these UCN-primed rats, the osmosensitive subfornical organ (SFO) may be a potential site that detects increases in plasma NaLac and mobilizes panic pathways since inhibiting the SFO blocks panic following NaLac in this model. Furthermore, since SFO neurons synthesize angiotensin II (A-II), we hypothesized that the SFO projects to the BLA and releases A-II to mobilizing panic responses in UCN/BLA-primed rats following NaLac infusions. To test this hypothesis, rats received daily bilateral injections of UCN or vehicle into the BLA daily for 3 days. Five to seven days following the intra-BLA injections, we microinjected either the nonspecific A-II type 1 (AT1r) and 2 (AT2r) receptor antagonist saralasin, or the AT2r-selective antagonist PD123319 into the BLA prior to the NaLac challenge. The UCN/BLA-primed rats pre-injected with saralasin, but not PD123319 or vehicle, had reduced NaLac-induced anxiety-associated behavior and panic-associated tachycardia and tachypnea responses. We then confirmed the presence of AT1rs in the BLA using immunohistochemistry which, combined with the previous data, suggest that A-II’s panicogenic effects in the BLA is AT1r dependent. Surprisingly, the SFO had almost no neurons that directly innervate the BLA, which suggests an indirect pathway for relaying the NaLac signal. Overall these results are the first to implicate A-II and AT1rs as putative neurotransmitter-receptors in NaLac induced panic-like responses in UCN/BLA-primed rats.
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影响因子：
1.7
作者：
KAISER, FC;PALMER, GC;HALLAM, C
通讯作者：
HALLAM, C
影响因子：
5.3
作者：
Hiyama, TY;Watanabe, E;Noda, M
通讯作者：
Noda, M
影响因子：
3.8
作者：
GALAVERNA, O;DELUCA, LA;EPSTEIN, AN
通讯作者：
EPSTEIN, AN
影响因子：
3.4
作者：
Kerr, DS;Bevilaqua, LRM;Cammarota, M
通讯作者：
Cammarota, M
影响因子：
10.6
作者：
Peskind, ER;Jensen, CF;Raskind, MA
通讯作者：
Raskind, MA