de Souza Armini Rubia, Bernabé Cristian Setúbal, Rosa Caroline Azevedo, Siller Carlos Antônio, Schimitel Fagna Giacomin, Tufik Sérgio, Klein Donald Franklin, Schenberg Luiz Carlos
Deparment of Physiological Sciences, Federal University of Espírito Santo, Vitória, ES, Brazil.
Department of Psychobiology, Federal University of São Paulo, São Paulo, SP, Brazil.
Psychoneuroendocrinology. 2015 Mar;53:136-47. doi: 10.1016/j.psyneuen.2014.12.022. Epub 2015 Jan 10.
Panic disorder patients are exquisitely and specifically sensitive to hypercapnia. The demonstration that carbon dioxide provokes panic in fear-unresponsive amygdala-calcified Urbach-Wiethe patients emphasizes that panic is not fear nor does it require the activation of the amygdala. This is consonant with increasing evidence suggesting that panic is mediated caudally at midbrain's dorsal periaqueductal gray matter (DPAG). Another startling feature of the apparently spontaneous clinical panic is the counterintuitive lack of increments in corticotropin, cortisol and prolactin, generally considered 'stress hormones'. Here we show that the stress hormones are not changed during DPAG-evoked panic when escape is prevented by stimulating the rat in a small compartment. Neither did the corticotropin increase when physical exertion was statistically adjusted to the same degree as non-stimulated controls, as measured by lactate plasma levels. Conversely, neuroendocrine responses to foot-shocks were independent from muscular effort. Data are consonant with DPAG mediation of panic attacks.
惊恐障碍患者对高碳酸血症极为敏感且具有特异性。在恐惧无反应的杏仁核钙化的乌-维二氏病患者中，二氧化碳引发惊恐这一现象表明，惊恐既不是恐惧，也不需要杏仁核的激活。这与越来越多的证据一致，这些证据表明惊恐是由中脑背侧导水管周围灰质（DPAG）在尾部介导的。明显自发的临床惊恐的另一个惊人特征是，通常被认为是“应激激素”的促肾上腺皮质激素、皮质醇和催乳素反而没有增加，这与直觉相反。在这里，我们表明，当在小隔间刺激大鼠以防止其逃脱时，DPAG诱发惊恐期间应激激素没有变化。通过血浆乳酸水平测量，当体力消耗在统计学上调整到与未刺激的对照组相同程度时，促肾上腺皮质激素也没有增加。相反，对足部电击的神经内分泌反应与肌肉努力无关。这些数据与DPAG介导惊恐发作一致。
