Spiacci A, Sergio T de Oliveira, da Silva G S F, Glass M L, Schenberg L C, Garcia-Cairasco N, Zangrossi H
Department of Pharmacology, School of Medicine of Ribeirao Preto, University of São Paulo, Avenue Bandeirantes, 3900, Ribeirão Preto CEP: 14049-900, Brazil.
Department of Physiology, School of Medicine of Ribeirao Preto, University of São Paulo, Ribeirão Preto, Brazil.
Neuroscience. 2015 Oct 29;307:191-8. doi: 10.1016/j.neuroscience.2015.08.045. Epub 2015 Aug 28.
It has been proposed that spontaneous panic attacks are the outcome of the misfiring of an evolved suffocation alarm system. Evidence gathered in the last years is suggestive that the dorsal periaqueductal gray (dPAG) in the midbrain harbors a hypoxia-sensitive suffocation alarm system. We here investigated whether facilitation of 5-HT-mediated neurotransmission within the dPAG changes panic-like defensive reactions expressed by male Wistar rats submitted to a hypoxia challenge (7% O2), as observed in other animal models of panic. Intra-dPAG injection of 5-HT (20 nmol), (±)-8-hydroxy-2-(di-n-propylamino) tetralin hydrobromide (8-OH-DPAT) (8 nmol), a 5-HT1A receptor agonist, or (±)-2,5-dimethoxy-4-iodo amphetamine hydrochloride (DOI) (16 nmol), a preferential 5-HT2A agonist, reduced the number of upward jumps directed to the border of the experimental chamber during hypoxia, interpreted as escape attempts, without affecting the rats' locomotion. These effects were similar to those caused by chronic, but not acute, intraperitoneal administration of the antidepressant fluoxetine (5-15 mg/kg), or acute systemic administration of the benzodiazepine receptor agonist alprazolam (1-4 mg/kg), both drugs clinically used in the treatment of panic disorder. Our findings strengthen the view that the dPAG is a key encephalic area involved in the defensive behaviors triggered by activation of the suffocation alarm system. They also support the use of hypoxia-evoked escape as a model of respiratory-type panic attacks.
有人提出,自发性惊恐发作是进化而来的窒息警报系统误触发的结果。过去几年收集的证据表明,中脑导水管周围灰质背侧(dPAG)存在对缺氧敏感的窒息警报系统。我们在此研究了在dPAG内促进5-羟色胺介导的神经传递是否会改变雄性Wistar大鼠在缺氧挑战(7%氧气)下表现出的类似惊恐的防御反应,正如在其他惊恐动物模型中所观察到的那样。向dPAG内注射5-羟色胺(20纳摩尔)、5-羟色胺1A受体激动剂(±)-8-羟基-2-(二正丙基氨基)四氢萘溴化物(8-OH-DPAT)(8纳摩尔)或优先的5-羟色胺2A激动剂(±)-2,5-二甲氧基-4-碘苯丙胺盐酸盐(DOI)(16纳摩尔),可减少缺氧期间指向实验箱边界的向上跳跃次数,这种跳跃被解释为逃跑企图,且不影响大鼠的运动。这些效应与慢性(而非急性)腹腔注射抗抑郁药氟西汀(5 - 15毫克/千克)或急性全身注射苯二氮䓬受体激动剂阿普唑仑(1 - 4毫克/千克)所引起的效应相似,这两种药物在临床上均用于治疗惊恐障碍。我们的研究结果强化了这样一种观点,即dPAG是参与由窒息警报系统激活所触发的防御行为的关键脑区。它们还支持将缺氧诱发的逃跑作为呼吸型惊恐发作的一种模型。