Herdade Karina Costa Paes, Strauss Christiana Villela de Andrade, Zangrossi Júnior Hélio, Viana Milena de Barros
Laboratório de Psicofarmacologia, FFCLRP, Universidade de São Paulo, 14040-901 Ribeirão Preto, Brazil.
Behav Brain Res. 2006 Sep 25;172(2):316-23. doi: 10.1016/j.bbr.2006.05.021. Epub 2006 Jun 27.
In the last years, the role played by the medial nucleus of the amygdala (MeA) in the modulation of fear- and anxiety-related behaviors has been increasingly investigated. This nucleus plays an important role in the processing of predator odor-induced defensive reactions, i.e. freezing and risk-assessment behaviors. Immunohistochemical evidence also indicates that the MeA may be involved in the regulation of escape, a defensive behavior related to panic attacks. In this study, we further addressed this question by investigating the effects of the reversible inactivation of the nucleus on escape behavior generated in male Wistar rats by two different aversive stimuli, electrical stimulation of the dorsal periaqueductal gray matter (dPAG) and exposure to one of the open arms of the elevated T-maze. Results showed that intra-MeA administration of either the reversible sodium channel blocker lidocaine (34 nmol/0.2 microl) or the GABA(A) receptor agonist muscimol (0.22 nmol/0.2 microl) raised the threshold of aversive electrical stimulation, increasing the amount of current that applied to the dPAG evokes escape, an antiaversive effect. Local microinjection of muscimol (0.22 nmol/0.2 microl) inhibited escape behavior in the elevated T-maze, also suggesting an antiaversive effect. In this latter test, muscimol did not affect inhibitory avoidance, a behavior associated with generalized anxiety disorder. Muscimol effect in the elevated T-maze was independent of changes in general exploratory activity as measured in an open-field. Taken together, our data corroborate previous evidences suggesting that the MeA is involved in the modulation of escape. Dysfunction of this regulatory mechanism may be of relevance in the genesis/maintenance of panic disorder.
在过去几年中，杏仁核内侧核（MeA）在调节恐惧和焦虑相关行为中所起的作用得到了越来越多的研究。该核在处理捕食者气味诱发的防御反应，即僵住和风险评估行为中起着重要作用。免疫组织化学证据还表明，MeA可能参与了逃跑行为的调节，逃跑是一种与惊恐发作相关的防御行为。在本研究中，我们通过研究该核的可逆失活对雄性Wistar大鼠由两种不同厌恶刺激所产生的逃跑行为的影响，进一步探讨了这个问题，这两种厌恶刺激分别是对背侧导水管周围灰质（dPAG）进行电刺激以及暴露于高架T迷宫的一个开放臂中。结果显示，向MeA内注射可逆性钠通道阻滞剂利多卡因（34 nmol/0.2微升）或GABA(A)受体激动剂蝇蕈醇（0.22 nmol/0.2微升）均提高了厌恶电刺激的阈值，增加了施加于dPAG诱发逃跑所需的电流量，这是一种抗厌恶作用。向MeA局部微量注射蝇蕈醇（0.22 nmol/0.2微升）可抑制高架T迷宫中的逃跑行为，这也表明了其抗厌恶作用。在后者的测试中，蝇蕈醇并不影响抑制性回避，抑制性回避是一种与广泛性焦虑障碍相关的行为。蝇蕈醇在高架T迷宫中的作用与在旷场中测量的一般探索活动的变化无关。综上所述，我们的数据证实了先前的证据，表明MeA参与了逃跑行为的调节。这种调节机制的功能障碍可能与惊恐障碍的发生/维持有关。
