Powell D A, Chachich M, Murphy V, McLaughlin J, Tebbutt D, Buchanan S L
Neuroscience Laboratory (151A), VA Medical Center, Columbia, South Carolina 29201, USA.
Behav Neurosci. 1997 Oct;111(5):1056-74. doi: 10.1037//0735-7044.111.5.1056.
Damage to the amygdala or medial prefrontal cortex (mPFC) produces deficits in learned autonomic adjustments. Whether connections between these 2 structures are necessary for acquiring classically conditioned heart rate (HR) decelerations was studied. Connections between them were interrupted by unilateral lesions of the mPFC and amygdala, but on opposite sides of the brain. One experiment focused on the mPFC and amygdala central nucleus and a second on the mPFC and amygdala basolateral complex. Bilateral lesions of either structure disrupted the HR conditioned response. The response of the 2 crossed lesioned groups also was smaller than that of the sham-operated and unilateral lesioned groups, but significant conditioned stimulus-evoked bradycardia occurred in both, suggesting that although interactions between the amygdala and mPFC may normally occur during associative emotional responding, these connections are not necessary for the acquisition of conditioned bradycardia.
杏仁核或内侧前额叶皮质(mPFC)受损会导致习得性自主调节功能出现缺陷。本研究旨在探讨这两个结构之间的连接对于获得经典条件性心率(HR)减速是否必要。通过在大脑相对两侧对mPFC和杏仁核进行单侧损伤来中断它们之间的连接。一项实验聚焦于mPFC与杏仁核中央核,另一项则聚焦于mPFC与杏仁核基底外侧复合体。对这两个结构中的任何一个进行双侧损伤都会破坏HR条件反应。两个交叉损伤组的反应也比假手术组和单侧损伤组小,但两组均出现了显著的条件刺激诱发的心动过缓,这表明尽管杏仁核和mPFC之间的相互作用通常可能在联想性情绪反应过程中发生,但这些连接对于获得条件性心动过缓并非必要。