Frankland P W, Yeomans J S
Department of Psychology, University of Toronto, Ontario, Canada.
Behav Neurosci. 1995 Aug;109(4):669-80. doi: 10.1037//0735-7044.109.4.669.
Startle amplitudes are increased when acoustic startle responses are elicited in the presence of a stimulus that has previously been paired with shock. This "fear-potentiated" startle response appears to be mediated via the caudal ventral amygdalofugal pathway to the brainstem. Electrical stimulation of this pathway evokes unconditioned startlelike responses. Collision tests have shown that a monosynaptic connection from amygdala to midbrain mediates these responses. Collision tests here localize these synapses mediating electrically evoked startlelike responses to the rostrolateral midbrain in awake rats. To test whether rostrolateral midbrain synapses also mediate fear-potentiated startle, we lesioned cells in these sites with ibotenic acid. These lesions completely blocked fear potentiation of acoustic startle. These same lesions did not block potentiation of startle by d-amphetamine (6 mg/kg).
当在先前已与电击配对的刺激存在的情况下引发听觉惊吓反应时,惊吓幅度会增加。这种“恐惧增强”的惊吓反应似乎是通过尾侧腹侧杏仁核传出通路介导至脑干的。对该通路进行电刺激会诱发无条件惊吓样反应。碰撞试验表明,从杏仁核到中脑的单突触连接介导了这些反应。此处的碰撞试验将介导电诱发惊吓样反应的这些突触定位在清醒大鼠的嘴侧外侧中脑。为了测试嘴侧外侧中脑突触是否也介导恐惧增强的惊吓反应,我们用鹅膏蕈氨酸损伤了这些部位的细胞。这些损伤完全阻断了听觉惊吓的恐惧增强。相同的损伤并未阻断右旋苯丙胺(6毫克/千克)对惊吓的增强作用。