Abstract—Intracerebral microdialysis in Sprague-Dawley rats showed that a conditioned sound signal (CS+) previously reinforced by unavoidable electrocutaneous stimulation (fear conditioning test) is accompanied by an increased level of extracellular serotonin in the medial prefrontal cortex and provokes freezing behavior (fear index). A differential sound signal (CS–) not associated with pain stimulation (fear generalization test) also led to an increase in the level of extracellular serotonin in the medial prefrontal cortex but with decreased freezing behavior. These changes were absent in control group animals (same procedures, no electrocutaneus stimulation). Administration of the selective serotonin reuptake inhibitor fluoxetine (1 µmol) in the medial prefrontal cortex increased the elevation of extracellular serotonin levels caused by CS+ and CS–. This pharmacological exposure did not affect the freezing response to CS+ or CS– during the tests, however, it did cause longer periods of immobility between CS+ signals but not CS–. The data show that activation of the serotonin system of the medial prefrontal cortex by potentially threatening conditioned signals, but not neutral differential signals, takes part in the regulation of defensive behavior in the intervals between signals.

摘要-Sprague-Dawley大鼠的脑内微透析显示，先前通过不可避免的电皮肤刺激（恐惧条件测试）增强的条件声音信号（CS +）伴随着额前内侧皮层中细胞外血清素水平的升高，并激发了冰冻行为（恐惧指数） 。与疼痛刺激（恐惧泛化测试）无关的差分声音信号（CS–）也导致内侧前额叶皮层中细胞外血清素水平的增加，但冷冻行为降低。对照组动物不存在这些变化（相同的程序，无皮肤电刺激）。在内侧前额叶皮层中使用选择性5-羟色胺再摄取抑制剂氟西汀（1 µmol）可增加由CS +和CS–引起的细胞外血清素水平的升高。在测试期间，这种药理学接触不会影响对CS +或CS–的冷冻反应，但是，它确实会导致CS +信号之间的固定时间更长，但不会导致CS–信号固定。数据表明，通过潜在威胁条件信号而不是中性差分信号激活内侧前额叶皮层的5-羟色胺系统，参与了信号间隔中防御行为的调节。