Hitchcock J M, Sananes C B, Davis M
Department of Psychiatry, Yale University School of Medicine, New Haven, Connecticut.
Behav Neurosci. 1989 Jun;103(3):509-18. doi: 10.1037//0735-7044.103.3.509.
Bilateral electrolytic lesions of the central, but not the lateral, nucleus of the amgydala blocked shock sensitization of startle (the increase in startle produced by presentation of ten 0.6-mA footshocks in rapid succession). Lesions of the central nucleus also decreased reactivity to shock (jumping and flinching) during shock presentation. However, this decrease in reactivity cannot account for the blockade of shock sensitization, because when a higher shock intensity (1.0 mA) was used, producing equivalent reactivity to that of controls at 0.6 mA, central nucleus lesions still blocked shock sensitization. Moreover, lesions of the caudal part of the ventral amygdalofugal pathway, which carries central nucleus efferents to the startle reflex pathway, also blocked shock sensitization. It is hypothesized that shock activates the central nucleus of the amygdala, which increases startle through modulation of the startle pathway. Activation of the amygdala by shock may be the unconditioned response relevant for fear conditioning.
双侧杏仁核中央核而非外侧核的电解损伤阻断了惊吓的电击敏化(连续快速呈现十次0.6毫安足底电击所产生的惊吓增强)。中央核损伤也降低了电击呈现期间对电击的反应性(跳跃和退缩)。然而,这种反应性的降低并不能解释电击敏化的阻断,因为当使用更高的电击强度(1.0毫安)时,产生的反应性与对照组在0.6毫安时相当,中央核损伤仍然阻断了电击敏化。此外,腹侧杏仁核传出通路尾部的损伤,该通路将中央核传出纤维传导至惊吓反射通路,也阻断了电击敏化。据推测,电击激活杏仁核中央核,其通过调节惊吓通路来增强惊吓。电击对杏仁核的激活可能是与恐惧条件反射相关的无条件反应。