MacLennan A J, Drugan R C, Hyson R L, Maier S F, Madden J, Barchas J D
J Comp Physiol Psychol. 1982 Dec;96(6):904-12.
Inescapably shocked rats perform poorly on a two-way shuttle box escape task 24 hr after the shock. Because inescapably shocked rats become analgesic upon reexposure to a small amount of shock 24 hr after inescapable shock, they are likely to be analgesic during the shuttle box escape task. Subjects receiving an equivalent amount of escapable shock display neither the escape dificit nor the analgesia. Both the analgesia and the escape deficit respond in a similar fashion to the manipulation of a variety of other variables. These findings have led to the suggestion that the analgesia ("long-term analgesia") may cause the inescapable-shock-produced escape deficit. However, the present experiments demonstrated that two pituitary manipulations that completely eliminate the analgesia have no effect on the escape deficit. Both hypophysectomy and dexamethasone administration blocked the analgesic consequences of inescapable shock but did not reduce the magnitude of the escape deficit. Therefore, the long-term analgesia produced by inescapable shock does not cause the deficit in shuttle box escape performance displayed by inescapably shocked rats. Furthermore, these results indicate that the pituitary is not essential in the production of this escape deficit.
不可逃避电击的大鼠在电击后24小时的双向穿梭箱逃避任务中表现不佳。由于不可逃避电击的大鼠在不可逃避电击24小时后再次暴露于少量电击时会产生镇痛作用，它们在穿梭箱逃避任务期间可能处于镇痛状态。接受等量可逃避电击的大鼠既没有表现出逃避缺陷，也没有出现镇痛作用。镇痛作用和逃避缺陷对各种其他变量的操纵都有类似的反应。这些发现表明，镇痛作用（“长期镇痛”）可能导致不可逃避电击产生的逃避缺陷。然而，目前的实验表明，两种完全消除镇痛作用的垂体操作对逃避缺陷没有影响。垂体切除和地塞米松给药都阻断了不可逃避电击的镇痛后果，但并没有减少逃避缺陷的程度。因此，不可逃避电击产生的长期镇痛作用并不会导致不可逃避电击的大鼠在穿梭箱逃避任务中表现出的缺陷。此外，这些结果表明，垂体在这种逃避缺陷的产生中并非必不可少。
