Kelsey J E
Behav Neural Biol. 1983 Mar;37(2):326-31. doi: 10.1016/s0163-1047(83)91406-1.
This study examined the role of neurochemical changes produced by inescapable shock, specifically the depletion of norepinephrine (NE) and enhancement of acetylcholine (ACh), in mediating subsequent inescapable shock-induced deficits in escape acquisition in rats. Enhancement of these neurochemical changes by injections of the NE synthesis inhibitor, FLA-63 (10 mg/kg), or the anticholinesterase, eserine sulphate (3 X 0.5 mg/kg), during the inescapable shock enhanced the subsequent escape deficits observed 3 days later. In contrast, these drugs had no effect on the subsequent escape behavior of rats that were not exposed to inescapable shock. Since these effects could not be attributed to carry-over or state-dependent effects of the drugs, these data suggest that the magnitude of the escape deficit produced by prior inescapable shock is dependent on the magnitude of the initial inescapable shock-induced changes in NE and ACh.
本研究考察了不可逃避电击所产生的神经化学变化的作用，具体而言，即去甲肾上腺素（NE）的耗竭和乙酰胆碱（ACh）的增强，在介导随后不可逃避电击诱发的大鼠逃避习得缺陷中的作用。在不可逃避电击期间，通过注射NE合成抑制剂FLA - 63（10毫克/千克）或抗胆碱酯酶硫酸新斯的明（3×0.5毫克/千克）来增强这些神经化学变化，会增强3天后观察到的后续逃避缺陷。相比之下，这些药物对未遭受不可逃避电击的大鼠的后续逃避行为没有影响。由于这些效应不能归因于药物的残留或状态依赖性效应，这些数据表明，先前不可逃避电击产生的逃避缺陷程度取决于初始不可逃避电击诱发的NE和ACh变化的程度。
