Johansson A K, Bergvall A H, Hansen S
Department of Psychology, Göteborg University, Sweden.
Behav Brain Res. 1999 Jul;102(1-2):17-29. doi: 10.1016/s0166-4328(98)00159-4.
Research on alcoholism have identified a subgroup in which the drinking problem is associated with high rates of violence, an impulsive disposition and signs of reduced serotonin functioning in the brain. The present study reports that male Wistar rats with ibotenic acid-induced (5 micrograms/0.5 microliter) neuron loss in the basal forebrain (ventral striatum, septal area and adjacent structures) showed behavioral and neurochemical signs not unlike this subtype of alcoholics. Thus, rats with this lesion exhibited excessive 6% alcohol drinking in a two-bottle choice test and showed augmentation of certain defensive behaviors, including defensive aggression and increased activity-during signal. In the punished drinking test, a passive avoidance task which taps psychological mechanisms underlying impulsivity [56], experimental rats were not different from sham-operated controls with regard to the number of punished licks, but punishment evoked less disruption of ongoing behavior in subjects with basal forebrain damage. The virtual absence of food hoarding in the face of normal feeding may constitute yet another sign of increased impulsivity, indicating as it does a diminished influence of future rewards on behavior. As expected, in view of ibotenic acid's selectivity for neuronal perikarya, the concentrations of dopamine, serotonin and norepinephrine were normal in the lesioned area. However, the levels of serotonin and norepinephrine in the cortex were reduced. A separate experiment examined the extent to which serotonin depletion alone reproduced the behavioral profile induced by basal forebrain neuron loss. However, measures of alcohol consumption, defensive behavior and impulsivity were not different from controls in rats given intracerebroventricular 5,7-DHT (150 micrograms/20 microliters), except for a modest increase in defensive aggression.
对酗酒问题的研究已经确定了一个亚组，在这个亚组中，饮酒问题与高暴力发生率、冲动性格以及大脑中血清素功能降低的迹象有关。本研究报告称，用鹅膏蕈氨酸（5微克/0.5微升）诱导基底前脑（腹侧纹状体、隔区及相邻结构）神经元损失的雄性Wistar大鼠表现出的行为和神经化学迹象与这类酗酒者亚型并无不同。因此，有这种损伤的大鼠在双瓶选择试验中过量饮用了6%的酒精，并表现出某些防御行为的增强，包括防御性攻击以及在信号期间活动增加。在惩罚性饮酒试验中，这是一种利用冲动背后心理机制的被动回避任务[56]，实验大鼠在惩罚性舔舐次数方面与假手术对照组没有差异，但惩罚对基底前脑损伤的受试者正在进行的行为造成的干扰较小。面对正常喂食时几乎没有食物囤积，这可能构成冲动增加的另一个迹象，因为这表明未来奖励对行为的影响减弱。正如预期的那样，鉴于鹅膏蕈氨酸对神经元胞体的选择性，损伤区域中多巴胺、血清素和去甲肾上腺素的浓度是正常的。然而，皮质中血清素和去甲肾上腺素的水平降低了。一项单独的实验研究了仅血清素耗竭在多大程度上重现了基底前脑神经元损失所诱导的行为特征。然而，除了防御性攻击略有增加外，给予脑室内5,7 -二羟色胺（150微克/20微升）的大鼠在酒精摄入量、防御行为和冲动性测量方面与对照组没有差异。
