Vergnes M, Penot C
Brain Res. 1976 Mar 5;104(1):107-19. doi: 10.1016/0006-8993(76)90650-8.
Shock-induced fighting behavior, flinch-jump thresholds and locomotor open-field activity were studied following dorsal and medial raphe lesions in rats. Attack scores were raised for low-intensity shocks (1 mA) only, whereas they remained unchanged for shocks of higher intensity (2 mA), as compared to controls. The jump threshold is decreased in raphe lesioned animals, but the flinch threshold is unchanged. Physostigmine (0,2-0,5 mg/kg) reduces the lesion-induced hyperreactivity: locomotor open-field activity is reduced to a greater extent than in the controls, and habituation to the open-field situation is restored. Doses of physostigmine (e.g. 0,2 mg/kg), that do not modify shock-induced aggression in controls, reduce aggression in lesioned animals to the level shown by controls for low-intensity shocks. In conclusion, shock-induced aggression is not directly dependent on a serotonergic brain mechanism. The behavioral changes observed are related to the hyperreactivity induced by raphe lesions. This hyperreactivity presumably results from a reduced activity of cholinergic brain mechanisms.
在大鼠中，研究了中缝背核和中缝内侧核损伤后休克诱发的战斗行为、惊跳阈值和自发活动。与对照组相比，仅低强度电击（1毫安）时攻击分数升高，而高强度电击（2毫安）时攻击分数保持不变。中缝核损伤动物的跳跃阈值降低，但惊跳阈值不变。毒扁豆碱（0.2 - 0.5毫克/千克）可降低损伤诱导的高反应性：自发活动比对照组有更大程度的降低，并且恢复了对旷场环境的适应。在对照组中不改变电击诱发攻击行为的毒扁豆碱剂量（例如0.2毫克/千克），可将损伤动物的攻击行为降低至对照组低强度电击时的水平。总之，电击诱发的攻击行为并不直接依赖于脑内的5-羟色胺能机制。观察到的行为变化与中缝核损伤诱导的高反应性有关。这种高反应性可能是由于脑内胆碱能机制活动降低所致。
