调控去甲肾上腺素能系统对防治创伤后应激障碍的影响

个体经历严重创伤性事件后可能会形成创伤后应激障碍(posttraumatic stress disorder, PTSD)。在创伤经历中形成的情绪记忆是以后发展为PTSD的重要病理机制。PTSD的形成涉及到情绪记忆的过度巩固, 而去甲肾上腺素能神经信号可增强情绪记忆的巩固和再巩固。因此, 在创伤记忆的巩固和再巩固期间阻断去甲肾上腺素能神经信号, 而在创伤记忆的消退期间增强去甲肾上腺素能神经信号, 可能会破坏和或抑制病理性的情绪记忆, 从而预防或治疗PTSD。     

Pharmacological antagonism of mouse-killing behavior in the olfactory bulb lesion-induced killer rat

Representative agents from all of the major classes of drugs that have been reported to be selective antagonists of spontaneous mouse-killing behavior (i.e., antidepres-sants, antihistamines, anticholinergics, and stimulants) were tested for their ability to antagonize the mouse-killing response in rats that became killers following removal of the olfactory bulbs (O.B. lesion-induced killer rat) and in spontaneous killers. All of the drugs tested selectively antagonized the killing behavior of both spontaneous and lesion-induced mouse-killing rats. Several drugs (i.e., imipramine, amitriptyline, d-amphetamine, and chlorpheniramine) were found to be significantly less potent antagonists of mouse killing in the 0.6. lesioned rat as compared to spontaneous killers. Since all of the drugs that exhibited significant differences in activity between the two models have been shown to possess the ability to elevate norepinephrine levels at receptor sites in the brain, alterations in noradrenergic systems may account for the differences in sensitivity that were observed in this study. The possibility that there may be a common neural substrate for mouse killing in the two models is discussed.