Hoebel B G
Fed Proc. 1979 Oct;38(11):2454-61.
This review begins with James Olds' discovery that self-stimulation at various brain sites can be influenced by food intake or androgen treatment. It then describes our research designed to reveal the functional significance of self-stimulation. The evidence suggests that lateral hypothalamic self-stimulation is controlled by many of the same factors that control feeding. We believe this control is exerted by at least two neural mechanisms. One is the classical, medial hypothalamic satiety system. Another is an adrenergic system ascending from the midbrain to the lateral hypothalamus. Damage to either one can disinhibit self-stimulation and feeding, thus contributing to obesity. Some of our studies use rats with two electrodes, one that induces feeding and one that induces mating. There are two response levers in the test cage, one for self-stimulation and one for escape from automatic stimulation. With the feeding electrode, rats self-stimulated less and escaped more after a meal than before. The same shift occurred after an anorectic dose of insulin or the commercial appetite suppressant phenylpropanolamine. With the sex electrode the shift from reward to aversion occurred after ejaculation. The review ends with credit to James Olds for pioneering this line of research into the neuropsychology of reinforcement.
本综述始于詹姆斯·奥尔兹的发现,即不同脑区的自我刺激可受食物摄入或雄激素治疗的影响。接着描述了我们旨在揭示自我刺激功能意义的研究。证据表明,下丘脑外侧的自我刺激受许多与控制进食相同的因素调控。我们认为这种调控至少通过两种神经机制实现。一种是经典的下丘脑内侧饱腹感系统。另一种是从中脑向上延伸至下丘脑外侧的肾上腺素能系统。对其中任何一个系统的损伤都会解除对自我刺激和进食的抑制,从而导致肥胖。我们的一些研究使用带有两个电极的大鼠,一个电极诱发进食,另一个电极诱发交配。测试笼中有两个反应杆,一个用于自我刺激,另一个用于逃避自动刺激。使用进食电极时,大鼠进食后自我刺激减少,逃避增多,与进食前相比发生了同样的变化。给予厌食剂量的胰岛素或商业食欲抑制剂苯丙醇胺后也出现了同样的变化。使用性电极时,射精后会从奖励转变为厌恶。综述最后赞扬詹姆斯·奥尔兹开创了这一关于强化神经心理学的研究领域。