Hypothalamic self-stimulation and stimulation escape in relation to feeding and mating

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.

Publication types

  • Review

MeSH terms

  • Animals
  • Body Weight
  • Brain Mapping
  • Electric Stimulation
  • Feeding Behavior / physiology*
  • Female
  • Hydroxydopamines / pharmacology
  • Hypothalamus / drug effects
  • Hypothalamus / physiology*
  • Male
  • Neural Pathways
  • Phenylpropanolamine / pharmacology
  • Rats
  • Reinforcement, Psychology
  • Self Stimulation / physiology*
  • Sexual Behavior, Animal / physiology*
  • Stimulation, Chemical
  • Sympathetic Nervous System / anatomy & histology


  • Hydroxydopamines
  • Phenylpropanolamine