PubMed1974
These experiments have examined several aspects of analgesia produced by focal electrical stimulation of the brain. (1) Anatomical locus of analgesic effects: only stimulation of the mesencephalic central gray matter and periventricular gray matter greatly reduced or totally abolished responsiveness to all noxious stimuli employed. Stimulation of other brain areas increased jump threshold to electric shock (septal nuclei, dorsomedial thalamic nucleus) and sometimes even abolished responsiveness to tissue destructive pinch (ventral tegmentum, dorsomedial thalamic nucleus), but never eliminated resonding to radiant heat applied to the tail. Stimulation of the ventrobasal complex of the thalamus and the lateral hypothalamus produced little or no analgesia at all. (2) Magnitude of analgesia: stimulation of the central and periventricular gray matter produced analgesia equal to or greater than 10 mg/kg morphine on all tests. (3) Relationship to reward: stimulation-produced analgesia was found not to be casually related to the rewarding properties of the stimulation. Analgesia was often produced by stimulation at electrode sites which did not support self-stimulation behavior; and many animals self-stimulated at high rates but were not analgesic. (4) Relationship to seizure activity: electrographic or overt motor seizure activity was not related to stimulation-produced analgesia. (5) By analogy with the site and mechanism of morphine action, it is proposed that focal electrical stimulation activates a pain suppressive system concentrated in periventricular and periaqueductal regions and its activation reduces responsiveness to noxious stimuli, at least in part, by blocking transmission of nociceptive information through the spinal cord.