Frontal cortex lesions block the opioid and nonopioid hypoalgesia elicited by brief shocks but not the nonopioid hypoalgesia elicited by long shocks.

Previous research (Grau, 1987a, 1987b) suggests that forebrain systems play an essential role in the hypoalgesia observed after brief shock but not long shock. Additional research has shown that pentobarbital anesthesia and decerebration block the hypoalgesia observed after 3 brief (0.75-s) shocks but not the hypoalgesia observed after 3 long (25-s) shocks. This is a study of whether a specific forebrain lesion, a frontal cortex lesion, would have a similar impact on hypoalgesia induced by brief (0.75 s) and long (25-s) shocks. Frontal cortex lesions, like decerebration and pentobarbital anesthesia, eliminated the hypoalgesia observed after brief but not long shocks. Because other research suggests that the stress of surgery may influence whether the hypoalgesia elicited by shock is opioid or nonopioid, the 2nd experiment was to examine whether the sham operation per se alters the form of the hypoalgesia observed after brief shock. It does not; in the sham-treated subjects, brief shock induced the usual transient nonopioid hypoalgesia followed by prolonged opioid hypoalgesia. These data suggest that frontal cortex lesions block nonopioid and opioid hypoalgesia observed after brief shock.