Abstract
The release of corticotrophin-releasing factor (CRF) in the human has been shown to be under a direct inhibitory control derived from the locus coeruleus (LC). Opioids have been shown to inhibit CRF release. Based on our hypothesis of deranged opioid-noradrenergic activity in Tourette's syndrome (TS), we studied the effect of a naloxone challenge on plasma cortisol levels in 6 TS patients. In all patients naloxone produced a significant rise in cortisol secretion. These results support our hypothesis and suggest that in TS, noradrenergic LC receptors involved in CRF release are supersensitive as a result of chronic excessive endorphinergic activity.