Subject(s)
Electroencephalography , Enkephalins/physiology , Sleep Deprivation/physiology , Sleep, REM/physiology , Animals , Cerebral Cortex/drug effects , Cerebral Cortex/physiopathology , Dose-Response Relationship, Drug , Electroencephalography/drug effects , Electroshock , Glycopeptides/pharmacology , Leucine/analogs & derivatives , Leucine/pharmacology , Male , Mice , Mice, Inbred Strains , Neprilysin/antagonists & inhibitors , Nitrous Oxide/pharmacology , Rats , Rats, Inbred Strains , Sleep, REM/drug effects , Substance Withdrawal Syndrome/physiopathology , Thiorphan/pharmacologyABSTRACT
beta-Endorphin levels in the whole rat brain were not changed during acute (25 min) or chronic (48 h) exposure of rats to N2O. However, a significant decrease of beta-endorphin was found in the whole brain, brain stem and subcortex during the withdrawal from chronic exposure to N2O. It has been suggested that decrease of beta-endorphin levels during N2O withdrawal could be ascribed to unspecific stress accompanying drug withdrawal. Decrease of central beta-endorphin during N2O withdrawal might have a significant modulatory effect on transmitter balance, neuronal excitability and corresponding withdrawal behaviour. Furthermore, the decrease of beta-endorphin levels in the whole brain during N2O withdrawal might contribute to the postanaesthesia N2O-excitatory syndrome in humans. This might explain the known therapeutic effect of the opioid drug, meperidine on the excitatory N2O withdrawal phenomena during recovery from N2O anaesthesia in man.
