[Relevance of brain prostaglandins to central effects of l-tetrahydropalmatine].
l-THP isa central depressant. It caused a marked sedation in various animals at 20—40 mg/kg (ip) and a profound sedation with catalepsy in rats at 70—100 mg/kg ( ip) . In this paper the interaction between brain prostaglandins (PGs) and l-THP was studied. 
 After ip l-THP10 mg/kg, the spontaneous locomotor activities (walking, washing and rearing) of rats were decreased, but no catalepsy was found. Previous intraventricular injection (icv) of PGE or PGFpotentiated significantly the depression on the spontaneous locomotor activities of l-THP and induced catalepsy. However, when the brain PGs level had been lowered by ip indomethacin 20 mg/kg×2, the depression of the locomotor activities caused by l-THP 10 mg/kg was not diminished, and catalepsy was facilitated. 
 The radioimmunoassay (sensitivity 0.01 ng) was used for measuring PGE or PGF in brain tissues. In rats or mice given ip l-THP 100 mg/kg, a considerable increment of brain PGF accompanying a profound central effects was observed. The endogenous biosynthesis of PGs in cortex homogenate was not influenced by l–THP (mice, ip 100 mg/kg) and (rats, mM), but was inhibited by indomethacin. The PGs levels in rabbits' CSF were not affected by im l-THP 40 mg/kg. 
 It is deduced that the central inhibitory effects of l-THP is not directly related to brain PGs.