The cerebral GABA-T activity of mice was determined by the modified coupled-enzyme spectroflourimctry

and the method was proved stable and feasible. The cerebral GABA degradation of mice in vitro was inhibited by the sera from the mice with hepatic coma induced by galactosamine. The supernatant of liver homogenate of both control and hepatic coma groups can inhibit the cerebral GABA degradation too. The inhibitory capacity is proportional to the volume of LHS added in certain conditions

and reaches a maximum inhibitory rate of 80%. The inhibition can not be relieved by pyridoxal phosphate.The inhibitory effector of cerebral GABA degradation has been regarded as liver specific or mainly presented in the liver since no appreciable inhibition was found after the addition of the supernaiants of kidney

heart

lung and spleen homogenates. The possible contribution of GABA degradation inhibition by LHS to the pathogenesis of hepatic encephalopathy has also been discussed