The GABA hypothesis of hepatic encephalopathy (H.E) was supported by many reports with regard to its content

metabolism

permeability against blood brain barrier

etc. But the experimental data which reflect the changes of GABA recep-ptors in H.E. were limitted only to rabbits and rats.We established a method with a small concentration of membrane protein (50ug/ 0.2ml) for the analysis of GABA receptors with satisfactory results (NSB

TB

SB: CV<10%; SB/TB: 66-30% at the concentrations of 3H-GABA 11

28-225.5 pmo-le/L). The synaptic membrane prepared from the brain of a single mouse was sufficient for an experiment

thus

avoiding the pooling of brain extracts from several mice.Our results showed for the first time that mice with H.E were associated with a loss of low-affinity receptors in Triton treated synaptic membrane

but the densities of the active binding sites were not changed. The increase of the affinities of GABA receptors in fresh and Triton treated synaptic membrane suggests the increase of GABA synaptic transmissional activity in mice with H.E. Boin the amount of protein extracted from the fresh membrane and its inhibitory activities as GABA-modulin of mice

with H.E. were significantly lower than those of the cont-rol(p<0.01) . These may explain partly for the increase of the affinities of GABA receptors in mice with H.E