Effects of D-galactose on the expression of hippocampal peripheral-type benzodiazepine receptor and spatial memory performances in rats.

The changes in spatial memory performances and the binding of hippocampal peripheral-type benzodiazepine receptor (PBR) induced by D-galactose (D-gal) were investigated in rats. The animals were randomly divided into two groups: saline-treated group and D-gal-induced aging group. All rats received 56 days of injection followed by 5 days of behavioral tests. The D-gal-induced aging rats presented significant impairment in water maze performance, compared with that in the saline-treated rats. A significant decrease in [3H]PK11195 binding in the synaptosomes from hippocampus in the D-gal-induced aging rats was observed, compared to that in the saline-treated rats. Meanwhile, the Scatchard analysis revealed that there was a decrease in Bmax, with no significant change in KD. Further analysis demonstrated that water maze performance was closely related to the PK11195 binding in all rats. These results suggest that D-gal decreased the density of PBR in hippocampal synaptosomes, which may be attributable to the progressive pathogenesis of aging in rats.

[Protective mechanism of tianmacuzhi granules in brain].

OBJECTIVE: To provide pharmacological evidence for the protective effects of Tianmacuzhi Granules (TMC) in mouse brain in a ischemia--reperfusion model. METHOD: Receptor binding test of NMDA receptor and M receptor in brain, GPx activity determination in brain and liver effected by different dose of TMC were performed. RESULT: TMC could reduce the NMDA receptor activity, increase the M receptor activity and GPx activity of cerebral cortex and hippocampus tissues significantly. CONCLUSION: TMC might antagonize ischemia-reperfusion injury of brain by reducing the glutamate neurotoxicity and increasing the function of cholinergic nerve and effects of anti-peroxidization in brain.

[Protection mechanism of huanshaodan decoction in the brain].

OBJECTIVE: To observe the protective effect of Huanshaodan (HSD) in mouse brain in a steady ischemia-reperfusion model. METHODS: Step-through experiment, receptor binding test and choline acetyl-transferase (CAT) activity determination was performed. RESULTS: After HSD treatment, mice made much less mistakes in step-through experiment than sham groups. Meanwhile the 3H-MK801 binding of cerebral cortex and hippocampus tissues was significantly decreased. CAT activity of cerebral cortex and hippocampus tissue were increased respectively. CONCLUSION: HSD might antagonize ischemia injury of brain through modulating excessive activation of glutamate N-methyl-D-Aspartic acid receptors.

Cysteine uptake and taurine biosynthesis in freshly isolated and primary cultured rat hepatocytes.

Analysis of the uptake and metabolism of [14C]cysteine in rat liver was undertaken using freshly isolated hepatocytes and hepatocytes maintained in primary culture. The uptake of [14C]cysteine by freshly isolated hepatocytes was by means of both saturable and non-saturable transport systems and the former system was thought to involve facilitated diffusion. The uptake of [14C]cysteine by hepatocytes maintained in primary culture for 24 h also consisted of non-saturated and saturated transport mechanisms. The magnitude of the saturable transport system in cultured hepatocytes was, however, much greater than that found in freshly isolated hepatocytes, and was considered to be operated by active transport. Both freshly isolated and primary cultured hepatocytes had cysteine sulphinic acid decarboxylase activity, but this enzyme activity in the latter cells was noticeably reduced in comparison with that found in freshly isolated hepatocytes. Hepatocytes maintained in primary culture produced not only radiolabelled taurine, but also radiolabelled cysteine sulphinic acid, hypotaurine and alanine when incubated with [14C]cysteine. The present results indicate that cultured hepatocytes actively transport cysteine as well as metabolizing cysteine to taurine via cysteine sulphinic acid and hypotaurine.

Preferential release of newly synthesized [(3)H]GABA from striatal slices to preloaded [(3)H]GABA.

The release of [(3)H]GABA which is newly synthesized from [(3)H]l-glutamic acid (GLU) has been examined using striatal slices obtained from the rat brain. It was found that 8-10% of [(3)H]GLU transported was converted to [(3)H]GABA during the incubation of striatal slices in the presence of nipecotic acid (5 x 10(?5) M). Nipecotic acid was added to the medium in order to prevent possible reuptake of [(3)H]GABA released during its synthesis, and it was found to have no significant effect on the formation of [(3)H]GABA from [(3)H]GLU as well as on the uptake of [(3)H]GLU. The application of high potassium (60 mM) stimulation exhibited a significant enhancement of the release of this newly synthesized [(3)H]GABA in a Ca(2+) dependent manner. Kinetic analysis revealed that the evoked release of newly synthesized [(3)H]GABA was approximately two times greater than that of previously-loaded [(3)H]GABA, whereas no significant difference was observed in the spontaneous release. An immobilization stress in water failed to affect the release of newly synthesized [(3)H]GABA from striatal slices despite the occurrence of a significant enhancement of GABA formation in this structure. These results suggest that newly synthesized GABA may be preferentially released from its nerve terminals in response to the excitation of neurons at least in the striatum as compared with previously accumulated GABA.