ZD7288 inhibits the synaptic transmission in the pathway from perforant pathway fibers to CA3 region in rat hippocampus / 药学学报

<p><b>AIM</b>To study the effect of ZD7288 on synaptic transmission in the pathway from perforant pathway (PP) fibers to CA3 region in rat hippocampus.</p><p><b>METHODS</b>The extracellular recording technique in vivo was used to record the CA3 region field potentials. High-performance liquid chromatography (HPLC) with fluorescence detection was applied to measure the content of amino acids in hippocampal tissues. The effect of ZD7288 and CsCl on the amplitudes of population spike (PS) in CA3 region evoked by stimulation (0.5 Hz) of the perforant pathway (PP) fibers, and the content of amino acids in hippocampal tissue were observed.</p><p><b>RESULTS</b>Microinjection of ZD7288 (20, 100 and 200 nmol) and CsCl (1, 5 and 10 micromol) into CA3 region decreased the population spike (PS) amplitudes in a dose-dependent manner. The inhibitory effects appeared at 5 min after microinjection and lasted at least 90 min. In those rats treated with ZD7288 (100 nmol), the contents of glutamate, aspartate, glycine and GABA decreased significantly as compared to those of saline control (all P < 0.01, except P < 0.05 for that of glycine). A similar decrease in the contents of amino acids was observed when the rats were microinjected with CsCl (5 micromol). CONCLUSION; ZD7288 could obviously inhibit synaptic transmission in the pathway from PP fibers to CA3 region in rat hippocampus, and this action of ZD7288 may be associated with altered contents of amino acids.</p>

Effect of kang naoxueshuan tablet on protecting ischemic brain injury in rats / 中国中西医结合杂志

<p><b>OBJECTIVE</b>To observe the protective effect of Kang Naoxueshuan Tablet (KNT) on ischemic brain injury in rats, and explore its possible mechanism.</p><p><b>METHODS</b>Rats were administrated with KNT twice per day for successive 14 days. Rat model of acute focal cerebral ischemia was established by middle cerebral artery occlusion (MCAO) with a nylon suture inserted through the right internal carotid artery to occlude the beginning of middle cerebral artery. After 24 hrs MCAO, the neurological deficit and the volume of cerebral infarct were observed, and the effect of KNT on the thrombosis of rats in vitro, platelet aggregation and blood viscosity were also determined.</p><p><b>RESULTS</b>KNT could alleviate volume of cerebral infarct caused by focal cerebral ischemia in a dose-dependent manner and improve neurological symptoms. The volume of cerebral infarct was 11. 18 +/- 3. 35% , 14. 60 +/- 7.00% and 15. 37 +/- 7. 21% in the high, middle and low-dose groups, respectively, and they were decreased 59. 36% , 46. 93% and 44. 13% than that in the model group 27. 51 +/- 4. 71% (P <0. 01 ). The wet and dry weigh of thrombosis in vitro of the three different dose groups were significantly decreased, and they were significantly different than that of the model group (P <0. 05, P <0. 01). KNT could significantly inhibit platelet aggregation induced by ADP and decrease blood viscosity, but it had no effect on plasma viscosity and hematocrit.</p><p><b>CONCLUSION</b>KNT has significant protective effect on ischemia, the mechanism is relateed to the improvement of blood viscosity and inhibiti on of platelet aggregation. But the exact mechanisms need to be probed into deeply.</p>