| 摘要: | 摘 要 本研究以黑白室及舉臂式十字形迷宮誘發動物焦慮模式，探討黃連粗抽物及小蘗鹼之抗焦慮作用；並測定腦幹單胺與其代謝物濃度及併用改變 GABAergic與serotonergic system 神經活性藥物，以探討小蘗鹼之抗焦慮作用機轉。 結果顯示，口服黃連甲醇粗抽物和小蘗鹼(0.1, 0.5g/kg)均可延長小鼠在黑白室之白室滯留時間及減少黑室之滯留時間並增加兩室間的穿梭次數；且均可增加小鼠在舉臂式十字形迷宮之開放臂的滯留時間及進入次數，並減少在封閉臂之滯留時間及進入次數。口服黃連甲醇粗抽物及小蘗鹼(0.5g/kg)均會延長hexobarbital誘發之睡眠時間及降低大鼠運動量。在高速液相層析法測定中，口服小蘗鹼(0.1, 0.5g/kg)均可減少腦幹內NE、DA、5-HT之濃度及增加VMA、HVA、5-HIAA之濃度。小蘗鹼0.1g/kg可拮抗DOI、WAY-100635、8-OH DPAT誘發之焦慮作用；及增強BUS、p-MPPI、RIT之抗焦慮作用。 綜合以上結果，顯示黃連及小蘗鹼 0.1 g/kg不論黑白室或舉臂式十字形迷宮誘發小鼠焦慮模式中均具明顯之抗焦慮作用，小蘗鹼之抗焦慮作用機轉可能與活化突觸前5-HT1A autoreceptors及降低突觸後5-HT1A及5-HT2 受體之活性，進而減少腦幹中5-HT之濃度有關。; ABSTRACT The present study was attempted to investigate the anxiolytic effects of the Methanol extract of Coptis rhizome (CRMEOH) or berberine (BER) by means of the black and white test and the elevated plus-maze. We further demonstrated the anxiolytic mechanism of BER by combining with DIZ, serotonergic agonists or antagonists,and measuring the concentrations of monoamines and their metabolites in the brain stem. In the black and white test, CRMEOH or BER(0.1 and 0.5 g/kg, p.o.) increased the time spent in the white compartment and total change between two compartment, and decreased the time spent in the black compartment. CRMEOH or BER(0.1 and 0.5 g/kg, p.o.) increased the arm entries and the time spent on the open arms, and decreased the arm entries and the time spent on the closed arms in the elevated plus-maze. On the other hand, CRMEOH(0.5 g/kg, p.o.) or BER(0.5 g/kg, p.o.) decreased the horizontal activity and prolonged the hexobarbital-induced sleeping times. BER at 0.1,0.5 g/kg decreased the concentrations of NE, DA, 5-HT and increased the concentrations of VMA, HVA, 5-HIAA in the brain stem. BER also attenuated the anxiogenic effect of DOI, 8-OH DPAT and WAY-100635 and enhanced the anxiolytic effect of BUS, p-MPPI, and RIT in the elevated plus-maze. From these results, both CRMEOH and BER at 0.1g/kg had the anxiolytic effect in the black and white test and the elevated plus-maze in rodents. The anxiolytic mechanisms of BER might be due to decrease the concentration of 5-HT in the brain stem via activating somatodendritic 5-HT1A autoreceptors and inhibiting postsynaptic 5-HT1A and 5-HT2 receptors. |
