【摘要】 应用细胞内生物电记录技术,观察到可乐定使离体豚鼠腹腔神经节突触前神经末梢自发的微小兴奋性突触后电位(mEPSP)频率减少,使刺激突触前神经引起的乙酰胆硷(Ach)量子释放的失败机率增加,平均量子含量减少,但对平均量子大小无影响,表明可乐定能减少突触前神经末梢Ach的量子性释放,但对Ach在囊泡中的平均含量无影响。本工作提示可乐定对交感神经节突触传递的阻断作用与可乐定减少突触前神经末梢Ach量子释放有关。更多还原

【Abstract】 The work was carried out to investigate the effects of clonidine on Ach quantal release of presynaptic nerve terminals in guinea pig celiac ganglia in vitro by means of intracellular recording technique. After perfusion of celiac ganglia with clonidine ( 10μmol/L ) for 7 ~10 min, the frequency of spontaneous miniature excitatory postsynaptic potentials ( mEPSP ) which was increased by high K+ (15 mmol/L ) , diminished about 35% with little change in amplitude. Under condition of low Ca2+( 0.5mmol/L )/high Mg2+( 5.5mmol/L ) presynaptic nerve was repetitively stimulated by 200 pulses ( 1 Hz), the failure number of EPSP increased from 82 to 145 in 200 stimuli and the quantal content ( m ) decreased about 62% with little change in quantal size ( q ) under clonidine ( 10μmol/L ) action. It is indicated that clonidine can decrease Ach auantal release from presynaptic nerve terminals without effecting Ach content in vesicles, and is one of the mechanisms for depressant effect of clonidine on synaptic transmission of the sympathetic ganglia.更多还原