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本文应用同位素示踪、脑片离体培育和侧脑室注射的方法,在体外和体内研究了惊厥剂青霉素和抗惊厥剂苯巴比妥钠对小白鼠全脑切片积聚~3H-GABA的影响。结果表明:(1)在含6.70—13.40×10~(-4)mol/L的苄青霉素钾(PG)100μl或19.60—39.20×10~(-4)mol/L的苯巴比妥钠(PhB)50μl的培育液(2ml)中,小鼠全脑切片对~3H-GABA的积聚作用明显降低(P<0.05)。6.70×10~(-4)mol/L的PG100μl和39.20×10~(-4)mol/L的PhB50μl同时注入培育液(2ml)时,脑片对~3H-GABA的积聚比PG单独试验时稍有升高。(2 )小鼠侧脑室注射20μl的 3.35×10~(-2)mol/L的PG可引起强烈的惊厥,脑片上的~3H-GABA积聚减少(P>0.05);脑室内注射10μl的3.88×10~(-2)mol/L的PhB能抗惊厥,也使~3H-GABA在脑片上的积聚减少(P>0.05);脑室内同时注射PG和PhB,使~3H-GABA在脑片上的积聚恢复正常。以上结果提示:青霉素可通过竞争突触后膜和神经末梢上的GABA受体,阻断GA-BA的突触后抑制效应及抑制GABA释放,显示惊厥作用;苯巴比妥钠也可和突触后膜上的GABA受体结合,产生GABA样作用或激活GABA受体,起抗惊厥作用。
In this paper, isotope tracing, brain slices in vitro and lateral ventricle injection method in vitro and in vivo studies penicillin convulsant and anticonvulsant phenobarbital sodium on the accumulation of ~ 3H-GABA whole brain slices. The results showed that: (1) In the presence of 100μl of penicillin potassium (PG) containing 6.70-13.40 × 10 -4 mol / L or 19.60-39.20 × 10 -4 mol / L of phenobarbital sodium PhB) 50μl culture medium (2ml), the accumulation of ~ 3H-GABA in mouse brain slices was significantly reduced (P <0.05). The accumulation of ~ 3H-GABA in brain slices was higher than that in PG alone when PG100μl of 6.70 × 10 -4 mol / L PG and 50μl PhB of 39.20 × 10-4 mol / L were simultaneously injected into the culture medium (2 ml) Slightly higher. (2) Injection of 20μl of 3.35 × 10 ~ (-2) mol / L PG into the lateral ventricle of mice resulted in a strong convulsion, a decrease of ~ 3H-GABA accumulation in brain slices (P> 0.05); intraventricular injection of 10μl of 3.88 × 10 -2 mol / L PhB could inhibit convulsion and reduce the accumulation of ~ 3H-GABA in brain slices (P> 0.05). PG and PhB were simultaneously injected into the brain to make ~ 3H-GABA on the brain slices The accumulation returned to normal. The above results suggest that penicillin can induce convulsion by competing with GABA receptors on the postsynaptic membrane and nerve endings to block the postsynaptic inhibitory effect of GA-BA and inhibit the release of GABA. The GABA receptor on the posterior membrane binds to produce GABA-like activity or activate GABA receptors for anticonvulsant effects.