论文部分内容阅读
采用急性海马脑片,分别于长时程增强诱导前、诱导后早期及晚期进行苯巴比妥预干预、早期及晚期干预,检测其对长时程增强诱导与维持两阶段的影响及其可能机制。膜片钳技术检测发现苯巴比妥预干预可抑制长时程增强的诱导,但对双脉冲易化现象无明显影响,而早期及晚期干预未能抑制长时程增强,提示苯巴比妥可能通过突触后机制抑制长时程增强的诱导,但对维持阶段无明显影响。对长时程增强关键蛋白的Western blot检测发现,预干预组p-CaMKⅡ表达降低,而CaMKⅡ表达无变化;早期及晚期干预组CaMKⅡ及p-CaMKⅡ表达均无明显变化,提示苯巴比妥可能通过降低突触后CaMKⅡ磷酸化抑制诱导过程,其对维持阶段无抑制作用可能与对CaMKⅡ自我磷酸化及新蛋白质合成无抑制作用密切相关。
Acute hippocampal slices were used in the early and late induction of phenobarbital pre-induction, early and late intervention, respectively, before and after induction of long-term potentiation to detect the impact of long-term potentiation induction and maintenance of two stages and its possible mechanism. Patch clamp testing showed that pretreatment with phenobarbital suppressed the induction of long-term potentiation but had no obvious effect on the phenomenon of double-pulse facilitated, whereas early and late intervention failed to inhibit long-term potentiation, suggesting that phenobarbital May inhibit the induction of long-term potentiation through the postsynaptic mechanism, but has no significant effect on the maintenance phase. Western blot analysis of the key proteins of long-term potentiation found that pre-intervention group p-CaMK Ⅱ expression decreased, while CaMK Ⅱ expression did not change; early and late intervention group CaMK Ⅱ and p-CaMK Ⅱ expression did not change significantly, suggesting that phenobarbital may By inhibiting the induction of post-synaptic CaMKII phosphorylation, its inhibitory effect on the maintenance phase may be closely related to the inhibition of CaMKII autophosphorylation and new protein synthesis.