Cx43 蛋白在丰富环境改善脑外伤大鼠学习记忆能力中的作用

目的观察Cx43 蛋白在丰富环境改善脑外伤(TBI)大鼠学习记忆能力中的作用。方法选用成年Sprague-Dawley 大鼠，采用液压颅脑损伤仪制作TBI 模型，将模型大鼠分为丰富环境刺激组(A 组)、常规饲养组(B 组)、Cx43 特异性反义寡聚核苷酸(Cx43-ASODN)+丰富环境刺激组(C 组)和乱序ODN(scrambled sequence ODN)+丰富环境刺激组(D组)，每组6 只。另设6 只正常大鼠作为对照组。C组和D组分别在海马区注射Cx43-ASODN(2 μl/d/rat, 1.5 mmol/L)和ScrbASODN(2 μl/d/rat, 1.5 mmol/L)。饲养14 d，采用水迷宫测试评估大鼠的学习记忆能力。结果B组大鼠潜伏期大于对照组(P<0.05)，穿越次数少于对照组(P<0.05)。A组潜伏期小于B组(P<0.05)，且从第9 天起与对照组比较无显著性差异(P>0.05)；穿越平台次数多于B组，与对照组比较无显著性差异(P>0.05)。C组大鼠的潜伏期大于A组(P<0.05)，穿越平台次数少于A组(P<0.05)。结论Cx43 蛋白参与丰富环境改善TBI 大鼠学习记忆能力的调控。

Effect of Cx43 Protein on Improvement of Learning and Memory Ability Induced by Enriched Environment in Rats with Traumatic Brain Injury

Objective To explore the effect of Cx43 protein on improvement of learning and memory ability induced by enriched environment (EE) in rats with traumatic brain injury (TBI). Methods TBI model was made by fluid percussion injury (FPI) in Sprague-Dawley rats. The TBI rats were divided into EE group (A), standard housing (ST) group (B), Cx43 specific antisense oligonucleotides (Cx43 ASODN)+EE group (C) and scrambled sequence ODN+EE group (D) with 6 rats in each group. Another 6 normal rats were taken as the control group. Groups C and D were given hippocampal microinjection of Cx43-ASODN (2 μl/d/rat, 1.5 mmol/L) and ScrbASODN (2 μl/d/ rat, 1.5 mmol/L) respectively. Morris water maze was used to evaluated the learning and memory ability. Results The latency was longer and the traversing times was less in group B than in the control group (P<0.05). The latency was shorter in group A than in group B (P<0.05), and there was no significant difference between group A and the control group (P>0.05) from the 9th day after injury. The traversing times was more in group A than in group B and there was no significant difference between group A and the control group (P>0.05). The latency was longer and the traversing times was less in group C than in group A (P<0.05). Conclusion Cx43 protein may participate in the improvement of the learning and memory ability induced by EE in rats with TBI.