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目的研究神经肽Y(NPY)对海人酸(KA)致癫痫大鼠AMPA受体GluR2亚单位功能的影响。方法用KA建立大鼠癫痫模型。将成年雄性SD大鼠随机分为对照组、模型组、实验A组、实验B组,每组10只。对照组予以0.9%Na Cl 1μL,于脑室注药点内注射,模型组予以5.5μg·μL~(-1)KA 1μL,于脑室注药点内注射;实验A组予以5μg·μL~(-1)NPY 1μL,于海马区注药点内注射;实验B组予以3μg·μL~(-1)BIBP3226 1μL,0.5 h后注入5μg·μL~(-1)NPY 1μL,于海马区注药点内注射。24 h后,实验A组和实验B组予以5.5μg·μL~(-1)KA 1μL,于脑室注药点内注射。用Western blot法检测4组大鼠海马CA3区的GluR2亚单位的总蛋白和磷酸化蛋白的变化,用实时荧光定量聚合酶链式反应(RT-PCR)法检测4组大鼠海马CA3区的GluR2 mRNA表达水平。结果对照组、模型组、实验A组和实验B组的GluR2亚单位的总蛋白分别为0.63±0.21,0.63±0.36,0.63±0.28和0.61±0.22,差异均无统计学意义(均P>0.05)。对照组、模型组、实验A组和实验B组的GluR2亚单位蛋白磷酸化分别为0.42±0.21,1.24±0.17,0.91±0.07和1.05±0.08,GluR2 mRNA分别为1.01±0.14,0.42±0.16,0.76±0.07和0.60±0.09,对照组与其他3组比较,差异均有统计学意义(均P<0.05),实验A组与模型组、实验B组比较,差异均有统计学意义(均P<0.05)。结论 NPY可以通过激活Y1受体,抑制大鼠癫痫发作,减轻癫痫所致的AMPA受体GluR2亚单位功能受抑制。
Objective To investigate the effect of neuropeptide Y (NPY) on the function of GluR2 subunit of AMPA receptor in epileptic rats induced by kainate (KA). Methods KA model of rat epilepsy was established. Adult male Sprague-Dawley rats were randomly divided into control group, model group, experimental group A and experimental group B, with 10 rats in each group. The control group was given 0.9% NaCl 1μL and injected intracerebroventricularly. The model group was given 5.5μg · μL ~ (-1) KA 1μL and injected intracerebroventricular injection. In the experimental group, 5μg · μL ~ (- 1) NPY 1 μL injected into the hippocampus in the injection site. The experimental group B received 3 μg · μL -1 BIBP3226 1 μL, 0.5 μg · μL -1 NPY 1 μL injected 0.5 h after injection into the hippocampus Internal injection. After 24 h, 5.5 μg · μL ~ (-1) KA 1 μL was injected into experimental group A and group B, and injected into intraventricular injection site. The total protein and phosphorylated protein of GluR2 subunit of hippocampal CA3 region of four groups were detected by Western blot. The hippocampal CA3 region of four groups were detected by real-time fluorescence quantitative polymerase chain reaction (RT-PCR) GluR2 mRNA expression level. Results The total protein of GluR2 subunits in control group, model group, experimental group A and experimental group B were 0.63 ± 0.21, 0.63 ± 0.36, 0.63 ± 0.28 and 0.61 ± 0.22, respectively, with no significant difference (all P> 0.05 ). GluR2 subunit phosphorylation of control group, model group, experimental group A and experimental group B were 0.42 ± 0.21, 1.24 ± 0.17, 0.91 ± 0.07 and 1.05 ± 0.08, respectively, GluR2 mRNA was 1.01 ± 0.14 and 0.42 ± 0.16, 0.76 ± 0.07 and 0.60 ± 0.09, respectively. There were significant differences between the control group and the other three groups (all P <0.05). The difference between the experimental group A and the model group and the experimental group B was statistically significant (P <0.05). Conclusion NPY can inhibit the function of GluR2 subunit of AMPA receptor induced by epilepsy by inhibiting the seizure activity of Y1 receptor.