目的: 探讨大鼠脑出血(intracerebral hemorrhage,ICH)模型中,丘脑网状核(thalamic reticular nucleus,TRN)中谷氨酸脱氢酶67(glutamate decarboxylase 67,GAD67)和m型阿片受体(m-opioid receptor,MOR)含量的变化。方法: 在立体定位仪下进行右侧丘脑腹后外侧核(ventral posteriorlateral thalamic nucleus,VPL)注射Ⅳ型胶原酶,建立大鼠丘脑出血模型,同一位置注射同等体积的生理盐水为对照组,尼氏染色观察VPL周围神经元形态,免疫荧光染色观察TRN中GAD67和MOR含量的变化。结果: 丘脑腹后外侧核出血大鼠模型的运动功能未见明显异常表现;模型组VPL内神经元尼氏体坏死,萎缩,空泡变性;对照组TRN内MOR数量为77.77±9.45,ICH后7天减少到30.00±4.90(P＜0.05),ICH后14天为23.30±2.05(P＜0.05),ICH后28天10.50±2.87(P＜0.05);GAD67阳性细胞数量对照组为78.67±7.77,而ICH后7天为27.00±5.35(P＜0.05),ICH后14天为41.67±5.44(P＜0.05),ICH后28天为26.00±6.13(P＜0.05)。结论: 大鼠VPL注射Ⅳ型胶原酶能成功制备丘脑出血模型,模型组大鼠的运动功能无明显变化,模型组大鼠TRN中GAD67蛋白减少,MOR数量减少。
Objective: To explore the expression changes of glutamate decarboxylase 67 (GAD67) and m-opioid receptor (MOR) in thalamic reticular nucleus (TRN) after rat intracerebral hemorrhage model (ICH). Methods: The right ventrolateral thalamic nucleus (VPL) was injected with type IV collagenase under the stereotaxic apparatus to establish the rat thalamus hemorrhage model. The same volume of normal saline was injected at the same position as the control group. The morphology of neurons around VPL was observed by Nissl staining, and the changes of GAD67 and MOR contents in TRN were observed by immunofluorescence staining. Results: No obvious abnormality of motor function was found in the thalamic hemorrhage model of VPL injection; Nissl body necrosis, atrophy and vacuolar degeneration of neurons in VPL of model group; In the control group, the number of MOR in TRN was 77.77±9.45, decreased to 30.00±4.90 at 7 days after ICH (P＜0.05), 23.30±2.05 at 14 days after ICH (P＜0.05), and 10.50±2.87 at 28 days after ICH (P＜0.05). The number of GAD67 positive cells in the control group was 78.67±7.77, which was 27.00±5.35 at 7 days after ICH (P＜0.05), 41.67±5.44 at 14 days after ICH (P＜0.05), and 26.00±6.13 at 28 days after ICH (P＜0.05). Conclusion: VPL injection of type IV collagenase in rats can successfully prepare the thalamus hemorrhage model. The motor function of rats in the model group has no significant change. The GAD67 protein in the TRN of rats in the model group is reduced, and the number of MOR is reduced.
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