目的以急性脱钠大鼠为模型,用免疫荧光双标记法观察体内钠平衡变化过程中,是否能激活杏仁中央核内GABA能神经元及其可能的作用。方法皮下注射呋塞米+24h无钠饮食诱导急性脱钠动物模型,利用0.3mol/LNaCI/DW双瓶饮水法给予适宜刺激.观察杏仁中央核内GABA/Fos免疫阳性双标记神经元数的变化。结果急性脱钠使大鼠杏仁中央核内Fos免疫阳性神经元数和GABA/Fos免疫阳性双标记神经元数显著性增多(分别为P〈0.0l,P〈0.05);摄入0.3mol/LNaCl溶液使Fos免疫阳性神经元数和GABA/FOS免疫阳性双标记神经元数显著性增多(分别为P〈0.001,P〈0.01)。结论杏仁中央核内GABA能神经元可能对急性脱钠大鼠钠摄入的调控起抑制性作用。
Objective To determine whether the GABA-containing neurons in rat central nucleus of amygdala (CeA) can be activated by acute sodium deprivation. Methods Acute sodium depletion was induced by subcutaneous injection of furosemide in rats followed by 24 h of dietary sodium deprivation. The rats underwent 0.3 mol/L NaCl/distilled water two bottle choice test, and the activated neurons were labeled and identified with GABA/Fos-double labeling immunohistochemistry. Results The rats with acute sodium depletion exhibited significantly more numerous c-fos-positive neurons and GABA/Fos double-labeled neurons in the CeA than the control group (P〈0.01, P〈0.05). Consumption of 0.3 mol/L NaC1 significantly increased the number of c-fos and GABA/Fos double labeled neurons compared to the distilled water group (P〈0.001, P〈0.01). Conclusion GABAergic neurons in the CeA may play an inhibitory role in the regulation of sodium intake in rats with acute sodium depletion.