采用形态学观察、β内啡肽（βＥｎｄ）放射免疫测定及单细胞内游离钙浓度［Ｃａ２＋］ｉ检测等方法，观察了βＥｎｄ对谷氨酸单钠（ＭＳＧ）诱发神经元损伤的影响，分析了可能的作用机制。结果表明，βＥｎｄ可以明显加重ＭＳＧ诱发的下丘脑弓状核神经元的损伤；βＥｎｄ和ＭＳＧ诱发的［Ｃａ２＋］ｉ增高可被维拉帕米部分逆转。另外，吗啡可以进一步加剧ＭＳＧ诱导的各脑区βＥｎｄ含量的变化。提示βＥｎｄ可以明显地加剧ＭＳＧ的神经毒性作用，其机制与ＭＳＧ能诱发脑内βＥｎｄ的含量的增多及βＥｎｄ可进一步破坏ＭＳＧ引起的胞内钙稳态失衡有关。 The effects of βEnd on glutamate monosodium (MSG) -induced neurons were observed by morphological observation, βendorphin (βEnd) radioimmunoassay and single intracellular free calcium concentration [Ca2 +] i detection. The impact of injury, the possible mechanism of action was analyzed. The results showed that β  End can significantly aggravate MSG-induced hypothalamic arcuate nucleus neurons injury; β  End and MSG-induced [Ca2 +] i increased by verapamil partially reversed. In addition, morphine can further exacerbate MSG-induced changes in brain β-End content. Suggesting that β  End can significantly aggravate the neurotoxic effect of MSG, and its mechanism and MSG can induce brain β  End content increased and β  End can further damage MSG-induced imbalance of intracellular calcium homeostasis.