目的　研究中枢 β肾上腺素受体 (β AR)及其亚型在大鼠点燃模型的调控机理。 方法　建立大鼠杏仁核电刺激点燃和戊四唑化学性点燃模型 ,观察 β AR亚型激动剂和拮抗剂对点燃和小鼠最大电休克的影响。 结果　β AR拮抗剂普萘洛尔明显延缓杏仁核点燃进程 ;普萘洛尔和 β1 AR拮抗剂美托洛尔均能显著抑制杏仁核点燃和化学性点燃 ;β1 AR激动剂多巴酚丁胺完全逆转普萘洛尔对点燃的抑制作用 ,β2 AR激动剂特布他林对普萘洛尔抑制作用无明显影响。结论　中枢 β1 AR参与杏仁核电刺激点燃和戊四唑化学性点燃的抑制作用。 Objective To study the regulation mechanism of central β-adrenergic receptor (β AR) and its subtypes in the rat model. Methods The electrical stimulation of amygdala and the pentylenetetrazolium chemical ignition model were established in rats to observe the effects of β AR subtype agonists and antagonists on the maximum electrical shock in mice. Results Propranolol, a β AR antagonist, significantly delayed the process of amygdala lighting. Propranolol and β1 AR antagonist metoprolol both inhibited the amygdala lighting and chemical ignition significantly. Β1 AR agonist dobutamine Complete reversal of propranolol on the ignition inhibition, beta 2 AR agonist terbutaline on propranolol inhibition had no significant effect. Conclusion Central β1 AR participates in the electrical stimulation of amygdala and the inhibition of pentylenetetrazolium chemical ignition.