β肾上腺素受体拮抗剂对点燃的调控机理

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。

ROLE OF BETA-ADRENOCEPTOR ANTAGONISTS IN THE CONTROL OF KINDLING MODELS IN RATS

AIM: To study the role of beta-adrenoceptors (beta-AR) and their subtypes in the control of kindling models in rats. METHODS: Electrical amygdala kindling, pentylenetetrazol (PTZ) kindling models in rats and maximal electroshock (MES) in mice were used to observe the effects of beta-AR agonists and antagonists. RESULTS: The beta-AR antagonist propranolol 15 mg.kg-1 i.p. delayed the development of amygdala kindling; while propranolol 1-20 mg.kg-1 i.p. and beta-AR antagonist metoprolol 25-400 mg.kg-1 ig significantly increased the afterdischarge threshold and reduced the seizure severity in both kindling models (P < 0.01). beta 1-AR agonist dobutamine completely reversed the inhibitory effect of propranolol, while the beta 2-AR agonist terbutaline showed no effect on propranolol. Metoprolol 200 and 800 mg.kg-1 ig significantly inhibited MES in mice (P < 0.01). CONCLUSION: Central beta 1-AR is involved in the inhibitory effects on amygdala kindling and PTZ kindling models in rats.