一氧化氮对一叶萩碱诱导的突触传递长时程增强的作用

EFFECT OF NO ON SECURININE-INDUCED LONG-TERM POTENTIATION IN DENTATE GYRUS OF THE HIPPOCAMPUS OF ANESTHETIZED RATS

目的 研究一叶碱对麻醉大鼠突触可塑性形成中一氧化氮 (nitricoxide ,NO)的作用。方法 以在体记录突触传递长时程增强 (long termpotentiation ,LTP)的电生理学方法 ,记录大鼠海马齿状回颗粒细胞层群峰电位(populationspike,PS) ;以硝酸还原酶法测定NO含量。结果 在侧脑室给予 0 2nmol·L- 1 一叶碱 (securinine ,5 μL)前给予 1μmol·L- 1 7 硝基吲唑可抑制LTP的诱导。给药前ipL 精氨酸 2 5 0mg·kg- 1 可逆转这种抑制作用。取脑进行NO含量测定 ,与一叶碱对照组相比 ,7 硝基吲唑 +一叶碱给药组的NO含量明显下降。结论 选择性一氧化氮合酶 (nNOS)抑制剂 7 硝基吲唑抑制一叶碱对LTP的诱导 ;由nNOS催化产生的NO参与了一叶碱诱导LTP的过程。

AIM To study the effect of NO on securinine-induced long-term potentiation in the dentate gyrus of anesthetized rats. METHODS The population spike (PS) was recorded by electrophysiological techniques. Then the rat brain was homogenized, of which the NO level was detected by spectrometry at 550 nm after the catalysis of nitric acid reductase. RESULTS Pretreatment with 7-nitroindazole (1 μmol·L -1, 5 μL icv) was shown to inhibit LTP induced by securinine (0.2 nmol·L -1, 5 μL icv) in anesthetic rats. The percentage of PS amplitude was (100±23)%, (106±16)% and (124±20)% at 15, 30 and 60 min, respectively (n=6, P<0.01). Meanwhile, the NO level was obviously higher in securinine group compared with that in 7-nitroindazole group (P<0.01). Nevertheless, L-arginine (250 mg·kg -1, ip) was found to reverse this inhibitory effect induced by 7-nitroindazole (P<0.05). CONCLUSION Selective nNOS inhibitor 7-nitroindazole inhibited the securinine-induced LTP in anesthetic rats, which demonstrated that NO was involved in securinine-induced LTP.