Williams J H, Bliss T V
Division of Neurophysiology and Neuropharmacology, National Institute for Medical Research, London, U.K.
Neurosci Lett. 1989 Dec 15;107(1-3):301-6. doi: 10.1016/0304-3940(89)90835-5.
The effects on tetanus-induced long-term potentiation (LTP) of the lipoxygenase and phospholipase A2 inhibitor nordihydroguaiaretic acid (NDGA), and of the cyclo-oxygenase inhibitor indomethacin have been investigated in area CA1 of the hippocampal slice. In the presence of NDGA, tetanic stimulation of Schaffer collaterals produces an attenuated potentiation of the population excitatory postsynaptic potential (EPSP) lasting for less than 1 h. Indomethacin does not impair LTP of the EPSP. Neither drug significantly reduces LTP of the population spike. NDGA, but not indomethacin, reversibly reduces pre-established LTP. The results suggest a role for arachidonic acid or its lipoxygenase metabolites, but not its cyclo-oxygenase metabolites, in the induction and expression of tetanus-induced LTP in area CA1.
已在海马切片的CA1区研究了脂氧合酶和磷脂酶A2抑制剂去甲二氢愈创木酸(NDGA)以及环氧化酶抑制剂吲哚美辛对破伤风诱导的长时程增强(LTP)的影响。在NDGA存在的情况下,对谢弗侧支进行强直刺激会使群体兴奋性突触后电位(EPSP)的增强减弱,持续时间不到1小时。吲哚美辛不会损害EPSP的LTP。两种药物均未显著降低群体峰电位的LTP。NDGA可可逆地降低预先建立的LTP,但吲哚美辛则不会。结果表明,花生四烯酸或其脂氧合酶代谢产物而非其环氧化酶代谢产物在CA1区破伤风诱导的LTP的诱导和表达中起作用。