Togashi H, Mori K, Itoh Y, Matsumoto M, Ueno K, Ohashi S, Otani H, Yoshioka M
Department of Pharmacology, Hokkaido University Graduate School of Medicine, Kita-15, Nishi-7, Kita-ku, 060-8638, Sapporo,
Neurosci Lett. 2001 Nov 9;313(3):133-6. doi: 10.1016/s0304-3940(01)02271-6.
To investigate whether postischemic cerebral dysfunction occurs via the interleukin-1 beta/nitric oxide (IL-1beta/NO) pathway, we examined the effects of an IL-1beta antagonist on long-term potentiation (LTP) impairment and excessive NO production in the rat hippocampus after 10-min global ischemia. Intracerebroventricilar administration of the IL-1beta antagonist attenuated NO production and rescued LTP impairment in the perforant path-dentate gyrus synapses, observed 1 day and 4 days after ischemic insult, respectively. There was an inverse relationship between LTP in the dentate gyrus synapses and hippocampal NO production. Centrally applied IL-1beta mimicked the consequences of transient ischemia in LTP formation and hippocampal NO production in non-ischemic rats. These findings indicate that the IL-1beta/NO pathway is involved in the hippocampal LTP impairment observed in the postischemic brain.
为了研究缺血后脑功能障碍是否通过白细胞介素-1β/一氧化氮（IL-1β/NO）途径发生，我们检测了IL-1β拮抗剂对大鼠海马在10分钟全脑缺血后长时程增强（LTP）损伤和过量NO产生的影响。分别在缺血损伤后1天和4天观察到，脑室内给予IL-1β拮抗剂可减弱NO的产生，并挽救穿通通路-齿状回突触中的LTP损伤。齿状回突触中的LTP与海马NO产生之间呈负相关。向非缺血大鼠脑内注射IL-1β可模拟短暂缺血在LTP形成和海马NO产生方面的后果。这些发现表明，IL-1β/NO途径参与了缺血后脑海马LTP损伤。
