Prostaglandins are necessary and sufficient to induce contextual fear learning impairments after interleukin-1 beta injections into the dorsal hippocampus
Prostaglandins are necessary and sufficient to induce contextual fear learning impairments after interleukin-1 beta injections into the dorsal hippocampus
复制标题
DOI：
10.1016/j.neuroscience.2007.10.003
复制
发表时间：
2007-12-19
期刊：
影响因子：
3.3
通讯作者：
Maier, S. F.
中科院分区：
文献类型：
--
作者：
Hein, A. M.;Stutzman, D. L.;Maier, S. F.
海马内施用白细胞介素-1 β（IL-1 β）以及诱导海马内升高但生理水平的IL-1 β干扰长期记忆的形成。有证据表明，IL-1 β诱导前列腺素（PG）形成与IL-1 β后工作记忆和空间记忆受损有关。本实验扩展了这些发现，表明PG是负责记忆缺陷的上下文恐惧条件反射发生后，IL-1 β注射到背海马的Sprague-Dawley大鼠。环氧合酶（考克斯）抑制阻断了由IL-1 β产生的背景恐惧条件反射的破坏，并且单独的考克斯抑制也破坏了背景记忆，表明PG水平和记忆之间存在倒U形关系。除了证明PG在IL-1 β介导的记忆缺陷中的必要性外，我们还表明，直接注射到背侧海马中的PG足以损害背景记忆，并显著降低海马内BDNF的后调节水平，这表明PG的记忆损害作用的可能机制。(c)2007年IBRO。由爱思唯尔有限公司出版。保留所有权利。
The intra-hippocampal administration of interleukin-1 ss (IL-1 ss) as well as the induction of elevated but physiological levels of IL-1 ss within the hippocampus interferes with the formation of long-term memory. There is evidence suggesting that the induction of prostaglandin (PG) formation by IL-1 ss is involved in impairments in working and spatial memory following IL-1 ss. The present experiments extend these findings by showing that PGs are responsible for memory deficits in contextual fear conditioning that occur following IL-1 ss injection into the dorsal hippocampus of Sprague-Dawley rats. Cyclooxygenase (COX) inhibition blocked the disruption in contextual fear conditioning produced by IL-1 ss and COX inhibition alone also disrupted contextual memory, suggesting an inverted U-shaped relationship between PG levels and memory. In addition to demonstrating the neces- sity of PGs in IL-1 ss-mediated memory deficits, we also show that PGs injected directly into the dorsal hippocampus are sufficient to impair context memory and significantly reduce post-conditioning levels of BDNF within the hippocampus, suggesting a possible mechanism for the memory-impairing effects of PGs. (c) 2007 IBRO. Published by Elsevier Ltd. All rights reserved.