Inositol phosphate metabolism has emerged as one of the key players in synaptic transmission. Previous studies have shown that the deletion of inositol hexakisphosphate kinase 1 (IP6K1), which is responsible for inositol pyrophosphate biosynthesis, alters probability of presynaptic vesicle release and short-term facilitation of glutamatergic synapses in mouse hippocampus. However, the behavioral and cognitive functions regulated by IP6K1 remain largely elusive. In this study, IP6K1-knockout mice exhibited decreased prepulse inhibition with no defects in Y-maze and elevated plus maze tests. Interestingly, IP6K1 knockout led to impaired short-term memory formation in a contextual fear memory retrieval test with no effect on long-term memory. Further, both hippocampal long-term potentiation and long-term depression in IP6K1-knockout mice were similar to those in the wild-type control. Taken together, the findings in this study suggest the physiological roles of IP6K1 and the associated inositol pyrophosphate metabolism in regulating sensorimotor gating as well as short-term memory.

中文翻译：

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肌醇六磷酸激酶-1是脉冲前抑制和短期恐惧记忆的关键介质。

肌醇磷酸代谢已成为突触传递的关键因素之一。以前的研究表明，负责肌醇焦磷酸生物合成的肌醇六磷酸激酶1（IP6K1）的删除，改变了小鼠海马中突触前囊泡释放的可能性和谷氨酸能突触的短期促进作用。但是，由IP6K1调节的行为和认知功能仍然难以捉摸。在这项研究中，IP6K1基因敲除小鼠表现出减少的前脉冲抑制作用，在Y迷宫中没有缺陷，在正迷宫试验中也没有升高。有趣的是，在上下文恐惧记忆检索测试中，IP6K1敲除导致受损的短期记忆形成，而对长期记忆没有影响。进一步，IP6K1敲除小鼠的海马长时程增强和长期抑郁都与野生型对照相似。两者合计，这项研究中的发现表明IP6K1和相关的肌醇焦磷酸代谢在调节感觉运动门控和短期记忆中的生理作用。