{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Kim MG"],"funding":["National Research Foundation of Korea"],"pagination":["72"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC7206715"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["13(1)"],"pubmed_abstract":["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."],"journal":["Molecular brain"],"pubmed_title":["Inositol hexakisphosphate kinase-1 is a key mediator of prepulse inhibition and short-term fear memory."],"pmcid":["PMC7206715"],"funding_grant_id":["NRF-2018R1A5A1024261","NRF-2017R1A2B4006535","NRF-2019M3C7A1031742","NRF-2018R1A2B2005913"],"pubmed_authors":["Kim S","Chung C","Park H","Zhang S","Park SJ","Kim MG"],"additional_accession":[]},"is_claimable":false,"name":"Inositol hexakisphosphate kinase-1 is a key mediator of prepulse inhibition and short-term fear memory.","description":"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.","dates":{"release":"2020-01-01T00:00:00Z","publication":"2020 May","modification":"2024-11-09T05:12:16.703Z","creation":"2020-05-22T20:09:00Z"},"accession":"S-EPMC7206715","cross_references":{"pubmed":["32381051"],"doi":["10.1186/s13041-020-00615-3"]}}