Permissive Role of Insulin in the Expression of Long-Term Potentiation in the Hippocampus of Immature Rats
Publication in refereed journal


摘要Many studies indicate that impairment in insulin signaling leads to learning and memory deficits. However, previous studies failed to establish a clear role of insulin in long-term potentiation (LTP), the best cellular model of memory formation. Here we show that while insulin pretreatment did not affect LTP magnitude in the adult rat hippocampus, it facilitated LTP expression in the immature hippocampus. The tyrosine kinase inhibitor AG-1024 abolished the effect of insulin in young rats, suggesting the involvement of the insulin receptor. On the other hand, increasing extracellular glucose concentration failed to facilitate LTP and application of an insulin-responsive glucose transporter-4 inhibitor did not impair the effect of insulin. These results suggest that the facilitatory action of insulin on LTP is not an indirect effect on glucose homeostasis/utilization. Involvement of the MAPK/ERK pathway, a known downstream pathway of insulin signaling, was revealed by pretreatment with PD98059, which blocked the insulin-mediated LTP facilitation. Consistent with this, high-frequency stimulation induced a significant increase in the level of phosphorylated Erk-2 in insulin-treated hippocampus. Taken together, these results suggest that insulin may be an essential factor in the immature brain, allowing the expression of LTP to facilitate learning and memory. Copyright (C) 2011 S. Karger AG, Basel
著者Zhao WC, Wu XM, Xie H, Ke Y, Yung WH
頁次236 - 245
關鍵詞Insulin; Long-term potentiation; Synaptic plasticity
Web of Science 學科類別Biochemistry & Molecular Biology; BIOCHEMISTRY & MOLECULAR BIOLOGY; Biophysics; BIOPHYSICS; Cell Biology; CELL BIOLOGY; Neurosciences; NEUROSCIENCES; Neurosciences & Neurology

上次更新時間 2021-14-01 於 23:32