Study on the expression of LTP in hippocampus of young rats by Med64

Permissive role of insulin in the expression of long-term potentiation in the hippocampus of immature rats

Induction of insulin on long-term potentiation (LTP) expression in hippocampus of young rats

Prof Yung WH/CUHK Chinese University of Hong Kong

Many studies have shown that insulin signaling errors lead to learning and memory disorders. However, previous studies were unable to determine the association of insulin with long-term potentiation (LTP) , although LTP is the best cellular model for memory formation. Here we show that insulin pretreatment has no effect on long-term potentiation of hippocampus in adult rats, but it can promote the expression of LTP in mature hippocampus . The tyrosine kinase inhibitor AG-1024 can abolish the effects of insulin on young rats. So insulin receptors may be involved in this process. on the other hand, Increasing extracellular glucose concentration does not promote LTP , Add a glucose transporter 4 inhibitor that acts on insulin ( Insulin-responsive glucose transporter-4 inhibitor ) does not reduce the effects of insulin. These results indicate that the promotion of insulin to LTP is not an indirect Insulin homeostasis / utilization mechanism. Using PD98059 to interrupt insulin-mediated LTP , it is known that the insulin signaling downstream pathway MAPK/ERK molecules are involved in the process. Consistent with the above results, high frequency stimulation of insulin treatment of hippocampus increased phosphorylated Erk-2 levels. In summary, these findings suggest that insulin may be an immature brain, a very important substance for LTP to appear. Strengthen brain learning

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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, Increased 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 facilitating 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 P D98059, 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.

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