Consistently, in the hippocampus of rodents, learning behavior modification is usually accompanied by changes in synaptic plasticity factors, such as dendritic spine morphology and LTP. Animal studies have shown that ovariectomized rats treated with estrogen replacement therapy exhibit enhanced LTP and increased dendritic spine density in the CA1 to CA3 regions of the hippocampus. Substantial evidence has proven the important effects of estrogen on learning and memory. However, the mechanisms by which estrogen affects Chloroxylenol memory formation remain D panthenol unknown. Glucose is the main source of energy in the brain. Uptaking of glucose is required by neurons during learning and memory. Alternatively, reduction of brain glucose metabolism caused the cognitive deficits. Therefore, normal glucose metabolism is crucial in improving and maintaining learning and memory. Glucose metabolism is regulated by a comprehensive molecular network. Among these molecules, insulin is an essential factor in this processing. Insulin-dependent glucose metabolism principally occurs in the hippocampus, and this process is mediated by glucose transporter type 4 . Previous study has been indicated that hippocampal neurons rapidly increase glucose utilization during hippocampal-dependent learning through the insulin-mediated translocation of GlLUT4 to the plasma membrane in rats. Another study has been suggested that estrogen can increase insulin sensitivity and enhance insulin gene transcription and insulin release via estrogen receptors . Increasing literatures have been shown cross-talk occurred between estrogen and insulin signals during metabolism. Therefore, the present study aims to determine whether or not the effects of estrogen on learning and memory is associated with the insulin signals in OVX rats. Ovariectomy is a surgical procedure wherein the ovaries are removed, resulting in estrogen depletion. OVX rats are commonly used subjects in studies involving menopause and menopause-associated conditions. Results showed that the regulatory effect of estrogen on memory was dependent on ERb.