earticle

영어

GQ1b is a tetrasialo-ganglioside that has four sialic acid residues, and seemed to be involved in the learning and memory. However, the molecular mechanisms and functions of GQ1b is not well understood. Studies were initiated to determine the effect of GQ1b on the improvement of the learning and memory of rats by using the Y-maze and Morris water maze test. The spatial learning and memory of rats was improved by GQ1b treatment into the rat brain. The improvements in spatial memory as measured by these two maze tests are dependent on the hippocampal learning and memory function and related to the N-methyl-D-aspartate (NMDA) receptor signaling pathway. Thus, we showed the activation of NMDA receptor signaling pathway by GQ1b treatment in rat hippocampal cells and rat hippocampus. The activation of NMDA receptor signaling pathway can leads to an enhancement of Brain-derived neurotropic factor(BDNF) mRNA levels and stimulates released of the BDNF protein. BDNF is known to support the survival, growth and differentiation of neurons and mainly expressed in synapses of the hippocampus, cortex, and basal forebrain. We investigated that the expression and the secretion of BDNF were increased by GQ1b treatment in SH-SY5Y cells and rat primary neurons. In addition, GQ1b treatment prevented the effect of D-PDMP, ganglioside synthesis inhibitor, on decrease of BDNF expression in SH-SY5Y cells. To investigate whether NMDA receptor signaling pathways was involved in GQ1b-induced BDNF expression, rat primary neurons were treated with GQ1b and NMDA receptor antagonist D-AP5. Pretreatment with the D-AP5 significantly abolished BDNF expression following GQ1b treatment in primary cortical neurons. These data suggested that GQ1b mediates its effect on BDNF expression through the NMDA receptor activation in the brain. Therefore, ganglioside GQ1b might improve spatial learning and memory and regulate the expression and the secretion of BDNF via activation of NMDA receptors signaling pathway.