期刊
BRAIN RESEARCH
卷 1355, 期 -, 页码 141-150出版社
ELSEVIER SCIENCE BV
DOI: 10.1016/j.brainres.2010.07.098
关键词
Baicalein; Memory; Passive avoidance task; Morris water maze task; Extracellular signal-regulated kinase; cAMP response element-binding protein; Brain-derived neurotrophic factor
资金
- Seoul Research and Business Development Program [10524]
Baicalein is one of the major flavonoids originally isolated from the roots of Scutellaria baicalensis Georgi (Labiatae). Reports on baicalein-induced changes in memory-related biochemical parameters including extracellular signal-regulated kinases (ERK), Akt, cAMP response element-binding protein (CREB), and brain-derived neurotrophic factor (BDNF) have been scarce, and the action of baicalein is controversial. Baicalein promotes phosphorylation of ERK under normal conditions; on the other hand, it inhibits phosphorylation of ERK extracellularly under oxidative conditions. In the present study, we observed that baicalein (20 mg/kg, p.o.) as compared to vehicle significantly increased the expression of phosphorylated ERK (pERK), phosphorylated CREB (pCREB), and BDNF but did not increase phosphorylated Akt expression in the hippocampus of naive mice. Baicalein also significantly increased the expression of pERK and BDNF in the cortex of naive mice. However, baicalein had no effect on memory acquisition in the step-through passive avoidance task. On the contrary, baicalein (20 mg/kg, p.o.) co-injected with flumazenil (10 mg/kg, i.p.) significantly increased the retention latency in the passive avoidance task in comparison to the flumazenil-treated group, baicalein-treated group, and vehicle-treated control group. In addition, the number of platform crossings in the Morris water maze test during the probe trial session was significantly increased by co-administration of baicalein with flumazenil. Furthermore, the expressions level of BDNF was significantly increased in the baicalein with flumazenil-treated group compared to the baicalein- or flumazenil-treated groups in the hippocampus after an acquisition trial. These results suggest that the reasons why baicalein does not exert cognitive enhancement although it enhances the expression levels of pERK, pCREB, and BDNF are, in part, derived from its GABA(A) receptor agonistic property which is antagonized by flumazenil. (C) 2010 Elsevier B.V. All rights reserved.
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