Effect and Mechanism of Baicalein on Synaptic Plasticity of CA1 Subfield in Rat Hippocampal Slices
|School||Huazhong University of Science and Technology|
|Keywords||Baicalein Hippocampal Long-term potentiation NMDA receptor Learning and memory Calcium / calmodulin-dependent protein kinase II Neurogranin Calcium / calmodulin|
The first part of baicalein purpose synaptic plasticity of hippocampal CA1 region: that baicalein (Baicalein, BAI) is the main flavonoids extracted from the dried root of Scutellaria one. Previous studies have shown that the pharmacological effects of the BAI has anti-inflammatory, anti-viral, anti-oxidative damage, and can improve the cognitive impairment caused by brain damage. Natural flavonoid compounds have been reported to improve the animal's cognitive abilities, enhance LTP. But the baicalein whether skullcap flavonoid monomers can improve the cognitive abilities of normal animals affect LTP has not been reported. This study was designed to observe the BAI term potentiation in CA1 region of rat hippocampal slices (Long-term potentiation, LTP) and further explore its mechanism. Method: acutely isolated rat hippocampal slices recorded by extracellular field potentials in the hippocampal CA1 region observed BAI the basic synaptic pass the CA1 region of the hippocampus, presynaptic reaction, the impact of long-term potentiation. Results: Low concentrations of BAI not affect basal synaptic transmission, high concentration (100μmol / L) BAI significantly enhance the fEPSP slope and amplitude. 10μmol / L BAI significantly enhanced LTP of hippocampal CA1 region. 10μmol / L BAI role in brain slices after two indicators reflect presynaptic reaction PPR and input - output reaction did not significantly change. N-methyl-D-aspartate (NMDA) receptor antagonist APV completely blocked BAI facilitation of LTP role; intracellular calcium chelator BAPTA-AM significantly inhibited the BAI to enhance the role of the LTP. L-type voltage-dependent calcium channel blocker verapamil did not block the BAI to enhanced LTP role. Conclusion: BAI enhances hippocampal CA1 region of the NMDA receptor-dependent LTP, and the role of the calcium-dependent. The purpose of the second part of baicalein synaptic plasticity related protein expression in rat hippocampal CA1 region: neurogranin (Ng) neurons with calmodulin (CaM) binding protein, whose main role is to regulate Ca2 and calcium / calmodulin (Ca2 / CaM)-mediated signaling pathways. The calcium / calmodulin-dependent protein kinase Ⅱ (CaMKII) the brain Ca2 / CaM-dependent kinase, modulating neuronal function, learning and memory are closely related. CaMKII 286 threonine autophosphorylation sites, through autophosphorylation CaMKII mediated brief intracellular calcium concentration ([Ca] i) elevated trigger some of the physiological function of long-term change. CaMKII is known to the NMDA receptor-dependent LTP necessary. The purpose of this study is to observe Ng, CaMKII BAI facilitation of LTP, to further explore the BAI enhanced LTP mechanisms. Methods: Using western blot method, after the end of the field potentials recorded extract the CA1 region of the protein, to observe the effects of BAI CA1 region of hippocampal slices CaMK Ⅱ, pCaMK Ⅱ, Ng, pNg expression. The result: high-frequency stimulation (HFS) can increase the brain slices pCaMK Ⅱ pNg expression; 10 μmol / L of BAI increase HFS brain slices pCaMK Ⅱ and pNg of expression. Conclusion: The role of BAI facilitated LTP, its increase pCaMK Ⅱ, and pNg expression.