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Ginkgo (Ginkgo biloba) in the Earth about 200 million years, was widely distributed in the Northern Hemisphere, Europe, Asia, the Americas, known as gymnosperms \Its seeds as \Ginkgolide (ginkgolides) is an active ingredient in the Ginkgo biloba extract, ginkgolide A, B, C, M, J, etc., are strong platelet activating factor (Platelet activating factor, PAF) antagonists. Which ginkgolide B (Ginkgolide B, GB) most active to date on the pharmacological effects of ginkgolide B is most concentrated. The ginkgolide competition antagonized PAF binding to its receptor, so that the PAF can not G protein transduction activation of phospholipase C, gland cyclase and tyrosine protein kinase, thereby blocking the PAF receptor signal transduction guide, blocking the biological effects of PAF. Ginkgolide a certain role in the prevention and treatment of a variety of diseases of the central nervous system. Protection of cerebral ischemia, reduce reperfusion injury, anti-Alzheimer's disease (AD), inhibition of neuronal apoptosis, and many other aspects that ginkgolide has a bright future in the treatment of central nervous system diseases. About the the hub protection mechanism of action of the ginkgolide B, especially electrophysiological unclear. Hippocampal structure is simple, easy to separate, and fiber nuclei involved in the cardiovascular center, is commonly used parts of the neurophysiological studies. Hypothalamic paraventricular nucleus (paraventricular nucleus, PVN) is very important to integrate parts of the regulation of cardiovascular activity, and to accept from the hippocampus, fornix fiber. Ginkgolide B on rat central neurons electrophysiological properties has not been reported. Therefore, this paper these two parts. Purpose of the Ⅰ Ginkgolide B spontaneous discharges of hippocampal CA1 neurons: study of ginkgolide B (Ginkgolide B, BN52021) on hippocampal slices of neuronal activity in the resting state. Method: The experiment was the choice of 20 ± 3 days of male Sprague-Dawley rats. The rats were quickly decapitated, stripped of the skull and the dura mater, remove the brain tissue at 0-4 ℃ in advance with 95% O 2 and 5% CO 2 of mixed gas saturated artificial cerebrospinal fluid, fast isolated side of the hippocampus, cut into the thickness of 350-500μm brain slices. Brain slices and then transferred to artificial cerebrospinal fluid, continuous pass 2 and 5% CO 2 95% O incubated for 60-90 min at room temperature. Using extracellular recording technique to observe the impact of of ginkgolide B of rat hippocampal slices neurons discharge. Results: (1) given in 43 CA1 neurons discharge unit ginkgolide B (0.1,1,10 μmol / L), 2 minutes, 42 discharge units (97.67%) discharge frequency was significantly reduced, and a dose-dependent sex; (2) pre-0.2 mmol / L of L-glutamate (L-Glu) perfused hippocampal slices, 10 units, the discharge frequency was significantly increased performance for epileptiform discharges based on perfusion ginkgo bitter lactone B (1μmol / L) 2 minutes, the epileptiform discharges all inhibition; (3) pre-L-type calcium channel agonist Bay K 8644 perfusion eight hippocampal slices, 8 units (100%) of all discharge increase in based on the discharge frequency was significantly reduced; perfusion ginkgolide B (1μmol / L) 2 minutes, 7 discharge units (87.5%) (4) 8 CA1 neurons discharge units, ginkgolide B (1μmol / L), the inhibitory effect can be widely potassium channel blockers (tetraethylammonium, TEA) 1 mmol / L was completely blocked. Conclusion: ginkgolide B (Ginkgolide B, BN52021) inhibited hippocampal neurons spontaneous discharge, and inhibited by L-glutamate-induced neuron discharge. Prompted ginkgolide B on central neurons by reducing their activities with a certain degree of protection, and this effect may be related to the ginkgolide B inhibition of L-type calcium channels, and may be delayed rectifier potassium channel (delayed rectifier potassium channel, KDR). Objective: Research ginkgolide B (Ginkgolide B, BN52021) II ginkgolide B on the rat hypothalamic paraventricular nucleus neurons discharge spontaneously nucleus neuron activity in the paraventricular hypothalamic slices resting state the impact. Method: The experiment was the choice of 20 ± 3 days of male Sprague-Dawley rats. The rats were quickly decapitated, stripped of the skull and the dura mater, remove the brain tissue at 0-4 ℃ in advance with 95% O 2 and 5% CO 2 of saturated artificial cerebrospinal fluid mixed gas, according to the anatomical landmarks cut block contains the paraventricular nucleus of the hypothalamus brain slices, thickness of 350-500μm, and placed in artificial cerebrospinal fluid, continuous pass the 95% O , 2 and 5% CO 2 , the mixture was incubated at room temperature for 60-90 min. Using extracellular recording technique, the observed of ginkgolide B of paraventricular nucleus neurons from impact. Results: (1) 27 hypothalamic paraventricular nucleus neurons units give ginkgolide B (0.1,1,10 μmol / L), 2 minutes, 26 discharge units (96.30%) significantly lower discharge frequency, and a dose-dependent manner; (2) pre-perfused hypothalamic slices of 0.2 mmol / L L-glutamate (L-Glu) 8 discharge unit discharge frequency increased significantly performance epileptiform discharges based on perfusion Ginkgo bitter lactone B (1μmol / L) 2 minutes, the epileptiform discharges all inhibition; (3) pre-L-type calcium channel agonist Bay K 8644 perfusion eight hypothalamic slices, all eight units (100%) the discharge increased based on perfusion ginkgolide B (1 μmol / L) 2 minutes, 8 discharge unit (100%) was significantly lower discharge frequency; (4) in the the eight hypothalamic paraventricular nucleus yuan discharge unit inhibitory effect of ginkgolide B (1μmol / L) has been widely potassium channel blockers (tetraethylammonium, TEA) 1 mmol / L completely blocked. Conclusion: ginkgolide B (Ginkgolide B, BN52021) inhibit spontaneous discharge of hypothalamic paraventricular nucleus neurons and inhibit neurons by L-glutamate-induced discharge. Prompted ginkgolide B has a certain degree of protection by reducing their activities of cardiovascular, central nervous, this effect may ginkgolide B inhibition of L-type calcium channels, and may be related to the delayed rectifier potassium channel ( delayed rectifier potassium channel, KDR).
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