Maturation of presynaptic transmitter secretion machinery is a critical step in synaptogenesis. Here we report that a brief train of presynaptic action potentials rapidly converts early nonfunctional contacts between cultured hippocampal neurons into functional synapses by enhancing presynaptic glutamate release. The enhanced release was confirmed by a marked increase in the number of depolarization-induced FM4-64 puncta in the presynaptic axon. This rapid presynaptic maturation can be abolished by treatments that interfered with presynaptic BDNF and Cdc42 signaling or actin polymerization. Activation of Cdc42 by applying BDNF or bradykinin mimicked the effect of electrical activity in promoting synaptic maturation. Furthermore, activity-induced increase in presynaptic actin polymerization, as revealed by increased concentration of actin-YFP at axon boutons, was abolished by inhibiting BDNF and Cdc42 signaling. Thus, rapid presynaptic maturation induced by neuronal activity is mediated by presynaptic activation of the Cdc42 signaling pathway.

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Oxidative stress-induced cell damage has been implicated in a variety of neurodegenerative disorders. In the current study, we investigated the protective role of ginsenoside Rd against the cytotoxicity induced by exposure to hydrogen peroxide (H 2 O 2 ) and the underlying mechanism in the PC12 cell line. The protective effects of ginsenoside Rd (1, 10 m mM) on H 2 O 2 -induced cytotoxicity may be ascribed to its antioxidative properties by reducing the intracellular reactive oxygen species level; decreasing malondialdehyde production, a common index of lipid peroxidation; and enhancing the antioxidant enzymatic activities of superoxide dismutase and glutathione peroxidase. Additionally, ginsenoside Rd could stabilize the mitochondrial membrane potential after H 2 O 2 exposure. These findings suggested that ginsenoside Rd may be considered a potential antioxidant agent and should encourage further research in neurodegenerative diseases to explore the potential neuroprotective effects of ginsenoside Rd.Key words ginsenoside Rd; neuroprotection; oxidative stress; PC12 cell Biol. Pharm. Bull. 31(10) 1923-1927(2008 © 2008 Pharmaceutical Society of Japan * To whom correspondence should be addressed. e-mail: zhaogang@fmmu.edu.cn

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