Ginkgo Biloba Extracts Inhibit Ischemic LTP Through Attenuating EPSCs In Rat Hippocampus

Abstract Ginkgo biloba extract 761 (Egb761), a standardized extract from the Ginkgo biloba leaf, is purported to inhibit NMDA receptor-mediated neuronal excitotoxicity and protect neurons form ischemic injury. However, the specific signal pathway involved in the effects of Egb761 on synaptic plasticity is still in dispute. In this article, effects of Egb761 and its monomer component Ginkgolide A (GA), Ginkgolide B (GB) and Ginkgolide C (GC) on rat hippocampal synaptic plasticity were studied. The evoked Excitatory postsynaptic currents (EPSCs) and miniature EPSCs were recorded on hippocampal slices from SD rats (14–21 days of age) by whole-cell patch-clamp recording and long-term potentiation (LTP) was induced by theta-burst stimulation. Acutely applied Egb761 inhibited the LTP, but bilaterally affect the EPSCs, that is EPSC increase at lower concentration of Egb761, then EPSC decrease at higher concentration of Egb761. Egb761 monomer component GA, GB and GC could also inhibit the TBS-induced LTP and EPSC amplitude but not paired-pulse ratio (PPR). Simultaneously, Egb761 and its monomer components inhibited the post-ischemic LTP (i-LTP) by inhibiting the EPSCs and the AMPA receptor subunit GluA1 expression on postsynaptic membrane. The results indicated that high concentration of Egb761 might inhibit LTP and i-LTP through inhibition effects of GA, GB and GC on AMPA receptors.