Early in postnatal development, inhibitory inputs to rat lateral superior olive (LSO) neurons change from releasing predominantly GABA to releasing predominantly glycine into the synapse. Here we show that spontaneous miniature inhibitory postsynaptic currents (mIPSCs) also change from GABAergic to glycinergic over the first two postnatal weeks. Many 'mixed' mIPSCs, resulting from co-release of glycine and GABA from the same vesicles, are seen during this transition. Immunohistochemistry showed that a large number of terminals contained both GABA and glycine at postnatal day 8 (P8). By P14, both the content of GABA in these mixed terminals and the contribution of GABA to the mixed mIPSCs had decreased. The content of glycine in terminals increased over the same period. Our results indicate that switching from GABAergic to glycinergic inputs to the LSO may occur at the level of a single presynaptic terminal. This demonstrates a new form of developmental plasticity at the level of a single central synapse.
Cisplatin (CDDP) was incorporated inside single-wall carbon nanohorns with holes opened (SWNHox) by a nanoprecipitation method that involved dispersion of CDDP and SWNHox in a solvent followed by the solvent evaporation. The incorporated CDDP quantity increased from the previously reported value of 15 to 46%, and the total released quantity of CDDP also increased from 60 to 100% by changing the solvent from dimethylformamide to water. Concurrently, in vitro anticancer efficiency of CDDP@SWNHox increased to 4-6 times greater than that of the intact CDDP. In vivo, CDDP@SWNHox intratumorally injected to transplanted tumors of mice suppressed the tumor growth more than the intact CDDP. We observed that CDDP@SWNHox adhered to the cell surfaces in vitro and stayed within the tumor tissues in vivo. Therefore, we think that the CDDP released from SWNHox realized high concentrations locally at the cells in vitro and in the tissues in vivo and could efficiently attack the tumor cells. We also found that SWNHox itself had an in vivo anticancer effect, which might increase the anticancer activities of CDDP@SWNHox.
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