However, we do not know to what extent their development depends on the specific milieu. In this study, we transplanted mouse PGCs collected from male and female gonads at 12.5 days postcoitum, together with gonadal somatic cells, under kidney capsules of adult mice. The transplanted PGC and gonadal somatic cells constructed testis-like and ovary-like tissues, respectively, under the kidney capsules within 4 wk. Normal-appearing KU-57788 round spermatids and fully grown germinal vesicle (GV) oocytes developed

within these tissues. Ectopic spermatogenesis continued thereafter, while oogenesis consisted of only a single wave. The injection of these round spermatids directly into mature in vivo-derived oocytes led to the birth at term of normal pups. PGC-derived GV oocytes were isolated, induced to mature in vitro, and injected with normal spermatozoa. The injected oocytes were successfully fertilized and developed into normal pups. Our findings demonstrate the remarkable flexibility of PGC development, which can proceed up to the functional gamete stage under spatially Pinometostat molecular weight and temporally noninnate

conditions. This transplantation system may provide a unique technical basis for induction of the development of early germ cells of exogenous origins, such as those from embryonic stem cells.”
“The human neuroblastoma cell line SH-SY5Y is a potentially useful model for the identification and LB-100 nmr characterisation of Na-v modulators, but little is known about the pharmacology of their endogenously expressed Na(v)s. The aim of this study was to determine the expression of endogenous Na-v alpha and beta subunits in SH-SY5Y cells using PCR and immunohistochemical approaches, and pharmacologically characterise the Na-v isoforms endogenously expressed in this cell line using electrophysiological and fluorescence approaches. SH-SY5Y human neuroblastoma cells were found to endogenously express several Na-v isoforms including Na(v)1.2

and Na(v)1.7. Activation of endogenously expressed Na(v)s with veratridine or the scorpion toxin 001 caused membrane depolarisation and subsequent Ca2+ influx through voltage-gated L- and N-type calcium channels, allowing Na-v activation to be detected with membrane potential and fluorescent Ca-2 dyes. mu-Conotoxin TIIIA and ProTxII identified Na(v)1.2 and Na(v)1.7 as the major contributors of this response. The Na(v)1.7-selective scorpion toxin OD1 in combination with veratridine produced a Na(v)1.7-selective response, confirming that endogenously expressed human Na(v)1.7 in SH-SY5Y cells is functional and can be synergistically activated, providing a new assay format for ligand screening. Crown Copyright (C) 2012 Published by Elsevier Inc. All rights reserved.