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It was previously reported that suppressing glycine signaling from the beginning of development in zebrafish embryos caused an abnormal maintenance of the progenitor population and a specific reduction of spinal interneurons but not of other cell populations. Here, we show that cells including progenitors in the embryonic spinal cord had occasional spontaneous, glycine\u2010mediated calcium transients that were blocked by the glycine antagonist strychnine and the L\u2010type calcium channel blocker nifedipine. As shown previously for chronic block by strychnine, block of these transients by nifedipine reduced interneuron differentiation. Our results indicate that glycinergic depolarization of neural progenitors evokes spontaneous calcium transients that may enhance the interneuron neurogenic program. \u00a9 2012 Wiley Periodicals, Inc. 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