[Validation Study of Analytical Method for Determination of Amnesic Shellfish Poison in Bivalves].

Amnesic shellfish poison (ASP) is regarded as one of the shellfish poison groups in the EU, though it is not subject to regulation in Japan. We have developed an analytical method of ASP based on the report by Hatfield et al. and other methods. Validation studies were carried out with certified compositional reference materials (CRM). Performance parameters were estimated based on 17 analytical results. The estimate of trueness was 97.5%, and the estimate of intralaboratory reproducibility (RSD) was 1.5%. The HorRat(r) value was 0.16. These performance parameters meet the criteria in the Codex Procedural Manual. Furthermore, internal quality control was performed by using the CRM. The action limits were set based on the performance parameters of the method. Most of the results of the internal quality control were within the action limit range. The results confirmed that the quality of the analyses was well maintained. The purpose of the analytical method is to confirm that the level of ASP in scallop is less than 4.6 mg/kg. The applicability of the analytical method to scallops was confirmed by using spiked samples.

Fgf16 is required for specification of GABAergic neurons and oligodendrocytes in the zebrafish forebrain.

Fibroblast growth factor (Fgf) signaling plays crucial roles in various developmental processes including those in the brain. We examined the role of Fgf16 in the formation of the zebrafish brain. The knockdown of fgf16 decreased cell proliferation in the forebrain and midbrain. fgf16 was also essential for development of the ventral telencephalon and diencephalon, whereas fgf16 was not required for dorsoventral patterning in the midbrain. fgf16 was additionally required for the specification and differentiation of γ-aminobutyric acid (GABA)ergic interneurons and oligodendrocytes, but not for those of glutamatergic neurons in the forebrain. Cross talk between Fgf and Hedgehog (Hh) signaling was critical for the specification of GABAergic interneurons and oligodendrocytes. The expression of fgf16 in the forebrain was down-regulated by the inhibition of Hh and Fgf19 signaling, but not by that of Fgf3/Fgf8 signaling. The fgf16 morphant phenotype was similar to that of the fgf19 morphant and embryos blocked Hh signaling. The results of the present study indicate that Fgf16 signaling, which is regulated by the downstream pathways of Hh-Fgf19 in the forebrain, is involved in forebrain development.