To identify new loci predisposing to insulin-dependent diabetes mellitus (IDDM), we have investigated 250 families with more than one diabetic child. Affected sibling pair linkage analysis revealed strong evidence for an IDDM susceptibility locus near D15S107 on chromosome 15q26 (P = 0.0010) termed IDDM3. Families less predisposed through genes in the HLA region provided most of the evidence for linkage. In these families, discordant sibling pairs also showed linkage (P = 0.0052), and sibling pair disease concordance or discordance was strongly related to the proportion of genes the pair shared at D15S107 (P = 0.0003). Our study also revealed evidence for an IDDM locus on chromosome 11q13 (IDDM4) using affected siblings (P = 0.0043), but no evidence using discordant siblings.

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We re-investigated the occurrence of substance P-like immunoreactivity in the retina of the goldfish Carassius auratus using antisera to substance P and other tachykinins. Most antisera labelled a previously described single class of mono-stratified amacrine cells arborizing in layer 3 of the inner plexiform layer. Preabsorption experiments showed that these amacrine cells contained at least one tachykinin-like peptide. One antiserum (INC 353) to substance P labelled not only these amacrine cells but also fibres in layer 1 of the inner plexiform layer and fibres in the optic nerve. These fibres were identified as retinopetal projections of the nervus terminalis, in part because of colocalized labelling with antisera against gonadotropin-releasing hormone and FMRFamide. Preabsorption experiments showed that the substance P-immunoreactive material in the nervus terminalis was not substance P or any other typical tachykinin. Labelling of the nervus terminalis with INC 353 was blocked by preabsorption with two bovine FMRF-amide-like peptides, F8Famide and A18Famide, which contain a substance P(4-7)-like region. Antisera to F8Famide and A18Famide strongly labelled ganglia of the nervus terminalis and retinopetal fibres. We suggest that labelling of the nervus terminalis by antisera to substance P and FMRFamide occurs because of homologies between these antigens and a non-tachykinin, endogenous peptide that is similar to F8Famide and A18Famide.

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