Inhibition by anti-(nicotinic acetylcholine receptor) antibodies of acetylcholine-induced dopamine release from striatal nerve terminals

with urease. A third minor metabolite was present in urine collected after intraperitoneal administration but remains unidentified. The quantitative distribution of pterin-dcarboxylic acid and urea in the 0-24 h urine samples is shown in Table 1. Fukushima & Nixon (1980) reported the degradation of [2-14C]pterin-6-carboxylic acid to 14C02 by the gut microorganisms of the rat. It is possible that this has occurred in vivo in these experiments and the resulting 14C0, lost. Thus it appears that the pterin ring is not stable in vivo as pterin6-carboxylic acid is metabolized to urea and possibly CO, in the rat. The contribution of the gut microflora to this process remains to be established. Labelled urea and 14C0, are detected as metabolites after the administration of [ 2-l4Clfolates to rats and guinea pigs (Connor et al., 1977; Connor & Blair, 1979; R. Choolun, personal communication). The results reported here suggest that pterin6-carboxylic acid may be an intermediate in the formation of these catabolites from folate. However, pterin-6-carboxylic acid is excreted at least partly unchanged and the absence of pterin-6-carboxylic acid from the urine of rats given folate suggests the oxidative breakdown of dihydropteroyl-L-glutamate is a minor route of metabolism under normal circumstances. Rats treated with methotrexate excrete pterin-6-carboxylic acid as a catabolite of folate polyglutamates (A. Saleh, unpublished work). In these rats the inhibition of dihydrofolate reductase causes a build-up of dihydropteroyl-L-glutamate derivatives and leads to increased folate breakdown.