—The stability of the GABA content of synaptosomal‐enriched fractions was evaluated by two approaches. Firstly, the addition of 10−3m‐aminooxyacetic acid to the homogenizing medium totally inhibited the GABA‐degrading enzyme in the fractions but did not affect the GABA levels. This indicated that GABA was not being metabolized during the normal preparation of the synaptosomal‐enriched fraction. Secondly, when synaptosomal‐enriched fractions were re‐fractionated by discontinuous density gradient centrifugation, the GABA contents of the fractions before and after the second fractionation were very similar provided they were expressed on a per mg protein basis. It was therefore concluded that the GABA content of the organelles was not subject to change during the fractionation procedures. On the basis of these findings and others it was suggested that the synaptosomal‐enriched fraction could be used as a model to evaluate drug‐induced changes in GABA levels in nerve endings. In vivo experimentation indicated that the convulsant agents hydrazine, isonicotinic acid hydrazide and aminooxyacetic acid brought about similar decreases in the GABA content of the synaptosomal‐enriched fractions prepared from tissue at the onset of seizures despite the fact that no correlation was observed between seizure activity and whole brain GABA levels.
Lesions induced in the gills of rainbow trout (Salmo gairdneri) by exposure to acutely lethal aqueous concentrations of inorganic mercury and copper were examined by light and electron microscopy. Lesions were most severe during the first 48 hours of exposure to the metals and were characterized primarily by apoptosis of lamellar epithelial cells and lamellar fusion. The latter process occurred either by simple apposition of adjacent lamellae to each other or through epithelial hypertrophy and hyperplasia. Except for hypertrophy of and increased number of primary lysosomes in lamellar epithelial cells of animals exposed to mercury, branchial lesions were not prominent in fish collected between 48 and 96 hours. The branchial lesions observed in this study are compared with pathological processes occurring in mammals.
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