A set of 29 monoclonal antibodies (MAbs) specific for the rabies virus nucleoprotein (N protein) was prepared and used to analyze the topography of antigenic sites. At least four partially overlapping antigenic sites were delineated on the N protein of rabies virus by competitive binding assays. Indirect immunofluorescent antibody tests using MAbs with a series of rabies and rabiesrelated viruses showed that epitopes shared by various fixed and street strains of rabies virus were mainly localized at antigenic sites II and III, while epitopes representing the genus-specific antigen of Lyssavirus were widely presented at sites I, III and IV. All but one of seven MAbs specific for antigenic sites I, IV and bridge site (I and II) reacted with the antigen that had been denatured by sodium dodecyl sulfate or 2-mercaptoethanol, as well as with the denatured N protein in Western blotting assays. However, none of the MAbs against antigenic sites II and III reacted with the denatured antigen. These data indicate that antigenic sites I and IV, and sites II and III on the N protein of rabies virus are composed of linear and conformation-dependent epitopes, respectively.

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Aims: Although it is commonly recognized that ethanol suppresses gluconeogenesis, the influence of alcohol intake on blood glucose levels remains controversial. Ethanol may act on both glucose production and glucose consumption in the liver. Thus, we studied each effect of ethanol on glucose oxidation, gluconeogenesis, glycogenesis and glycogenolysis in the liver. Methods: The rat liver was isolated and cyclically perfused with a medium containing 50 mmol/l ethanol. Results: Ethanol enhanced ¹⁴C-glucose oxidation in the liver from 1.09 ± 0.11 to 1.41 ± 0.14 µmol for 20 min (p < 0.05). Gluconeogenesis from ¹⁴C-lactate was markedly reduced by ethanol from 8.0 ± 1.3 to 1.5 ± 0.6 µmol for 12 min (p < 0.01). Ethanol increased glycogenolysis (net hepatic glucose output, 0.47 ± 0.10 vs. 0.22 ± 0.04 mmol/30 min, p < 0.01), and then decreased hepatic glycogen content (179 ± 38 vs. 273 ± 39 mg in the presence of 1 mU/ml insulin after 30 min of perfusion, p < 0.05). Ethanol decreased the direct glycogenesis from ¹⁴C-glucose from 0.55 ± 0.08 to 0.33 ± 0.05 µmol per 100 mg glycogen for 30 min (p < 0.01). Ethanol inhibited the indirect glycogenesis from ¹⁴C-lactate from 0.21 ± 0.04 to 0.09 ± 0.01 µmol per 100 mg glycogen for 30 min (p < 0.01). Discussion: The influence of ethanol on the blood glucose regulation by the liver seems to be different between fasted and fed states. Namely, ethanol has both the hypoglycemic effects through decreased gluconeogenesis and increased glucose oxidation and the hyperglycemic effects through decreased glycogenesis and increased glycogenolysis.

We examined the developing synaptic junctions in the rat frontal cortex in cases of fetal alcohol syndrome, the objective being to determine the synapse-mental retardation relationship. On day 21 of gestation, the ultrastructural synaptic junction revealed no obvious differences between the ethanol-exposed and control rats; however, the number of synapses in ethanol-exposed rats was one third that of the controls. The possible relationship between synaptic density in the frontal cortex and mental development has to be considered.