Lectin histochemistry of the rat brain following thioacetamide-induced hepatic failure.

Abstract

Biotinyl derivatives of several lectins were used to study the localization of glycoconjugates in the cerebral microcapillaries and various brains of rats given at 24-h intervals two i.p. administrations of a hepatotoxin-thioacetamide (TAA) and examined 21 d posttreatment. At this time, the rats were asymptomatic with regard to hepatic encephalopathy but showed specific and selective changes in the blood-brain-barrier (BBB) transport of basic amino acid, but no BBB damage, and region-specific neuronal injury in the hippocampus and neocortex. The lectins tested recognized the following sugar residues: beta-D-galactosyl (Ricinus communis agglutinin [RCA-1]); N-acetyl-glucosaminyl and N-acetyl-neuraminic acid (wheat-germ agglutinin [WGA]); N-acetyl-D-galactosaminyl (Helix pomatia agglutinin [HPA]); beta-D-galactosyl and D-galactosyl neuraminic acid (peanut agglutinin [PNA]), and alpha-D-galactosyl and alpha-D-mannosyl (concanavalin A [Con A]). The treatment markedly decreased the binding to the cerebromicrovascular network of the hippocampus and neocortex of RCA-1 and WGA. The binding of these two lectins to their complementary monosaccharide residues appears to reflect subtle changes in BBB function, with a detection threshold below the conventional BBB permeability tests. The changes in the binding of the other two lectins: an increase of HPA binding and a decrease of Con A binding, confined to neocortical neurons and pyramidal cells of hippocampus injured by TAA treatment.