The permeability of isolated and in situ mouse hepatic gap junctions studied with enzymatic tracers

Abstract

We have studied the effects of phospholipasc C from Clostridium welchii on gap junctions in the intact mouse liver and in a junction-rich fraction prepared from mouse liver. Treatment of the isolated junctions results in the disappearance of both the 20 A gap and of thc polygonal lattice visible with lanthanum. The junctions are morphologically unaltered, however, when whole livers are perfused with phospholipasc via the portal vein. These results suggest that cxtracellular phospholipase cannot diffuse into the junctional area, but that the enzyme may affect structures within the gap from its cytoplasmic surfaces which become exposed in the isolated preparations. Horseradish peroxidase, which has physical dimensions similar to those of Clostridium phospholipase is also denied access to the 20 A gap in whole liver, while pcroxidase reaction product can be seen in the gap in isolated preparations. Beef liver catalase, however, a tracer molecule much larger than peroxidase, cannot penetrate even in isolated fractions. If the cytoplasmic approaches to the gap junction used by peroxidase and phospholipase arc available in vivo, and have not been created during the process of mechanical isolation, thcy may play a role in cell-to-cell passage of molecules larger than ions. © 1971, Rockefeller University Press. All rights reserved.