Morphometrical analysis of the gap-junctional area in parenchymal cells of the rat liver after administration of dibutyryl cAMP and aminophylline

• Published in: Cell and tissue research 1988-06, Vol.252 (3), p.611-618
• Main Authors: De Mazière, A M, Scheuermann, D W
• Format: Article
• Language: English
• Subjects: Aminophylline - pharmacology; Animals; Bucladesine - pharmacology; Freeze Fracturing; Intercellular Junctions - drug effects; Intercellular Junctions - ultrastructure; Liver - cytology; Liver - drug effects; Liver - ultrastructure; Microscopy, Electron; Rats; Rats, Inbred Strains; Reference Values
• ISSN: 0302-766X; 1432-0878
• DOI: 10.1007/BF00216648

In view of the presumed involvement of gap junctions in the coordination of metabolic activities, the influence of cAMP as a regulatory signal of cell metabolism on gap junctions of hepatocytes has been examined. Male rats received two intraperitoneal doses of 10 mg dibutyryl cAMP/100 g body weight with a time interval of 2.5 h and were decapitated 2.5 h later. After this 5-h interval, analysis of freeze-fracture replicas of fixed liver tissue revealed an increase in the mean (+/- SEM) gap-junctional membrane portion on the lateral hepatocyte membranes from 0.049 +/- 0.003 (n = 66) in controls to 0.061 +/- 0.003 (n = 70) in treated rats, while the configuration of the connexons appeared unaltered. This effect could not be reinforced by prior administration of aminophylline: the relative gap-junctional area is similarly extended from 0.054 +/- 0.003 (n = 126) in the control group to 0.065 +/- 0.004 (n = 105) in the experimental animals. Probing for the time course of the junctional response, a group of rats was sacrificed 3 h after the onset of treatment. Already within this time, the gap-junctional area is augmented from 0.042 +/- 0.004 (n = 63) in the concurrent controls to 0.069 +/- 0.006 (n = 42) in the treated rats. These statistically significant increases in area may suggest a stimulating effect of cAMP on gap junctions of hepatocytes in vivo.