Ultrastructural changes related to functional activity in gastric oxyntic cells.
When stimulated to secrete HCl the gastric oxyntic cell undergoes profound morphological change. The identifiable apical cell surface is greatly expanded in the stimulated oxyntic cell as compared with nonsecreting ones. To account for this change, one hypothesis proposes that the expanded surface is derived from the fusion of cytoplasmic tubulovesicular membranes with the existing limited apical membrane surface. An alternative hypothesis suggests that the tubulovesicular compartment is actually confluent with the apical surface at all times and that the morphological appearance follows the expansion of this supercollapsed compartment as HCl secretion commences. A variety of morphological evidence is reviewed here including transmission electron microscopy during various stages of secretion and inhibition, analysis of freeze-fracture replicas, penetration of macromolecular tracers, and membrane surface-staining characteristics. It is concluded that the weight of evidence favors a membrane fusion process. Moreover, recent comparative studies of membrane fractions from resting and secreting stomachs show different morphological and functional properties that are also consistent with a fusion hypothesis as a fundamental event in the membrane transformation of the oxyntic cell.
D000818:Animals; D002462:Cell Membrane / Q000187:drug effects / Q000648:ultrastructure; D005614:Freeze Fracturing; D005750:Gastric Juice / Q000378:metabolism; D005753:Gastric Mucosa / Q000166:cytology / Q000187:drug effects / Q000648:ultrastructure*; D005947:Glucose / Q000494:pharmacology; D006632:Histamine / Q000494:pharmacology; D006863:Hydrogen-Ion Concentration; D008854:Microscopy, Electron; D013552:Swine; D013861:Thiocyanates / Q000494:pharmacology
D013861:Thiocyanates; D006632:Histamine; D005947:Glucose