Crustecdysone-induced modulation of electrical coupling and gap junction structure in crayfish hepatopancreatocytes.
Crustecdysone, the hormone responsible for onset and regulation of the molt cycle in Crustacea, causes an increase in ionic coupling of cells of the hepatopancreas concomitant with the events of the molt. Hepatopancreatic tissue incubated for up to 4 hr in modified Eagle Basal Medium containing crustecdysone, exhibited an approximate 29% decrease in intercellular resistance as compared with tissue incubated in control medium. This represents a 29% increase in ionic coupling between hepatopancreatocytes following treatment with crustecdysone. Examination of platinum replicas of freeze-fractured, crustecdysone-treated hepatocyte plasma membrane revealed that most of the gap junction plaques were round with tightly packed intramembrane particles; a condition indicative of highly coupled cells. Similar preparations of control plasmalemmae demonstrated many gap junction plaques which were round or irregular in shape with very loosely packed particles and were indicative of uncoupled junctions. Results of this study are identical to those from a previous investigation of the electrophysiology and freeze-fracture morphology of hepatopancreatocytes during the molt cycle (McVicar and Shivers, 1984), and are thus presumed to reflect a crustecdysone-controlled increase in cell communications in vivo.
D000818:Animals; D003400:Astacoidea / Q000502:physiology* / Q000648:ultrastructure; D004594:Electrophysiology; D005614:Freeze Fracturing; D007365:Intercellular Junctions / Q000648:ultrastructure; D008099:Liver / Q000187:drug effects / Q000502:physiology / Q000648:ultrastructure; D008297:Male; D008854:Microscopy, Electron; D010179:Pancreas / Q000187:drug effects / Q000502:physiology / Q000648:ultrastructure