Mesenteric mast cell degranulation is not essential for conditioned taste aversion.
The possible role of mesenteric mast cell degranulation as the mediator of the initial UCS effects in the complex sequences leading to conditioned taste aversion (CTA) was studied. Both LiCl and Compound 48/80, a potent mast cell degranulator, produced CTA to 10% sucrose. Whereas the Compound 48/80 groups displayed massive mast cell degranulation, neither the LiCl treated nor saline control groups demonstrated any histologically determinable alterations. Administration of the antihistamine chlorpheniramine at dosages known to block radiation-induced CTA before the sucrose CS-UCS pairings did not block either LiCl- or Compound 48/80-induced CTA; the antihistamine actually facilitated the aversion. However, pretreatment with the antihistamine did not alter mesenteric mast cell morphology.
D000818:Animals; D001362:Avoidance Learning / Q000502:physiology*; D002744:Chlorpheniramine / Q000494:pharmacology; D003594:Cytoplasmic Granules / Q000502:physiology*; D004327:Drinking Behavior / Q000187:drug effects; D008094:Lithium / Q000494:pharmacology; D008297:Male; D008407:Mast Cells / Q000502:physiology* / Q000648:ultrastructure; D008643:Mesentery / Q000166:cytology*; D051381:Rats; D013649:Taste / Q000502:physiology*; D003189:p-Methoxy-N-methylphenethylamine / Q000494:pharmacology
D002744:Chlorpheniramine; D003189:p-Methoxy-N-methylphenethylamine; D008094:Lithium