ABSTRACT
Adult male mice infected with the M variant of encephalomyocarditis virus develop hyperglycaemia acutely as a consequence of B cell injury. The severity of the metabolic disease is variable and many animals become normoglycaemic during convalescence. The islets of Langerhans of these mice exhibit minor structural changes, but there are no significant abnormalities of insulin and glucagon secretion. In contrast, animals with persistent hyperglycaemia exhibit striking morphological alterations in the islets. The A cell mass is prominent, whereas B cells are reduced in number and exhibit striking cytological features. These changes are associated with both hypoinsulinaemia and hyperglucagonaemia.
Subject(s)
Diabetes Mellitus, Experimental/etiology , Enterovirus Infections/pathology , Islets of Langerhans/pathology , Animals , Diabetes Mellitus, Experimental/metabolism , Diabetes Mellitus, Experimental/pathology , Encephalomyocarditis virus , Enterovirus Infections/metabolism , Glucagon/metabolism , Glucose Tolerance Test , Immunoenzyme Techniques , Insulin/metabolism , Male , Mice , Time FactorsABSTRACT
The M variant of encephalomyocarditis virus (EMC) produces a disease similar to human insulin-dependent diabetes mellitus in some but not all strains of mice. This diabetogenic M variant was found to induce fivefold more interferon than non-diabetogenic strains of EMC in cultures of mouse L 929 fibroblasts. When interferon induced by the M variant was added to monolayers of B cells from both diabetes-'susceptible' CD-1 mice and 'resistant' C57 bl/6 mice before EMC infection, B cell damage and virus replication were delayed. In addition, viral production in B cell cultures from C57 bl/6 mice was reduced five- to tenfold. A similar effect was not found when cultures from CD-1 mice were treated with interferon. Thus, interferon might play an important role in modulating the severity of the initial infection of B cells.
Subject(s)
Encephalomyocarditis virus/physiology , Interferons/pharmacology , Islets of Langerhans/microbiology , Animals , Cells, Cultured , Diabetes Mellitus/etiology , Disease Susceptibility , Encephalomyocarditis virus/genetics , Enterovirus Infections , Insulin/metabolism , Insulin Secretion , Interferons/metabolism , Islets of Langerhans/metabolism , Male , Mice , Mice, Inbred C57BLABSTRACT
The cranial cervical sympathetic ganglion (CCG) provides the primary innervation of the pineal gland in several gallinaceous species. The CCG is located at the base of the skull near the exoccipital bone, dorsal to the level of the vagus and glossopharyngeal nerves. It occupies a much larger volume and appears pinkish-gray, instead of white, when compared to the petrosal ganglion. To surgically remove the CCG, chicks were anesthetized with halothane vapor. Following a small skin incision, blunt dissection was used to expose the CCG lying adjacent to the internal carotid. The ganglion was grasped with small forceps and pinched free of its fine neural connections to adjacent nerves. The success of the surgery was confirmed visually and by complete adrenergic dennervation of the pineal gland. The entire surgical procedure required approximately 20 min per bird. Mortality was less than 20% overall.
