Abstract
Rats and mice were submitted either to the convulsant methionine sulfoximine (MSO) alone or to MSO combined with actinomycin D or methionine, respectively. At 24 h after the i.p. administration of these compounds, the animals were killed and tissue samples were prepared for EM. MSO induced grand mal type seizures which were abolished by methionine. In saline controls, glycogen was as .beta. particles located in the cytoplasm of astrocytes, i.e., in perikarya and processes. Liver glycogen was as perinuclear masses of .alpha. and .beta. particles or as .alpha. particles scattered in all the cytoplasm. When treated with MSO, glycogen was as .alpha. and .beta. particles which invaded all areas of the astrocyte cytoplasm, this increase being tremendous in perivascular end feet. Actinomycin D slowed down the accumulation of glycogen particles while methionine completely abolished it. Glycogen particles were confined to the astrocytes and were never seen in other types of cells. In liver, MSO induced an important decrease or a complete disappearance of glycogen particles. When the convulsant was combined with actinomycin D or with methionine, the figures looked like those of controls. These results have been discussed in relation to the mechanism of glycogenesis in central nervous system of rodents submitted to MSO.