Brain
glycogen could be considered as an energy store for neuronal activity, with high relevance in
epilepsies. We selected two lines of mice based upon their latency to
methionine sulfoximine (MSO) dependent-
seizures: MSO-Fast and MSO-Slow, and their neurochemical characterization was attempted in order to look for the mechanisms of epileptogeny. We determined the MSO effect on brain
glycogen in the two selected lines and their eight parental strains, and on indolamines and
catecholamines. The increase in brain
glycogen content induced by MSO is significantly lower in MSO-Fast than in MSO-Slow. At the onset of
seizures the degradation of accumulated
glycogen was higher in MSO-Slow mice than in MSO-Fast ones. Moreover, a positive correlation was observed between the magnitude of latency toward MSO-induced
seizures and brain
glycogen content in the eight parental strains used for selection. A striking proportionality between the content of
glycogen and
5-hydroxytryptamine (5-HT) was observed in cerebral cortices of both selected lines. However, the cortical
5-HT level is higher in MSO-Fast than in MSO-Slow, and it is significantly decreased at the onset of
seizures in both lines. Brain
glycogen content is implicated in the developed model of mice with different latency to MSO-dependent
seizures: The higher the brain
glycogen content, the longer the latency; and
5-HT is involved in the control of latency to
seizures-induced by MSO in these two lines. Our model of MSO "sensitive" (MSO-Fast) and "resistant" (MSO-Slow) mice could lead to a better understanding of MSO mechanisms of epileptogenesis, and the relationship between epileptogenic and glycogenic MSO effects.