Altered expression levels of G protein subclass mRNAs in various seizure stages of the kindling model

Functional significance of stimulatory GTP‐binding protein in hippocampus is associated with kindling‐elicited epileptogenesis

“… 8,9 We presented experimental findings to suggest that the G‐protein‐, including G s , mediated process may be associated with kindling‐elicited epileptogenesis. 10–12 Our results support the hypothesis that kindling‐related epileptogenesis might cause functional imbalance between G‐protein subclasses. From these observations, it has been proposed that G protein‐mediated, especially G s , mechanisms have an impact on the basic pathogenesis of epileptic syndromes.…”

“…We reported previously of an increase in the G sα mRNA level in the cerebral cortex both at 24 h after and 4 weeks after the last seizure in the amygdaloid kindling model. 12 Therefore, we supposed that the increase of G s mRNA in the cerebral cortex is associated with the basic mechanisms of the induction of seizure generation and is also related to the maintenance of long‐lasting epileptogenesis. Because the increase in expression level of G sα mRNA in the hippocampus was observed only at 24 h after the last seizure, the alteration of G s in the hippocampus might be related to the mechanism of the generalization of epileptic seizures rather than to the acquisition process and/or maintenance of epileptogenesis.…”

G protein β3 subunit C825T polymorphism modifies the presentation of temporal lobe epilepsy

“…In particular, there are data suggesting a role of the inhibitory G protein G i . In a rat kindling model, brain mRNA level for both G s a (bilaterally) and G i2 a (only on stimulated side) were increased (12). In a rat kindling model, brain mRNA level for both G s a (bilaterally) and G i2 a (only on stimulated side) were increased (12).…”

“…Thus, inhibition of the G i protein with pertussis toxin increases the severity of status epilepticus in a rat model (10), while in rats with genetic absence epilepsy from Strasbourg, inhibition of G i through injections with pertussis toxin resulted in decrease of seizures (11). In a rat kindling model, brain mRNA level for both G s a (bilaterally) and G i2 a (only on stimulated side) were increased (12). Mice deficient of the G protein c 3 subunit appear to be more susceptible to seizures (13).…”

Target Discovery and Validation Reviews and Protocols

“…There are few drugs in this group: butanoic (105), valproic (106, 107), and 4-phenylbutanoic (108). Despite being much less potent than the hydroxamic acids and their pleiotropic effects, these are currently among the best studied HDAC inhibitors: valproic acid and phenylbutyrate have already been approved for use in treating epilepsy and some cancers, respectively, whereas butanoic acid is undergoing clinical trials (109,110).…”