Amygdaloid Kindling Elicits Persistent Changes in Pertussis Toxin‐Catalyzed ADP‐Ribosylation

Abstract

We examined the changes in pertussis toxin (PTX)-catalyzed ADP-ribosylation in amygdaloid-kindled rats to clarify the role of G proteins in the basic mechanisms of epilepsies. Autoradiographic analysis showed a remarkable increase in PTX-catalyzed ADP-ribosylation in 39-41-kDa proteins in hippocampus and cerebral cortex of kindled animals. The 39- to 41-kDa proteins were shown to be alpha-subunits of Gi and Go by immunoblotting with specific anti-Gi alpha and anti-Go alpha. The increase in ADP-ribosylation of these proteins was observed on stimulated and unstimulated sides of brains 24 h after the last generalized seizure and persisted for at least 3-4 weeks. These results suggest that persistent alterations in signal transduction through Gi and Go might be related to acquisition of long-lasting epileptogenesis.

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.…”