Ca2+/calmodulin-dependent protein phosphorylation is not altered by amygdaloid kindling.
Kindling is a process in which episodic electrical stimulation permanently increases seizure susceptibility. One mechanism to account for a change in seizure susceptibility is some alteration in signal transduction, possibly at the level of second messenger systems. In this study, male Long-Evans rats were kindled in the amygdala, and Ca2+/calmodulin (Ca2+/CaM)-dependent protein phosphorylation was assessed at the site of the primary kindled focus using one- and two-dimensional gel electrophoresis. In vitro phosphorylation of membrane and cytosol fractions in the presence of absence of Ca2+/CaM did not differentiate kindled from nonkindled amygdaloid tissue. These results suggest that changes in Ca2+/CaM-dependent phosphorylation are not related to the mechanism(s) underlying the establishment of an amygdaloid kindled focus.
Burdette
L J
LJ
Department of Neurology, Graduate Hospital, Philadelphia, PA 19146.
O'Callaghan
J P
JP
D000679:Amygdala / Q000502:physiology*; D000818:Animals; D002118:Calcium / Q000378:metabolism*; D002147:Calmodulin / Q000378:metabolism*; D003600:Cytosol / Q000378:metabolism; D007696:Kindling, Neurologic / Q000502:physiology*; D008297:Male; D008566:Membranes / Q000187:drug effects / Q000378:metabolism; D009419:Nerve Tissue Proteins / Q000378:metabolism*; D010766:Phosphorylation; D051381:Rats; D012640:Seizures / Q000503:physiopathology
D002147:Calmodulin; D009419:Nerve Tissue Proteins; D002118:Calcium