Inositol trisphosphate (IP3) receptors and epileptic seizure.
The effects of anticonvulsants and Ca2+ channel antagonists on the inositol trisphosphate (IP3) binding and IP3-induced Ca2+ release were examined in brain membrane fractions. Anticonvulsant (PHT and valproate) and Ca2+ channel antagonists (verapamil, diltiazem, flunarizine, nicardipine and cinnarizine), examined did not significantly inhibit the IP3-receptor binding. The Kd and Bmax values of the IP3 binding did not change significantly in the various brain regions of the amygdala-kindled rats, killed 10 days after the last seizure, compared to those of controls. On the other hand, PHT, PB and carbamazepine inhibited the Ca2+ releasing activity of IP3 in the cerebellar membrane fractions by approximately 20% at therapeutic concentrations.
Imazawa
M
M
National Institute of Neuroscience, NCNP, Nodaira, Japan.
Kabuto
Y
Y
Miyamoto
K
K
Nishimura
S
S
Yagi
K
K
D000679:Amygdala / Q000503:physiopathology*; D000818:Animals; D001931:Brain Mapping; D002118:Calcium / Q000502:physiology; D015220:Calcium Channels / Q000502:physiology; D004827:Epilepsy / Q000503:physiopathology*; D005071:Evoked Potentials / Q000502:physiology; D053496:Inositol 1,4,5-Trisphosphate Receptors; D007696:Kindling, Neurologic / Q000502:physiology*; D008297:Male; D051381:Rats; D011919:Rats, Inbred Strains; D011956:Receptors, Cell Surface / Q000502:physiology*; D018160:Receptors, Cytoplasmic and Nuclear
D015220:Calcium Channels; D053496:Inositol 1,4,5-Trisphosphate Receptors; D011956:Receptors, Cell Surface; D018160:Receptors, Cytoplasmic and Nuclear; D002118:Calcium