S336 A COMPARISON
774 YOSHIKI
BETWEEN
UNILATERAL
AND BILATERAL
KINDLING
OF THE RABBIT
HIPPOCAMPI MATSUDA’,
SHINICHI
KOGLJRE’,
AYAKO
UEHARA’,
MASAOMI
KITAYAMA’,
YOSHIMI
KATO’,
YASUO URATA’ ‘Dept. of Bioengn.,
Fat of Engn.,
I-236, Hachioji,
Soka Univ.,
Biotech., Tokyo Insti. of Tech., 4259, Nagatsuga, In previous studies on unilateral hippocampal
Midori-ku,
Tokyo
192-8577,
‘Dept. of Biotech.,
The present
(BK_group:n=8).
The characteristics
BK were kindled. stimulations
experiment
was designed
obtained
ii) Those animals
in BK. iii) Complex IIDs occurred
incomplete
UK-group
responses
in BK-group.
stage 5 convulsions at a higher frequency
(n=7), whereas the frequencies It is concluded
to reveal the contralateral
from UK- and BK-group
developed
of Biosci.&
Yokohama 227-0026
kindling of the rabbits (UK-group:n=
17) simple type of interictal
(IIDs), of which origin was situated in the contralateral side, seemed to have suppressive epileptogenesis.
Fat.
influence
effect in bilateral
on the kindling-induced hippocampal
kindling
animals are as follows. i) 5996 in UK, but 100% in with a mean of 18 stimulations in kindled
UK-group
in UK. while 29
(n=lO) but simple IIDs did in
of both types of IIDs were related to the enhancement
that both processes,
discharges
excitatory one based on the kindling completion
of behavioral and higher rate
of complex IIDs, and inhibitory one based on the delay of kindling and hrgher rate of simple IIDs. arc enhanced m the simultaneous kindling of bilateral hippocampl.
SEQUENTIAL
775
CHANGES
IN GLAST
PROTEIN
OF FECL+NDUCED
EPILEPSY
MODEL
TAKU DOIl. YUTO UEDAl,2, ‘Dept. of Psychiatry, 2Dept. Neurology,
L. JAMES WILLMORE
Miyazaki Medical College,
AND YOSHIO MITSUYAMA’
5200 Kihara, Kiyotake, Miyazaki 889-1692,
Univ. of Texas Medical Stool, 6431 Fannin, Houston, TX 77030, USA
Severe head injury in humans causes recurrent seizures; this form of epilepsy appears to correlate with occurrence of parenchymal hemorrhage. Injection of ferric cations, one component of hemoglobin, into rat amygdala, causes lipid peroxidation, and recurrent spontaneous seizures. We wondered whether regulation of glutamate might be perturbed as a mechanism of chronic epileptogenesis. Levels of glutamate transporter protein GLAST was measured in the ipislateral and contralateral hippocampi removed from rats having spontaneous iron-induced limbic seizures. At 15 days and 30 days after injection, when experimental animals were experiencing spontaneous limbic behavioral seizures, GLAST transporter protein was down-regulated. Epileptogenesis may correlate with impairment of glial glutamate transport, leading to excitation and imbalance of transmitter iniluences within the hippocampi.
776
ALTERATIONS POSTTRAUMATIC
YUTO UEDA1,2,TAKU ‘Dept. of Psychiatry, 2Dept. Neurology,
IN THE HIPPOCAMPAL EPILEPSY MODEL
GAT PROTEINS
OF
DOI’, L. JAMES WILLiMORE2 AND YOSHIO MITSUYAMAl
Miyazaki Medical College,
5200 Kihara, Kiyotake, Miyazaki 889-1692,
Univ. of Texas Medical Stool, 6431 Fannin, Houston, TX 77030, IJSA
Severe head injury in humans causes recurrent seizures; this form of epilepsy appears to correlate with occurrence of parenchymal hemorrhage. Injection of ferric cations, one component of hemoglobin, into rat amygdala, causes lipid peroxidation, and recurrent spontaneous seizures. We wondered whether regulation of gamma-aminobutyric acid (GABA) might be perturbed as a mechanism of chronic epileptogenesis. Levels of GABA transporter (GAT) proteins GAT-1, GAT-2 and GAT-3 in the hippocampus removed from rats having spontaneous iron-induced limbic seizures were measured by western blot. GAT- 1 and -2 were elevated up to 150%-80% at 15 days, and GAT-3 was elevated up to 250% at 5 days following the microinjection that initiated seizures. These increases of GAT proteins were observed at 30 days. In the experimental animals experiencing spontaneous limbic behavioral seizures, excessive reverse transport of GABA at ictal phase and excessive re-uptake at interictal phase will be induced by these up-regulation of GAT protein. Epileptogenesis may correlate with up-regulation of GABA transpoters in the hippocanpus, leading to excitation and imbalance of transmitter influences within the hippocampi.