Regional Accumulation of 14C-zonisamide in Rat Brain during Kainic Acid-induced Limbic Seizures

2001 ◽  
Vol 28 (4) ◽  
pp. 341-345 ◽  
Author(s):  
Koichi Akaike ◽  
Shigeya Tanaka ◽  
Hideshi Tojo ◽  
Shin-ichiro Fukumoto ◽  
Morikuni Takigawa ◽  
...  
Keyword(s):  
Status Epilepticus ◽  
Rat Brain ◽  
Kainic Acid ◽  
Sensorimotor Cortex ◽  
Dorsal Hippocampus ◽  
Femoral Vein ◽  
Experimental Studies ◽  
Phosphate Buffer Solution ◽  
Limbic Seizures ◽  
Secondary Generalization

Background:Zonisamide (ZNS) is an antiepileptic drug developed in Japan. Various experimental studies have investigated the effects of ZNS. However, the mechanism of action of ZNS against limbic seizures and secondary generalization is not well-known. We studied ictal regional accumulation of ZNS in the rat brain during kainic acid (KA)-induced limbic status epilepticus.Methods:Fourteen male Wistar rats underwent a stereotactic operation. For recording the electroencephalogram (EEG), electrodes were placed in the left amygdala (LA), left dorsal hippocampus, and over the left sensorimotor cortex. For microinjection, a stainless steel cannula was also inserted into the LA. Seven days after surgery, rats were anesthetized and a catheter was inserted into the femoral vein. The animals were immobilized and allowed to recover from anesthesia for at least two hours. In eight rats, 1.0μL (1.0μg) of KA was injected into the LA, and 1.0 μL of phosphate buffer solution was injected into the LA in six control rats. Sixty minutes after injection, 14C-ZNS was administered intravenously, and an autoradiographic study was done.Results:During limbic status epilepticus, only seizures in the sensorimotor cortex were markedly attenuated a few minutes after 14C-ZNS administration. Additionally, high uptake of 14C-ZNS was noted ipsilaterally in the sensorimotor cortex, parietal cortex and thalamus (lateral portion). In control rats, no EEG change was seen, and distribution of 14C-ZNS was rather homogeneous.Conclusion:These results suggested that ZNS suppresses secondary generalization of limbic seizures by a direct effect on the cerebral cortex.

scholarly journals Developmental Hypothyroidism Increases the Expression of Kainate Receptors in the Hippocampus and the Sensitivity to Kainic Acid-Induced Seizures in the Rat

Endocrinology ◽  
2010 ◽  
Vol 151 (7) ◽  
pp. 3267-3276 ◽  
Author(s):  
Elena Giné ◽  
Jose Angel Morales-Garcia ◽  
Ana Perez-Castillo ◽  
Angel Santos
Keyword(s):  
Status Epilepticus ◽  
Kainic Acid ◽  
Neuronal Loss ◽  
Immunohistochemical Analysis ◽  
Kainate Receptors ◽  
Normal Brain ◽  
Limbic Seizures ◽  
Neurotoxic Effects ◽  
Clear Increase ◽  
Normal Brain Development

Thyroid hormones are essential for normal brain development, and multiple alterations at behavioral, cognitive, cellular, and molecular levels have been described in animals made hypothyroid during development. Here we analyzed the effect of developmental hypothyroidism in the rat on the sensitivity to kainic acid-induced limbic seizures and the expression of kainate receptors in the hippocampus. Our results show that hypothyroid rats are extremely sensitive to the proconvulsant and neurotoxic effects of kainic acid (KA). Hypothyroid rats entered in status epilepticus at a dose of KA three times lower than that required to reach status epilepticus in control animals. In accordance with this, high levels of glial activation and neuronal loss after low KA dose injections were observed only in the hippocampus of hypothyroid rats. These effects correlated with an increased expression of kainate receptor subunits, excluding GluR5, in the hippocampus of hypothyroid animals. The concentrations of GluR6, GluR7, KAR1, and KAR2 (ionotropic glutamate receptor subunits of the kainic acid subtype) mRNAs were increased between 50 and 250% in hypothyroid animals relative to the values in controls. In agreement with these results, Western blot and immunohistochemical analysis showed a clear increase in the hippocampal content of GluR6/7 proteins in hypothyroid animals.

scholarly journals Spatiotemporal Characterization of mTOR Kinase Activity Following Kainic Acid Induced Status Epilepticus and Analysis of Rat Brain Response to Chronic Rapamycin Treatment

PLoS ONE ◽  
2013 ◽  
Vol 8 (5) ◽  
pp. e64455 ◽  
Author(s):  
Matylda Macias ◽  
Magdalena Blazejczyk ◽  
Paulina Kazmierska ◽  
Bartosz Caban ◽  
Agnieszka Skalecka ◽  
...  
Keyword(s):  
Status Epilepticus ◽  
Rat Brain ◽  
Kainic Acid ◽  
Kinase Activity ◽  
Brain Response ◽  
Rapamycin Treatment ◽  
Mtor Kinase

Dietary supplementation with α-tocopherol reduces neuroinflammation and neuronal degeneration in the rat brain after kainic acid-induced status epilepticus

2011 ◽  
Vol 45 (10) ◽  
pp. 1136-1142 ◽  
Author(s):  
Michele Betti ◽  
Andrea Minelli ◽  
Patrizia Ambrogini ◽  
Stefano Ciuffoli ◽  
Valentina Viola ◽  
...  
Keyword(s):  
Status Epilepticus ◽  
Rat Brain ◽  
Kainic Acid ◽  
Neuronal Degeneration ◽  
Dietary Supplementation

ADAM9, ADAM10, and ADAM15 mRNA levels in the rat brain after kainic acid-induced status epilepticus

2005 ◽  
Vol 137 (1-2) ◽  
pp. 272-275 ◽  
Author(s):  
R.M. Ortiz ◽  
I. Kärkkäinen ◽  
A.-P.J. Huovila ◽  
J. Honkaniemi
Keyword(s):  
Status Epilepticus ◽  
Rat Brain ◽  
Kainic Acid ◽  
Mrna Levels

scholarly journals Effect of the compound GIZH -290 and levetiracetam on epileptic activity in rat brain structures on EEG models of bemegrid-induced seizures

2021 ◽  
pp. 14-18
Author(s):  
T. A. Voronina ◽  
S. A. Litvinova ◽  
I. G. Kovalev
Keyword(s):  
Rat Brain ◽  
Lateral Hypothalamus ◽  
Sensorimotor Cortex ◽  
Dorsal Hippocampus ◽  
Brain Structures ◽  
High Amplitude ◽  
Epileptic Activity ◽  
Paroxysmal Activity ◽  
Epileptic Discharges ◽  
Generalized Epileptic Activity

The effect of levetiracetam (a derivative of 4-phenylpyrrolidone) and its original analog, the compound GIZH-290, on primary generalized epileptic activity (EpA) in rat brain structures (sensorimotor cortex, dorsal hippocampus-CA3 field and lateral hypothalamus field) on EEG models of bemegridinduced seizures was studied. It was found that EpA, after the introduction of bemegrid, appears in 1–2 minutes in the form of prolonged generalized high-amplitude discharges and is registered within 3 hours. GIZH-290 (5 mg/kg, intraperitoneal, 15 minutes after bemegrid) causes a significant (p < 0.05) decrease in the number of epileptic discharges in the cortex and at the level of the trend in the hippocampus, which is accompanied by a decrease in the amplitude of the Epi-discharges. Levetiracetam at a dose of 200 mg / kg does not significantly change the severity of paroxysmal activity (the number of convulsive discharges and their duration) caused by bemegrid.

Anterior pericaudate white matter is important for the secondary generalization of kainic acid-induced limbic seizures in rats

2007 ◽  
Vol 118 (9) ◽  
pp. e192-e193
Author(s):  
Shin-ichi Imamura ◽  
Shigeya Tanaka ◽  
Koichi Akaike ◽  
Hideshi Tojo ◽  
Norihiko Sakoda ◽  
...  
Keyword(s):  
White Matter ◽  
Kainic Acid ◽  
Limbic Seizures ◽  
Secondary Generalization

scholarly journals Blockade of Nitric Oxide Synthesis Inhibits Hippocampal Hyperemia in Kainic Acid-Induced Seizures

1994 ◽  
Vol 14 (4) ◽  
pp. 581-590 ◽  
Author(s):  
Anne-Sophie Rigaud-Monnet ◽  
Elisabeth Pinard ◽  
Josiane Borredon ◽  
Jacques Seylaz
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Kainic Acid ◽  
Dorsal Hippocampus ◽  
Limbic Seizures ◽  
Arterial Blood ◽  
Blood Flow Control ◽  
Baseline Values ◽  
Synthase Inhibitor ◽  
Spontaneously Breathing

We investigated whether the nitric oxide (NO) synthase inhibitor NG-nitro-l-arginine methyl ester (l-NAME) affects the cerebrovascular changes occurring in seizures induced by kainic acid (KA) in awake, spontaneously breathing rats. Blood flow and tissue Po2 and Pco2 were continuously and simultaneously measured by mass spectrometry from a cannula chronically implanted into the dorsal hippocampus. l-NAME (20 mg/kg; n = 8) or saline (n = 9) was administered i.p. 30 min prior to i.p. KA (10 mg/kg) injection. l-NAME significantly decreased hippocampal blood flow and Po2 and increased mean arterial blood pressure (MABP). In l-NAME-treated rats, seizure activity occurred about 10 min sooner than in control rats, and status epilepticus was inevitably followed by a flat electroencephalogram and sudden death. In contrast, control rats survived KA-induced seizures. Hippocampal blood flow was significantly less elevated during the seizures in l-NAME-treated rats than in control rats (maximal levels, 170 and 450%, respectively, of baseline values), though MABP remained significantly higher. Hippocampal Po2 was significantly decreased at all times after KA injection in l-NAME-treated rats, whereas it remained at or above normoxic levels in control rats. The present results show that l-NAME markedly attenuates the hippocampal blood flow and tissue Po2 changes in response to enhanced metabolic activity due to limbic seizures and suggest that NO is of major importance in cerebral blood flow control during KA-induced seizures.

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