المؤلفون: Ji-Eun Kim, Hui-Chul Choi, Duk-Soo Kim, Moo Ho Won, Yeong-In Kim, Hong-Ki Song, Tae-Cheon Kang, Soo Young Choi, Sung-Eun Kwak

المصدر: Neuropeptides. 39:507-513

مصطلحات موضوعية: medicine.medical_specialty, Central nervous system, Zonisamide, Hippocampus, Biology, Gerbil, Vigabatrin, Cellular and Molecular Neuroscience, Endocrinology, Seizures, Internal medicine, mental disorders, medicine, Animals, Neuropeptide Y, In Situ Hybridization, Endocrine and Autonomic Systems, Hippocampus proper, Dentate gyrus, Isoxazoles, General Medicine, Neuropeptide Y receptor, humanities, medicine.anatomical_structure, nervous system, Neurology, Anticonvulsants, Gerbillinae, medicine.drug

الوصف: Changed neuropeptide Y (NPY) system in the hippocampus has been reported in various experimental epileptic models. However, there have been little data concerning the alteration in the NPY system in the epileptic hippocampus following treatment of anti-epileptic drugs (AEDs). In the present study, therefore, we performed analyses of effects of vigabatrin (VGB) and zonisamide (ZNS) treatment on the NPY system in the hippocampus of the seizure sensitive (SS) gerbils. In SS gerbil, NPY immunoreactivity in the hippocampus was lower than that in seizure resistant gerbil. Following VGB treatment, the number of NPY immunoreactive neurons and NPY mRNA expression were increased in the hilus and the hippocampus proper. In contrast, ZNS treatment markedly elevated only the density of NPY immunoreactive fibers in the dentate gyrus, not in the hippocampus proper, as compared with saline-treated animals. These patterns were observed in the dose-dependent manners. These findings suggest that AEDs treatments may distinctly affect the NPY system in the SS gerbil hippocampus.

الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::f7a60e9dd2d00b42d9dd9a384a216a5cTest
https://doi.org/10.1016/j.npep.2005.08.003Test

المؤلفون: Ji-Eun Kim, Seung-Mook Jo, Tae-Cheon Kang, Sung-Eun Kwak

المصدر: Neurological research. 31(9)

مصطلحات موضوعية: Male, medicine.medical_specialty, Antineoplastic Agents, Convulsants, Status epilepticus, Suramin, P2 receptor, Biology, Proinflammatory cytokine, Rats, Sprague-Dawley, Status Epilepticus, Internal medicine, Glial Fibrillary Acidic Protein, medicine, Purinergic P2 Receptor Antagonists, Animals, Gliosis, Receptor, Cell Shape, Microglia, Cell Death, Receptors, Purinergic P2, Dentate gyrus, Pilocarpine, General Medicine, Rats, Disease Models, Animal, medicine.anatomical_structure, Endocrinology, nervous system, Neurology, Receptors, Purinergic P2X, Astrocytes, Immunology, Dentate Gyrus, Nerve Degeneration, Neurology (clinical), Receptors, Purinergic P2X7, medicine.symptom, Astrocyte, medicine.drug, Signal Transduction

الوصف: The P(2) receptor is involved in diverse signal cascades, including the initiation of the rapid release and processing of proinflammatory cytokines, the induction of cytoskeletal rearrangements and transcription factor activation. Therefore, we investigated whether blocking the P(2) receptor would prevent the astroglial death induced by status epilepticus (SE).We performed seizure induction and drug treatments. After tissue processing, we executed immunoreactivities: mouse anti-glial fibrillary acidic protein (GFAP) IgG (diluted 1 : 200; Chemicon, Billerica, MA, USA rabbit anti-P(2)X(7) receptor IgG (diluted 1 : 200; Chemicon).In control animals, P(2)X(7) receptor-immunoreactive (P(2)X(7)(+)) microglia had small cell bodies with thin ramified processes. Seven days after SE, P(2)X(7) receptor immunoreactivity in microglia was significantly elevated in the dentate gyrus, and the microglia appeared amoeboid or phagocytic. At this point, loss of GFAP immunoreactivity in the dentate gyrus was even more pronounced, indicating that the network of astrocytes was disrupted and a large empty zone was observed. Treatment with pyridoxal phosphate-6-azophenyl-2',4'-disulfonic acid and suramin (2, 20 and 200 mg/kg, i.p., respectively) markedly, but not completely, inhibited microglial activation following SE. The morphology of microglia was similar to that of the astrocytes in that they appeared hyper-ramified. In addition, P(2)X(7) receptor antagonist treatments effectively prevented astroglial degeneration.These findings suggest that astroglial death induced by ATP-mediated microglia activation may be an important pathophysiological pathway in epileptogenesis.

الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::4eff80aa203b54e55d9b74ecce672a81Test
https://pubmed.ncbi.nlm.nih.gov/19138473Test

المؤلفون: Ki-Yeon Yoo, Dae-young Kwon, Tae-Cheon Kang, Moo Ho Won, YoungSub Kim, Won-Kook Moon, Dong-Woo Kim, In-Koo Hwang

المصدر: Neurological research. 29(5)

مصطلحات موضوعية: Male, medicine.medical_specialty, Time Factors, medicine.medical_treatment, Hippocampus, Hippocampal formation, Biology, Western blot, Seizures, Internal medicine, medicine, Animals, Neurons, medicine.diagnostic_test, Dentate gyrus, Adrenalectomy, General Medicine, Endocrinology, Parvalbumins, nervous system, Neurology, Gene Expression Regulation, biology.protein, Immunohistochemistry, sense organs, Neurology (clinical), Gerbillinae, hormones, hormone substitutes, and hormone antagonists, Glucocorticoid, Parvalbumin, medicine.drug

الوصف: Neurons containing parvalbumin (PV), a calcium-binding protein, in the hippocampus, play an important role in hippocampal excitability in epilepsy. In this study, we examined temporal and spatial changes of PV immunoreactivity and protein content in the hippocampus after adrenalectomy (ADX) in seizure sensitive (SS) gerbils, which are hereditarily seizure-prone.PV distribution and change in SS gerbils after ADX were examined in the hippocampal CA1 region and in the dentate gyrus (DG) using immunohistochemistry and Western blot analysis.PV immunoreactivity in sham-operated SS gerbils was detected in many CA1 pyramidal cells. Three hours after ADX, PV immunoreactivity significantly decreased in CA1 pyramidal cells and thereafter PV immunoreactivity began to increase by 4 days after ADX. Four days after ADX, PV immunoreactivity was significantly higher than that in the sham-operated SS gerbils. In the DG of sham-operated SS gerbils, PV immunoreactivity was mainly detected in polymorphic cells. Three hours after ADX, PV immunoreactivity in the DG significantly decreased in the polymorphic layer. Thereafter, PV-immunoreactive neurons decreased with time after ADX. Western blot analysis showed that change in PV protein content was similar to immunohistochemical data after ADX in SS gerbils.Our results indicate that PV is changed in hippocampus after ADX and PV may be associated with the regulation of seizure activity.

الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::1e0d210cb03bdf81720cb1a515d78149Test
https://pubmed.ncbi.nlm.nih.gov/17535552Test

المؤلفون: Jae-Chul Lee, Yang Seok Oh, Tae-Cheon Kang, In Koo Hwang, Ki Yeon Yoo, Moo Ho Won, Jun Hwi Cho, Ju-Young Jung, Won Ki Kim

المصدر: Neurological research. 29(3)

مصطلحات موضوعية: Pathology, medicine.medical_specialty, Time Factors, Ischemia, Excitotoxicity, Cell Count, Hindlimb, Motor Activity, medicine.disease_cause, Lumbar, Anterior Horn Cells, medicine, Animals, Behavior, Animal, business.industry, Spinal Cord Ischemia, Lumbosacral Region, General Medicine, Anatomy, medicine.disease, Spinal cord, Lumbar Spinal Cord, Disease Models, Animal, medicine.anatomical_structure, Excitatory Amino Acid Transporter 3, Neurology, Isoflurane, Gene Expression Regulation, Spinal Cord, Phosphopyruvate Hydratase, Neurology (clinical), Rabbits, business, medicine.drug, Artery

الوصف: To examine temporal changes of EAAC1 immunoreactivity and its protein level in the spinal ventral horn after transient ischemia in the rabbit to investigate the correlation between neuronal cell death and EAAC1 in the ventral horn of spinal cord.White rabbits weighing 2.5-3.0 kg were anesthetized with a mixture of 2.5% isoflurane in 30% oxygen and 70% nitrous oxide, and the abdominal aortic artery below the left renal artery was occluded for 15 minutes. At designated times after reperfusion, the immunohistochemical and Western blot analysis for EAAC1 was conducted using tissues of the seventh lumbar spinal segment.EAAC1 immunoreactivity was detected in the neurons of the normal spinal cord. EAAC1 immunoreactivity and protein level reduced significantly 30 minutes after ischemia/reperfusion, but EAAC1 immunoreactivity and protein level again increased by 80% versus sham 3 hours after ischemia. At this time point, neurological defect in hindlimb was also detected. Thereafter, EAAC1 immunoreactivity and protein levels remained to be attenuated in the ventral horn of spinal cord until 48 hours after ischemia.The significant change in EAAC1 expression and motor defects at early time after transient spinal cord ischemia relates to the acute events following ischemia/reperfusion. These results indicate that EAAC1 has an important role in the modulation of glutamate homeostasis in ischemic neurons in the spinal ventral horn.

الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::230679eeec25bc9d103382764d03025fTest
https://pubmed.ncbi.nlm.nih.gov/17509232Test

المؤلفون: Tae-Cheon Kang, Ah-Reum Ko

المصدر: Seizure. :133-140

مصطلحات موضوعية: Male, medicine.medical_specialty, Levetiracetam, medicine.drug_class, Pyridines, Receptor expression, Endothelin B Receptor Antagonists, Clinical Neurology, Endothelin-1, Endothelin B receptor, Epilepsy, Levetiracetam, P-glycoprotein, Hippocampus, Pharmacology, p38 Mitogen-Activated Protein Kinases, Rats, Sprague-Dawley, Epilepsy, Piperidines, Seizures, Internal medicine, medicine, Animals, Enzyme Inhibitors, Receptor, business.industry, Imidazoles, Piracetam, Brain, p38 mitogen-activated protein kinase, General Medicine, medicine.disease, Receptor antagonist, Receptor, Endothelin B, Disease Models, Animal, Endocrinology, Treatment Outcome, Neurology, Chronic Disease, Anticonvulsants, Neurology (clinical), business, Oligopeptides, medicine.drug

الوصف: Purpose To elucidate the mechanisms that regulate p-glycoprotein (PGP) expression and function in pharmacoresistant epilepsy, we investigated the effect of an ET B receptor antagonist (BQ788) and a p38 mitogen-activated protein kinase (p38MAPK) inhibitor (SB202190) on intractable seizures in chronic epileptic rats. Methods Lithium-pilocarpine-induced chronic epileptic rats were used in the present study. Animals were given levetiracetam (LEV), LEV+SB202190, LEV+BQ788, SB202190 or BQ788 over a 3-day period using an osmotic pump. Seizure activity was recorded by video-EEG monitoring with 2h of recording per day at the same time of day. We also performed western blot after EEG analysis. Results Compared to control animals, PGP, ET B receptor and p38MAPK expression was increased in the hippocampus of epileptic animals. Neither SB202190 nor BQ788 affected the spontaneous seizure activity in epileptic rats. Three of ten rats were responders and achieved complete seizure control or significant reduction in seizure activity by LEV. In four of ten rats, seizure frequency was unaltered by LEV (non-responders). LEV+SB202190 reduced seizure duration, but not seizure frequency, in both responders and non-responders. LEV+BQ788 alleviated seizure frequency and seizure duration in both responders and non-responders. Compared to responders, PGP and ET B receptor expression was enhanced in the hippocampus of non-responders. Conclusion To the best of our knowledge, these findings are the first indications of the role of ET B receptor in pharmacoresistant epilepsy. Therefore, the present data suggest that the regulation of the ET B receptor-mediated signaling pathway may be important for identification of new therapeutic strategies for improving antiepileptic drug efficacy.

الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::f1f86122b6291bb7926970f4b7813f51Test

المؤلفون: Yeong-In Kim, Hui-Chul Choi, Duk-Shin Lee, Ji-Eun Kim, Hong-Ki Song, Tae-Cheon Kang, Hea Jin Ryu

المصدر: Seizure. (5):368-377

مصطلحات موضوعية: Phenytoin, Levetiracetam, medicine.drug_class, Neuronal death, Clinical Neurology, Status epilepticus, Pharmacology, Hippocampus, Rats, Sprague-Dawley, Epilepsy, medicine, Oxiracetam, Hippocampus (mythology), Animals, Neurons, Vasogenic edema, Benzodiazepine, Valproate, Diazepam, Behavior, Animal, Cell Death, business.industry, Valproic Acid, Pilocarpine, General Medicine, medicine.disease, Fluoresceins, Piracetam, Rats, Disease Models, Animal, Neurology, Drug Therapy, Combination, lipids (amino acids, peptides, and proteins), Neurology (clinical), medicine.symptom, business, medicine.drug

الوصف: Purpose Levetiracetam has been reported to be well tolerated and effective in status epilepticus (SE) refractory to benzodiazepine. Because of little preclinical or clinical data concerning the outcomes of LEV in SE-induced neuronal death and vasogenic edema, we investigated the effect of LEV on SE-induced injury in comparison to diazepam (DZP), and valproate (VPA). Methods Two hours after pilocarpine-induced SE, rats were given one of the following drugs; (1) DZP, (2) LEV, (3) VPA, (4) DZP+LEV, (5) DZP+VPA, and (6) DZP+oxiracetam. Three–four days after SE, neuronal damage and vasogenic edema were evaluated by Fluoro-Jade B (FJB) staining and serum-protein extravasation, respectively. Results LEV (≥50mg/kg) was effective to protect neuronal damage from SE in comparison to DZP and VPA. LEV as an add-on drug with DZP could not alleviate neuronal damage as compared to LEV alone. VPA (≥100mg/kg) was effective to protect neuronal damage from SE, as compared to DZP. VPA as an add-on drug with DZP reduced neuronal damage, as compared to DZP alone. Conclusion These findings suggest that LEV may negatively interact with DZP, and be more effective to prevent SE-induced neuronal death as a first line drug than as a second line therapy after BDZ treatment.

الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::6a3c4f481f154c1286486f658e5966faTest