Abstract |
We examined whether acupuncture can reduce both the incidence of seizures and hippocampal cell death using a mouse model of kainic acid (KA)-induced epilepsy. ICR mice were given acupuncture once a day at acupoint HT8 (sobu) bilaterally during 2 days before KA injection. After an intracerebroventricular injection of 0.1 microg of KA, acupuncture treatment was subsequently administered once more (total 3 times), and the degree of seizure was observed for 20 min. Three hours after injection, the survival of neuronal cells and the expressions of c-Fos, c-Jun, and glutamate decarboxylase (GAD)-67 in the CA1 and CA3 were determined using immunohistochemistry and Western blotting techniques. Acupuncture reduced the severity of the KA-induced epileptic seizure and the rate of neural cell death, and it also decreased the expressions of c-Fos and c-Jun induced by KA in the hippocampus. Furthermore, acupuncture increased GAD-67 expressions in the same areas. These results demonstrated that it could inhibit the KA-induced epileptic seizure and hippocampal cell death by increasing GAD-67 expressions.
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Authors | Seung-Tae Kim, Songhee Jeon, Hae Jeong Park, Mee-Sook Hong, Wu Byung Jeong, Jang-Hyun Kim, Yeonjung Kim, Hye-Jung Lee, Hi-Joon Park, Joo-Ho Chung |
Journal | The journal of physiological sciences : JPS
(J Physiol Sci)
Vol. 58
Issue 1
Pg. 31-8
(Feb 2008)
ISSN: 1880-6546 [Print] Japan |
PMID | 18186956
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Excitatory Amino Acid Agonists
- Neurotoxins
- Proto-Oncogene Proteins c-fos
- JNK Mitogen-Activated Protein Kinases
- Glutamate Decarboxylase
- glutamate decarboxylase 1
- Kainic Acid
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Topics |
- Acupuncture
- Animals
- Cell Death
(physiology)
- Enzyme Activation
- Epilepsy
(chemically induced, pathology, therapy)
- Excitatory Amino Acid Agonists
(toxicity)
- Glutamate Decarboxylase
(metabolism)
- Hippocampus
(pathology)
- JNK Mitogen-Activated Protein Kinases
(metabolism)
- Kainic Acid
(toxicity)
- Male
- Mice
- Mice, Inbred ICR
- Neurons
(metabolism, pathology)
- Neurotoxins
(metabolism)
- Proto-Oncogene Proteins c-fos
(metabolism)
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