Acupuncture inhibits kainic Acid-induced hippocampal cell death in mice.

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.
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)
Chemical References	Excitatory Amino Acid Agonists Neurotoxins Proto-Oncogene Proteins c-fos JNK Mitogen-Activated Protein Kinases Glutamate Decarboxylase glutamate decarboxylase 1 Kainic Acid
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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