title: 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.affiliation: Acupuncture and Meridian Science Research Center, Kyung Hee University, Seoul, Republic of Korea.
authors.forename: Seung-Tae
authors.initials: ST
authors.lastname: Kim
authors.forename: Songhee
authors.initials: S
authors.lastname: Jeon
authors.forename: Hae Jeong
authors.initials: HJ
authors.lastname: Park
authors.forename: Mee-Sook
authors.initials: MS
authors.lastname: Hong
authors.forename: Wu Byung
authors.initials: WB
authors.lastname: Jeong
authors.forename: Jang-Hyun
authors.initials: JH
authors.lastname: Kim
authors.forename: Yeonjung
authors.initials: Y
authors.lastname: Kim
authors.forename: Hye-Jung
authors.initials: HJ
authors.lastname: Lee
authors.forename: Hi-Joon
authors.initials: HJ
authors.lastname: Park
authors.forename: Joo-Ho
authors.initials: JH
authors.lastname: Chung
mesh_terms: D026881:Acupuncture; D000818:Animals; D016923:Cell Death / Q000502:physiology*; D004789:Enzyme Activation; D004827:Epilepsy / Q000139:chemically induced / Q000473:pathology* / Q000628:therapy*; D018690:Excitatory Amino Acid Agonists / Q000633:toxicity; D005968:Glutamate Decarboxylase / Q000378:metabolism; D006624:Hippocampus / Q000473:pathology*; D048031:JNK Mitogen-Activated Protein Kinases / Q000378:metabolism; D007608:Kainic Acid / Q000633:toxicity; D008297:Male; D051379:Mice; D008813:Mice, Inbred ICR; D009474:Neurons / Q000378:metabolism / Q000473:pathology; D009498:Neurotoxins / Q000378:metabolism; D016760:Proto-Oncogene Proteins c-fos / Q000378:metabolism
chemical_list: D018690:Excitatory Amino Acid Agonists; D009498:Neurotoxins; D016760:Proto-Oncogene Proteins c-fos; D048031:JNK Mitogen-Activated Protein Kinases; D005968:Glutamate Decarboxylase; C402565:glutamate decarboxylase 1; D007608:Kainic Acid