NDLI: Electroacupuncture attenuates both glutamate release and hyperemia after transient ischemia in gerbils.

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Electroacupuncture attenuates both glutamate release and hyperemia after transient ischemia in gerbils.

Content Provider	Semantic Scholar
Author	Pang, Jinning Itano, Toshifumi Sumitani, Kaznori Negi, Tetsuro
Copyright Year	2003
Abstract	Although many studies have indicated that electroacupuncture (EA) provides a neuroprotective effect against ischemic brain damage, the protective mechanism is not fully understood. Glutamate release and hippocampal blood flow in ischemia with EA were investigated to elucidate the neuroprotective mechanism of EA. Transient 5-minute ischemia was induced in gerbils. EA (7 Hz, 6 mA, for 30 minutes) delivered to the points called Fengfu (GV16) and Shendao (GV11) was administered pre-, intra- or post-ischemia. The procedure rescued hippocampal neurons from ischemic insult and significantly attenuated both ischemia-induced glutamate release and transient increase of cerebral blood flow (CBF) during reperfusion (hyperemia). Hyperemia as well as excessive glutamate after ischemia are regarded as important factors in brain damage as they lead to reperfusion injury. These results suggest that EA protects neurons bysuppressing both glutamate release and reperfusion injury after ischemia.
Starting Page	295
Ending Page	303
Page Count	9
File Format	PDF HTM / HTML
Alternate Webpage(s)	http://www.encognitive.com/files/Electroacupuncture%20Attenuates%20Both%20Glutamate%20Release%20and%20Hyperemia%20After%20Transient%20Ischemia%20in%20Gerbils.pdf
PubMed reference number	12856868v1
Volume Number	31
Issue Number	2
Journal	The American journal of Chinese medicine
Language	English
Access Restriction	Open
Subject Keyword	Brain Damage, Chronic Brain Neoplasms Cerebrovascular Circulation Each (qualifier value) Electroacupuncture Ethacrynic Acid Gerbils Glutamic Acid Hertz (Hz) Hyperemia Hypoxia-Ischemia, Brain Hypoxic-Ischemic Encephalopathy Ischemia Reperfusion Injury Reperfusion Therapy
Content Type	Text
Resource Type	Article

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