DOPA cyclohexyl ester, a competitive DOPA antagonist, protects glutamate release and resultant delayed neuron death by transient ischemia in hippocampus CA1 of conscious rats

2001 ◽  
Vol 299 (3) ◽  
pp. 213-216 ◽  
Author(s):  
Nobutaka Arai ◽  
Nobuya Furukawa ◽  
Takeaki Miyamae ◽  
Yoshio Goshima ◽  
Yukio Sasaki ◽  
...  
Keyword(s):  
Glutamate Release ◽  
Transient Ischemia ◽  
Neuron Death ◽  
Conscious Rats ◽  
Cyclohexyl Ester

scholarly journals Evaluation of Formalin-Induced Pain Behavior and Glutamate Release in the Spinal Dorsal Horn Using In Vivo Microdialysis in Conscious Rats

2012 ◽  
Vol 120 (2) ◽  
pp. 129-132 ◽  
Author(s):  
Alba Vidal-Torres ◽  
Alicia Carceller ◽  
Daniel Zamanillo ◽  
Manuel Merlos ◽  
Jos^|^eacute; Miguel Vela ◽  
...  
Keyword(s):  
Dorsal Horn ◽  
Spinal Dorsal Horn ◽  
Glutamate Release ◽  
In Vivo Microdialysis ◽  
Pain Behavior ◽  
Conscious Rats ◽  
Spinal Dorsal

Electroacupuncture Attenuates Both Glutamate Release and Hyperemia After Transient Ischemia in Gerbils

2003 ◽  
Vol 31 (02) ◽  
pp. 295-303 ◽  
Author(s):  
Jinming Pang ◽  
Toshifumi Itano ◽  
Kazunori Sumitani ◽  
Tetsuro Negi ◽  
Osamu Miyamoto
Keyword(s):  
Blood Flow ◽  
Reperfusion Injury ◽  
Brain Damage ◽  
Hippocampal Neurons ◽  
Neuroprotective Effect ◽  
Glutamate Release ◽  
Protective Mechanism ◽  
Ischemic Insult ◽  
Transient Ischemia ◽  
Ischemic Brain

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 by suppressing both glutamate release and reperfusion injury after ischemia.

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