Cannabidiol prevents infarction via the non-CBI cannabinoid receptor mechanism

被引：48

作者：

Hayakawa, K

Mishima, K

Abe, K

Hasebe, N

Takamatsu, F

Yasuda, H

Ikeda, T

Inui, K

Egashira, N

Iwasaki, K

Fujiwara, M

机构：

[1] Fukuoka Univ, Fac Pharmaceut Sci, Dept Neuropharmacol, Fukuoka 8140180, Japan

[2] Fukuoka Univ, Adv Mat Inst, Fukuoka 8140180, Japan

[3] Miyazaki Univ, Miyazaki Med Coll, Dept Obstet & Gynecol, Miyazaki 8891692, Japan

[4] Osaka Univ, Fac Med, Sch Allied Hlth Sci, Dept Med Phys, Suita, Osaka 5650871, Japan

来源：

NEUROREPORT | 2004年 / 15卷 / 15期

关键词：

cannabidiol; CBI receptor; hypothermia; middle cerebral artery occlusion; rectal temperature; Delta(9)-tetrahydrocannabinol;

D O I：

10.1097/00001756-200410250-00016

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Cannabidiol, a non-psychoactive constituent of cannabis, has been reported as a neuroprotectant. Cannabidiol and Delta(9)-tetrahydrocannabinol, the primary psychoactive constituent of cannabis, significantly decreased the infarct volume at 4 h in the mouse middle cerebral artery occlusion model. The neuroprotective effects of Delta(9)-tetrahydrocannabinol but not cannabidiol were inhibited by SR141716, a cannabinoid CB1 receptor antagonist, and were abolished by warming of the animals to the levels observed in the controls. Delta(9)-Tetrahydrocannabinol significantly decreased the rectal temperature, and the hypothermic effect was inhibited by SR141716. These results surely show that the neuroprotective effect of Delta(9)-tetrahydrocannabinol are via a CB1receptor and temperature-dependent mechanisms whereas the neuroprotective effects of cannabidiol are independent of CB1 blockade and of hypothermia.

引用

页码：2381 / 2385

页数：5

共 16 条

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