Parmentier-Batteur Sophie, Jin Kunlin, Mao Xiao Ou, Xie Lin, Greenberg David A
Buck Institute for Age Research, Novato, California 94945, USA.
J Neurosci. 2002 Nov 15;22(22):9771-5. doi: 10.1523/JNEUROSCI.22-22-09771.2002.
Endogenous cannabinoid signaling pathways have been implicated in protection of the brain from hypoxia, ischemia, and trauma, but the mechanism for these protective effects is uncertain. We found that in CB1 cannabinoid receptor knock-out mice, mortality from permanent focal cerebral ischemia was increased, infarct size and neurological deficits after transient focal cerebral ischemia were more severe, cerebral blood flow in the ischemic penumbra during reperfusion was reduced, and NMDA neurotoxicity was increased compared with wild-type littermates. These findings indicate that endogenous cannabinoid signaling pathways protect mice from ischemic stroke by a mechanism that involves CB1 receptors, and suggest that both blood vessels and neurons may be targets of this protective effect.
内源性大麻素信号通路已被证实与保护大脑免受缺氧、缺血和创伤有关，但其保护作用的机制尚不清楚。我们发现，与野生型同窝小鼠相比，CB1大麻素受体基因敲除小鼠永久性局灶性脑缺血的死亡率增加，短暂性局灶性脑缺血后的梗死面积和神经功能缺损更严重，再灌注期间缺血半暗带的脑血流量减少，NMDA神经毒性增加。这些发现表明，内源性大麻素信号通路通过涉及CB1受体的机制保护小鼠免受缺血性中风，并提示血管和神经元可能都是这种保护作用的靶点。
