Rivest Serge
Laboratory of Molecular Endocrinology, CHUL Research Center, and Department of Anatomy and Physiology, Laval University, Québec, Canada G1V-4G2.
Neuron. 2006 Jan 5;49(1):4-8. doi: 10.1016/j.neuron.2005.12.004.
Microglia are the resident immune cells of the brain, and they are under permanent activity to patrol the cerebral microenvironment. A proper inhibitory feedback onto these cells is critical during both intact and injury conditions. In this issue of Neuron, Eljaschewitsch and colleagues report that such feedback is provided by the endogenous cannabinoid anandamine and CB(1/2) receptor signaling, which ultimately leads to mitogen-activated protein kinase phosphatase-1 (MKP-1) induction. MKP-1 interferes with lipopolysaccharide-induced toll-like receptor 4 signaling and limits brain damage due to exaggerated microglial reactivity following acute NMDA injury.
小胶质细胞是大脑中的常驻免疫细胞，它们持续活跃以巡查大脑微环境。在正常和损伤状态下，对这些细胞进行适当的抑制性反馈都至关重要。在本期《神经元》杂志中，埃尔亚施维茨及其同事报告称，内源性大麻素花生四烯乙醇胺和CB(1/2)受体信号传导提供了这种反馈，最终导致丝裂原活化蛋白激酶磷酸酶-1（MKP-1）的诱导。MKP-1干扰脂多糖诱导的Toll样受体4信号传导，并限制急性NMDA损伤后因小胶质细胞反应过度而导致的脑损伤。
