Abstract：
:Endocannabinoids are released after brain injury and believed to attenuate neuronal damage by binding to CB(1) receptors and protecting against excitotoxicity. Such excitotoxic brain lesions initially result in primary destruction of brain parenchyma, which attracts macrophages and microglia. These inflammatory cells release toxic cytokines and free radicals, resulting in secondary neuronal damage. In this study, we show that the endocannabinoid system is highly activated during CNS inflammation and that the endocannabinoid anandamide (AEA) protects neurons from inflammatory damage by CB(1/2) receptor-mediated rapid induction of mitogen-activated protein kinase phosphatase-1 (MKP-1) in microglial cells associated with histone H3 phoshorylation of the mkp-1 gene sequence. As a result, AEA-induced rapid MKP-1 expression switches off MAPK signal transduction in microglial cells activated by stimulation of pattern recognition receptors. The release of AEA in injured CNS tissue might therefore represent a new mechanism of neuro-immune communication during CNS injury, which controls and limits immune response after primary CNS damage.
journal_name
Neuronjournal_title
Neuronauthors
Eljaschewitsch E,Witting A,Mawrin C,Lee T,Schmidt PM,Wolf S,Hoertnagl H,Raine CS,Schneider-Stock R,Nitsch R,Ullrich Odoi
10.1016/j.neuron.2005.11.027subject
Has Abstractpub_date
2006-01-05 00:00:00pages
67-79issue
1eissn
0896-6273issn
1097-4199pii
S0896-6273(05)01008-1journal_volume
49pub_type
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