We characterized the time-course, intensity of expression and cellular origin of components of the endothelin (ET) system in the rat brain after a standardized neurotrauma (cryogenic lesion of the parietal cortex). ET mRNAs were expressed at sham level after neurotrauma, whereas immunoreactivity for ET-1 was enhanced in glia and endothelium of the lesioned hemisphere and both hippocampi. The number of ET-3 positive mononuclear cells in the lesion perimeter increased starting at 24h after injury. At 48h after neurotrauma, ET-receptor immunoreactivity was increased in astrocytes. In basilar artery endothelium, ETB-immunoreactivity was reduced at 48h to 72h recovering at 7 days whereas ETA-receptor and ET-peptide immunoreactivities were not altered. In summary, neurotrauma leads to a multicellular stimulation of endothelins in the brain along with a delayed selective loss of vascular ETB-receptors. These changes seem to be posttranscriptional and cell type specific. They favor vasoconstriction increasing the risk of late vasospasm and ischemia.