The cytokine interleukin-1 (IL-1) is implicated in a broad spectrum of CNS pathologies, in which it is thought to exacerbate neuronal loss. Here, the effects of injecting recombinant rat IL-1 into the striatum of 3-week-old rats were followed noninvasively from 2 to 123 hr using magnetic resonance imaging and spectroscopy. Four hours after injection of IL-1 (1 ng in 1 l), cerebral blood volume was significantly increased, the blood-brain barrier (BBB) became permeable to intravenously administered contrast agent between 4.5 and 5 hr, and the apparent diffusion coefficient (ADC) of brain water fell by 6 hr (5.42 Ϯ 0.35 ϫ 10 Ϫ 4 mm 2 /sec treated, 7.35 Ϯ 0.77 ϫ 10 Ϫ 4 mm 2 /sec control; p Ͻ 0.001). At 24 hr the BBB was again intact, but the ADC, although partially recovered, remained depressed at both 24 and 123 hr ( p Ͻ 0.03). Depleting the animals of neutrophils before IL-1 injection prevented the BBB permeability at all time points, but the ADC was still depressed at 6 hr (6.64 Ϯ 0.34 ϫ 10 Ϫ 4 mm 2 /sec treated, 7.49 Ϯ 0.38 ϫ 10 Ϫ 4 mm 2 /sec control; p Ͻ 0.005). No changes were seen in brain metabolites using proton spectroscopy at 6 hr after IL-1.Intraparenchymal injection of IL-1 caused a neutrophildependent transient increase in BBB permeability. The presence of neutrophils within the brain parenchyma significantly contributed to the IL-1-induced changes in cerebral blood volume and the ADC of brain water. However, IL-1 apparently had a direct effect on the resident cell populations, which persisted well after all recruited leukocytes had disappeared. Thus the action of IL-1 alone can give rise to magnetic resonance imaging-visible changes that are normally attributed to alterations to cellular homeostasis.