| First Author | Xu ZH | Year | 2016 |
| Journal | Neuroscience | Volume | 328 |
| Pages | 22-9 | PubMed ID | 27133574 |
| Mgi Jnum | J:235971 | Mgi Id | MGI:5804066 |
| Doi | 10.1016/j.neuroscience.2016.04.036 | Citation | Xu ZH, et al. (2016) Interleukin-1 receptor is a target for adjunctive control of diazepam-refractory status epilepticus in mice. Neuroscience 328:22-9 |
| abstractText | Proinflammatory cytokine interleukin-1 beta (IL-1beta) may accumulate in the brain during status epilepticus, but whether it contributes to the progressive refractoriness of SE remains unclear. By using a kainic acid-induced SE mice model, we tested whether pharmacological blockade or knock-out of interleukin-1 receptor type 1 (IL-1R1) could influence the diazepam-refractory phenomenon of prolonged SE. We confirmed diazepam failed to terminate prolonged SE (allowed to continue for 40min before diazepam administration). The expression level of IL-1beta in the hippocampus during prolonged SE was significantly higher than that of baseline. Interestingly, prolonged SE was not diazepam-refractory in IL-1R1 knock-out mice. Moreover, administration of interleukin-1 receptor antagonist (IL-1RA) combined with diazepam terminated established prolonged SE, while IL-1RA alone is not capable to terminate prolonged SE. On the contrary, administration of recombinant human IL-1beta weakens the efficacy of diazepam by prolonging its latency to terminate non-prolonged SE. Thus, the present study provides direct evidence that accumulated IL-1beta contributed to the diazepam refractoriness of prolonged SE, and suggests that interleukin-1 receptor is a target for adjunctive control of diazepam-refractory SE. |
