['Extreme hyperbilirubinemia is treated with double volume exchange transfusion, which may take hours to commence. A neuroprotective agent that could be administered immediately might be clinically useful. Minocycline, an anti-inflammatory and anti-apoptotic semisynthetic tetracycline, prevents hyperbilirubinemia-induced cerebellar hypoplasia in Gunn rats. Acute brainstem auditory evoked potential (BAEP) abnormalities occur after giving sulfadimethoxine to 16-day-old jaundiced Gunn rats to displace bilirubin into tissue including brain.', 'To assess whether minocycline is neuroprotective in this model of acute bilirubin encephalopathy.', 'We recorded BAEPs at baseline and 6 h after injecting sulfadimethoxine. Minocycline 0.5 mg/kg (n = 4), 5 mg/kg (n = 9), 50 mg/kg (n = 9) or 500 mg/kg (n = 3, all died) was administered 15 min before sulfadimethoxine (0 h). Controls received saline followed by either sulfadimethoxine (n = 13) or saline (n = 7).', 'At 6 h total plasma bilirubin decreased from 10.84 +/- 0.88 mg/dl (mean +/- SD) to 0.70 +/- 0.35 mg/dl (p <10(-9)) in all sulfadimethoxine-injected groups. At 6 h, there was complete protection against decreased amplitudes of BAEP waves II and III and increased I-II and I-III interwave intervals (brainstem conduction times corresponding to I-III and I-V in humans) with 50 mg/kg minocycline, and partial protection with lower doses.'] Does minocycline block acute bilirubin-induced neurological dysfunction in jaundiced Gunn rats?