An experimental rat model of aluminum accumulation in the brain was developed to aid in determining neurotoxity of aluminum (Al). Al was administered orally, intravenously, and intraperitoneally, in the absence or presence of citric acid or maltol. Oral administration of Al hydroxide [Al (OH)3] or aluminum chloride (AlC13) with citric acid for 7 wk was not found to increase brain Al levels. Similarly, a single intravenous injection of AlCl3 in the presence or absence of either citric acid or maltol did not alter brain Al levels after 48 h. Only daily intraperitoneal injections of AlC13 (8 mg Al/kg body weight) and an equimolar amount of maltol over a 14-d period enhanced accumulation of Al in rat brain. No significant increases were observed for the experimental groups receiving intraperitoneal AlCl3 alone or with citric acid. This result suggests that the chemical form of Al strongly influences its bioavailability and that intraperitoneal administration of the Al-maltol complex appears to be useful in creating subacute model of Al accumulation in brain tissue.