The RAS/PI3K Pathway is Involved in the Impairment of Long-term Potentiation Induced by Acute Aluminum Treatment in Rats

• Published in: Biomedical and environmental sciences Vol. 29; no. 11; pp. 782 - 789
• Main Authors: SONG, Jing, LIU, Ying, ZHANG, Hui Fang, NIU, Qiao
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier B.V 01.11.2016; Department of 0ccupational Health, School of Public Health, Shanxi Medical University, Taiyuan 030001, Shanxi, China
• Subjects: Aluminum; Aluminum - toxicity; AMPA receptor; Animals; ELISA检测; Epidermal Growth Factor - metabolism; Hippocampus - drug effects; Hippocampus - metabolism; Injections, Intraventricular; Long-term potentiation; Long-Term Potentiation - drug effects; Male; Phosphatidylinositol 3-Kinases - metabolism; Phosphorylation - drug effects; PKB; Proto-Oncogene Proteins c-akt - metabolism; Random Allocation; RAS; ras Proteins - metabolism; Rats; Receptors, AMPA - metabolism; Signal Transduction - drug effects; 信号转导通路; 大鼠; 急性; 表皮生长因子; 铝诱导; 长时程增强; AMPA receptor; Aluminum; RAS; Long-term potentiation; PKB
• ISSN: 0895-3988; 2214-0190
• DOI: 10.3967/bes2016.105

Objective To explore the role of RAS/PI3K pathway in the impairment of long-term potentiation （LTP） induced by acute aluminum （AI） treatment in rats in vivo. Methods First, different dosages of aluminum-maltolate complex [Al（mal）3] were given to rats via acute intracerebroventricular （i.c.v.） injection. Following AI exposure, the RAS activity of rat hippocampus were detected by ELISA assay after the hippocampal LTP recording by field potentiation technique in vivo. Second, the antagonism on the aluminum-induced suppression of hippocampal LTP was observed after the treatment of the RAS activator epidermal growth factor （EGF）. Finally, the antagonism on the downstream molecules （PKB activity and the phosphorylation of GluR1 $831 and $845） were tested by ELISA and West-blot assays at the same time. Results With the increasing aluminum dosage, a gradually decreasing in RAS activity of the rat hippocampus was produced after a gradually suppressing on LTP. The aluminum-induced early suppression of hippocampal LTP was antagonized by the RAS activator epidermal growth factor （EGF）. And the EGF treatment produced changes similar to those observed for LTP between the groups on PKB activity as well as the phosphorylation of GluR1 S831 and s845. Conclusion The RAS-PI3K/PKB-GluR1 S831 and S845 signal transduction pathway may be involved in the inhibition of hippocampal LTP by aluminum exposure in rats. However, the mechanisms underlying this observation need further investigation.