title: Early chronic aluminium exposure impairs long-term potentiation and depression to the rat dentate gyrus in vivo.
abstract: As an important neurotoxin, aluminium can cause cognitive dysfunctions and mental diseases. Previous studies have reported that aluminium impaired long-term potentiation (LTP) in vivo and in vitro. Here, we utilise two models of synaptic plasticity, LTP and long-term depression (LTD) to study the effects of aluminium on synaptic plasticity in vivo. Neonatal Wistar rats were chronically exposed to aluminium from birth to weaning via the milk of dams fed with 0.3% aluminium chloride solution. Excitatory postsynaptic potential (EPSP) and population spikes (PS) were recorded from the dentate gyrus (DG) of adult rats by electrically stimulating the perforant path. THE FOLLOWING RESULTS WERE OBTAINED: (1) The input/output function indicated that, as compared to controls, aluminium increased the baseline amplitude of the PS, but decreased the baseline slope of EPSP. (2) Aluminium significantly prevented LTD in PS (controls: 77.36+/-6.7%, n=7; aluminium-exposed: 102.01+/-9.1%, n=7; P<0.05) and decreased the LTD amplitude in EPSP (controls: 76.61+/-4.1%, n=7; aluminium-exposed: 94.31+/-7.9% n=7, P<0.05). (3) Aluminium reduced the amplitude of LTP in both PS (controls: 190+/-16.1%, n=7; aluminium-exposed: 135+/-9.7%, n=7; P<0.05) and EPSP (control: 132+/-9.3%, n=7; aluminium-exposed: 115+/-10.6%, n=7; P<0.05). As for LTD and LTP, PS was impaired more seriously than EPSP in aluminium-exposed rats. (4) Aluminium exposure decreased the paired-pulse facilitation (PPF) of PS at 30-150 ms interpulse interval (IPI), and reduced 93.5% of PPF at 80 ms IPI in PS (controls: 243.4+/-39.8%, n=7; aluminium-exposed: 149.9+/-12.3%, n=7). There was no significant difference in EPSP of PPF. From these results we conclude that aluminium exposure in neonatal rats thus reduces the amplitude of LTP and PPF and blocks the induction of LTD in the DG. We suggest that aluminium affects both presynaptic and postsynaptic mechanisms of synaptic transmission.
authors.affiliation: School of Life Science, University of Science and Technology of China, P.O. Box 4, Hefei, Anhui 230027, China.
authors.forename: J
authors.initials: J
authors.lastname: Chen
authors.forename: M
authors.initials: M
authors.lastname: Wang
authors.forename: D
authors.initials: D
authors.lastname: Ruan
authors.forename: J
authors.initials: J
authors.lastname: She
mesh_terms: D000535:Aluminum / Q000633:toxicity*; D000818:Animals; D000831:Animals, Newborn; D018891:Dentate Gyrus / Q000187:drug effects* / Q000503:physiopathology*; D015536:Down-Regulation / Q000187:drug effects; D004594:Electrophysiology; D005260:Female; D017774:Long-Term Potentiation / Q000187:drug effects*; D008297:Male; D001523:Mental Disorders / Q000139:chemically induced; D051381:Rats; D017208:Rats, Wistar; D009435:Synaptic Transmission / Q000187:drug effects
chemical_list: D000535:Aluminum