Vasopressin reverses aluminum-induced impairment of synaptic plasticity inthe rat dentate gyrus in vivo

Citation
M. Wang et al., Vasopressin reverses aluminum-induced impairment of synaptic plasticity inthe rat dentate gyrus in vivo, BRAIN RES, 899(1-2), 2001, pp. 193-200
Citations number
43
Categorie Soggetti
Neurosciences & Behavoir
Journal title
BRAIN RESEARCH
ISSN journal
00068993 → ACNP
Volume
899
Issue
1-2
Year of publication
2001
Pages
193 - 200
Database
ISI
SICI code
0006-8993(20010427)899:1-2<193:VRAIOS>2.0.ZU;2-W
Abstract
Aluminum (Al), an important neurotoxin, contributes to a variety of cogniti ve dysfunction and mental diseases. previous studies have demonstrated that Al impairs hippocampal long-term potentiation (LTP) in vitro and in vivo. In the present study. both LTP and LTD (long-term depression) were recorded in the same animal to investigate the Al-induced impairment of synaptic pl asticity. Another aim of the present research was to verify whether the imp airment of synaptic plasticity induced by Al could be reversed by vasopress in (VP) treatment. Neonatal Wistar rats were exposed to Al from parturition through adulthood (pre- and post-weaning) by the drinking of 0.3% aluminum chloride (AlCl3) solution. The input-output (IIO) function, paired-pulse r eaction (PPR), excitatory postsynaptic potential (EPSP) and population spik e (PS) amplitude were measured in the dentate gyrus (DG) of adult rats (60- 90 days) in response to stimulation applied to the lateral perforant path. The results showed: (1) Al reduced the amplitudes of both EPSP LTP(control: 132+/-7%, n=7; Al-exposed: 115+/-10%, n=8, P<0.05) and PS LTP (control: 24 2+/-18%, n=7; Al-exposed: 136+/-7%, n=8, P<0.01) significantly. The amplitu des of EPSP LTD (control: 82+/-6%. n=7. Al-exposed: 92+/-7%, n=8, P<0.05) a nd PS LTD (control: 81+/-4%. n=7; Al-exposed: 98+/-5%, n=8, P<0.05) were al so decreased by Al treatment. The Al-induced impairments of PS LTP and PS L TD were more serious than that of EPSP LTP and EPSP LTD. (2) In control rat s. VP had an increase in the PS LTP amplitude (control: 242+/-18%. n=7; con trol+VP: 358+/-23%, n=6, P<0.01), while it had no significant effects on PS LTD (control: 81+/-4%, n=7; control+VP: 76+/-7% n =6, P>0.05). (3) In Al-e xposed rats, VP had a significant increase in the amplitudes of both PS LTP (Al-exposed: 136+/-7%, n=8, Al-exposed+VP: 255+/-16%, n=6, P<0.01) and PS LTD (Al-exposed: 98+/-5%, n=8; Al-exposed+VP: 81+/-6%. n=6, P<0.05). After the application of VP, the range of synaptic plasticity (PS LTP+PS LTD) in Al-exposed rats increased from 38% to 174%. which surpassed that in control rats (161%). It was suggested that VP could reverse Al-induced impairment of synaptic plasticity and might be an effective medicine to cure Al-induce d neurological disorders. (C) 2001 Elsevier Science B.V. All rights reserve d.