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Reparatory effects of nicotine on NMDA receptor‐mediated synaptic plasticity in the hippocampal CA1 region of chronically lead‐exposed rats
Author(s) -
Wang HuiLi,
Chen XiangTao,
Luo Le,
Lou ZhiYi,
Wang Shu,
Chen JuTao,
Wang Ming,
Sun LiGuang,
Ruan DiYun
Publication year - 2006
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1111/j.1460-9568.2006.04645.x
Subject(s) - methyllycaconitine , long term potentiation , mecamylamine , nicotine , synaptic plasticity , nmda receptor , nicotinic antagonist , chemistry , nicotinic agonist , neuroscience , excitatory postsynaptic potential , bicuculline , pharmacology , nicotinic acetylcholine receptor , antagonist , biology , receptor , biochemistry , inhibitory postsynaptic potential
Activation of neuronal nicotinic acetylcholine receptors (nAChRs) modulates the induction of long‐term potentiation (LTP): a possible cellular mechanism of learning. To investigate the effect of nicotine on synaptic plasticity in chronically lead‐exposed rats, field excitatory postsynaptic potentials and paired‐pulse facilitation (PPF) were recorded in the CA1 area of hippocampal slices from chronically lead‐exposed 23–30‐day‐old rats. The results showed the following. (1) Nicotine (1 µ m ) facilitated the induction of LTP in CA1 by a weak tetanic stimulation (100 Hz, 20 pulses), which does not by itself produce LTP in lead‐exposed rats. This effect was significantly suppressed by mecamylamine, a nicotinic antagonist, suggesting that the facilitation of LTP was through nAChRs. (2) The nicotine‐facilitated LTP was blocked by dihydro‐β‐erythroidine (DHβE), a non‐α7 nAChR antagonist, whereas long‐term depression (LTD) was produced by the combination of nicotine and methyllycaconitine, a α7‐nAChR antagonist. This type of LTD was blocked by DHβE. This suggested that several nAChR subtypes were involved in the nicotine‐facilitated synaptic plasticity. (3) Nicotine enhanced PPF in the hippocampal CA1 region, and the nicotine‐facilitated LTP in lead‐exposed rats was blocked by either d ‐(–)‐2‐amino‐5‐phosphonopentanoic acid, the N ‐methyl‐ d ‐aspartate (NMDA) receptor antagonist, or picrotoxin, an antagonist of γ‐aminobutyric acid A receptors. We suggest that nicotine‐facilitated synaptic plasticity was due to the activation of NMDARs by disinhibition of pyramidal cells through presynaptic nAChRs. This may represent the cellular basis of nicotine‐facilitated cognitive enhancement observed in chronically lead‐exposed rats.