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Reparatory effects of nicotine on NMDA receptor-mediated synaptic plasticity in the hippocampal CA1 region of chronically lead-exposed rats.
Eur J Neurosci. 2006 Mar; 23(5):1111-9.EJ

Abstract

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 microm) 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-beta-erythroidine (DHbetaE), a non-alpha7 nAChR antagonist, whereas long-term depression (LTD) was produced by the combination of nicotine and methyllycaconitine, a alpha7-nAChR antagonist. This type of LTD was blocked by DHbetaE. 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 gamma-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.

Authors+Show Affiliations

Department of Neurobiology and Biophysics, School of Life Science and Institute of Polar Environment, University of Science & Technology of China, Hefei, Anhui.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

16553775

Citation

Wang, Hui-Li, et al. "Reparatory Effects of Nicotine On NMDA Receptor-mediated Synaptic Plasticity in the Hippocampal CA1 Region of Chronically Lead-exposed Rats." The European Journal of Neuroscience, vol. 23, no. 5, 2006, pp. 1111-9.
Wang HL, Chen XT, Luo L, et al. Reparatory effects of nicotine on NMDA receptor-mediated synaptic plasticity in the hippocampal CA1 region of chronically lead-exposed rats. Eur J Neurosci. 2006;23(5):1111-9.
Wang, H. L., Chen, X. T., Luo, L., Lou, Z. Y., Wang, S., Chen, J. T., Wang, M., Sun, L. G., & Ruan, D. Y. (2006). Reparatory effects of nicotine on NMDA receptor-mediated synaptic plasticity in the hippocampal CA1 region of chronically lead-exposed rats. The European Journal of Neuroscience, 23(5), 1111-9.
Wang HL, et al. Reparatory Effects of Nicotine On NMDA Receptor-mediated Synaptic Plasticity in the Hippocampal CA1 Region of Chronically Lead-exposed Rats. Eur J Neurosci. 2006;23(5):1111-9. PubMed PMID: 16553775.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Reparatory effects of nicotine on NMDA receptor-mediated synaptic plasticity in the hippocampal CA1 region of chronically lead-exposed rats. AU - Wang,Hui-Li, AU - Chen,Xiang-Tao, AU - Luo,Le, AU - Lou,Zhi-Yi, AU - Wang,Shu, AU - Chen,Ju-Tao, AU - Wang,Ming, AU - Sun,Li-Guang, AU - Ruan,Di-Yun, PY - 2006/3/24/pubmed PY - 2006/9/19/medline PY - 2006/3/24/entrez SP - 1111 EP - 9 JF - The European journal of neuroscience JO - Eur. J. Neurosci. VL - 23 IS - 5 N2 - 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 microm) 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-beta-erythroidine (DHbetaE), a non-alpha7 nAChR antagonist, whereas long-term depression (LTD) was produced by the combination of nicotine and methyllycaconitine, a alpha7-nAChR antagonist. This type of LTD was blocked by DHbetaE. 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 gamma-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. SN - 0953-816X UR - https://www.unboundmedicine.com/medline/citation/16553775/Reparatory_effects_of_nicotine_on_NMDA_receptor_mediated_synaptic_plasticity_in_the_hippocampal_CA1_region_of_chronically_lead_exposed_rats_ L2 - https://doi.org/10.1111/j.1460-9568.2006.04645.x DB - PRIME DP - Unbound Medicine ER -