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Lead-induced impairment of learning and memory in the nervous

  • Neurotoxicology Lab,School of Life Science, University of Science and Technology of China, Hefei 230027, China

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  • Received Date: 28 June 2008
  • Rev Recd Date: 01 July 2008
  • Publish Date: 31 August 2008
    Abstract

  • Abstract

    The advances made in lead-induced impairment of learning and memory in the nervous system and mechanisms of pharmacals repair in Neurotoxicolog Lab in University of Science and Technology of China were described. They include: ①the effect of lead on synaptic plasticity in hippocampus; ②the mechanism of effect of lead on ion channels; ③lead-induced impairment of NMDA receptor, non NMDA receptors and receptor channels; ④the interaction between lead and neurotransmitters; ⑤the effect of lead on gene regulation; ⑥the repair mechanism of pharmacals (Taurine, Ganglioside, antioxidants, etc.) on lead-induced impairment.

    Abstract

    The advances made in lead-induced impairment of learning and memory in the nervous system and mechanisms of pharmacals repair in Neurotoxicolog Lab in University of Science and Technology of China were described. They include: ①the effect of lead on synaptic plasticity in hippocampus; ②the mechanism of effect of lead on ion channels; ③lead-induced impairment of NMDA receptor, non NMDA receptors and receptor channels; ④the interaction between lead and neurotransmitters; ⑤the effect of lead on gene regulation; ⑥the repair mechanism of pharmacals (Taurine, Ganglioside, antioxidants, etc.) on lead-induced impairment.
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    • References(47)
  • [1]
    Pocock S J, Smith M, Baghurst P. Environmental lead and childrens intelligence: a systematic review of the epidemiological evidence[J]. BMJ,1994,309:1 189-1 197.
    [2]
    Shen X M, Rosen J F, Guo D, et al. Childhood lead poisoning in China[J]. Sci Total Environ, 1996,181:101-109.
    [3]
    Altmann L, Weinsberg F, Sveinsson K, et al. Impairment of long-term potentiation and learning following chronic lead exposure[J]. Toxicol Lett, 1993, 66:105-112.
    [4]
    Ruan D Y, Chen J T, Zhao C, et al. Impairment of long-term potentiation and paired-pulse facilitation in rat hippocampal dentate gyrus following developmental lead exposure in vivo[J]. Brain Res,1998, 806: 196-201.
    [5]
    Xu Y Z, Ruan D Y, Wu Y, et al. Nitric oxide affects LTP in area CA1 and CA3 of hippocampus in low-level lead-exposed rat[J]. Neurotoxicol Teratol, 1998,20: 69-73.
    [6]
    Zhao W F, Ruan D Y, Xu Y Z, et al. The effects of chronic lead exposure on long-term depression in area CA1 and dentate gyrus of rat hippocampus in vitro[J]. Brain Res,1999,818:153-159.
    [7]
    Sui L, Ge S Y, Ruan D Y, et al. Age-related impairment of long-term depression in area CA1 and dentate gyrus of rat hippocampus following developmental lead exposure in vitro[J]. Neurotoxicol Teratol,2000,22: 381-387.
    [8]
    Sui L, Ruan D Y, Ge SY, et al. Two components of long-term depression are impaired by chronic lead exposure in area CA1 and dentate gyrus of rat hippocampus in vitro[J]. Neurotoxicol Teratol, 2000,22：741-749.
    [9]
    Ge S Y, Ruan D Y, Yu K, et al. Effects of Fe2+ on ion channels: Na+ channel, delayed rectified and transient outward K+ channels[J]. Food Chem Toxicol, 2001, 39: 1 271-1 278.
    [10]
    Sui L, Ruan D Y. Impairment of the Ca2+-permeable AMPA/kainate receptors by lead exposure in organotypic rat hippocampal slice cultures[J]. Pharmacol Toxicol,2000,87: 204-210.
    [11]
    Zhang X Y, Liu A P, Ruan D Y, et al. Effect of developmental lead exposure on the expression of specific NMDA receptor subunit mRNAs in the hippocampus of neonatal rats by digoxigenin-labeled in situ hybridization histochemistry[J]. Neurotoxicol Teratol, 2002,24:149-160.
    [12]
    Wang M, Ruan D Y, Chen J T, et al. Lack of effects of vitamin E on aluminum-induced deficit of synaptic plasticity in rat dentate gyrus in vivo[J]. Food Chem Toxicol, 2002,40: 471-478.
    [13]
    Yu K, Ge S Y, Dai X Q, et al. Effects of Pb2+ on the transient outward potassium current in acutely dissociated rat hippocampal neurons[J]. Can J Physiol Pharmacol, 2003,81:825-833.
    [14]
    Meng X M, Ruan D Y, Kang L L, et al. Age-related morphological impairments in the rat hippocampus following developmental lead exposure: An MRI, LM and EM study[J]. Envir Toxicol Pharmacol, 2003,13:187-197.
    [15]
    Ruan D Y. The effects of developmental lead exposure on morphology and electrophysiology of rat hippocampus and brain function of children[J]. Toxicology, 2003,191:34-34.
    [16]
    Meng X M, Zhu D M, Ruan D Y, et al. Effects of chronic lead exposure on 1H MRS of hippocampus and frontal lobes in children[J]. Neurology,2005,64:1 644-1 647.
    [17]
    He S J, Xiao C, Wu Z Y, et al. Caffeine-dependent stimulus-triggered oscillations in the CA3 region of hippocampal slices from rats chronically exposed to lead[J]. Exp Neurol, 2004,190: 525-534.
    [18]
    Yu K, Yu S S, Ruan D Y. Opposite effects of lead exposure on taurine-and HFS-induced LTP in rat hippocampus[J]. Brain Res Bull,2005,64:525-531.
    [19]
    Zhu D M, Wang M, Ruan D Y. Protection by a taurine supplemented diet from lead-induced deficits of long-term potentiation/depotentiation in dentate gyrus of rats in vivo[J]. Neuroscience,2005,134: 215-224.
    [20]
    Gu Y, Wang L, Xiao C,et al. Effects of lead on voltage-gated sodium channels in rat hippocampal CA1 neurons[J]. Neuroscience, 2005,133:679-690.
    [21]
    Sheng W, Hang H W, Ruan D Y. In vivo microdialysis study of the relationship between lead-induced impairment of learning and neurotransmitter changes in the hippocampus[J]. Envir Toxicol Pharmacol, 2005,20,233-240.
    [22]
    Wang H L, Chen X T, Luo L,et al. Reparatory effects of nicotine on NMDA receptor-mediated synaptic plasticity in the hippocampal CA1 region of chronically lead-exposed rats[J]. Eur J Neurosci, 2006,23:1 111-1 119.
    [23]
    Li X M, Gu Y, She J Q, et al. Lead Inhibited N-methyl-D-aspartate receptor-independent long-term potentiation involved ryanodine-sensitive calcium stores in rat hippocampal area CA1[J]. Neuroscience,2006, 139:463-473.
    [24]
    Xiao C, Gu Y, Zhou C Y, et al. Pb2+ impairs GABAergic synaptic transmission in rat hippocampal slices: a possible involvement of presynaptic calcium channels[J]. Brain Res, 2006,1 088:93-100.
    [25]
    She J Q, Wang M, Zhu D M, et al. Effect of Ganglioside on synaptic plasticity of hippocampus in lead-exposed rats in vivo[J]. Brain Res, 2005, 1 060(1/2)：162-169.
    [26]
    Wang L, Luo L, Luo Y Y, et al. Effects of Pb2+ on muscarinic modulation of glutamatergic synaptic transmission in rat hippocampal CA1 area[J]. Neurotoxicology, 2007，28：499-507.
    [27]
    Yu S S, Wang M, Li X M, et al. Influences of different developmental periods of taurine supplements on synaptic plasticity in hippocampal CA1 area of rats following prenatal and perinatal lead exposure[J]. BMC Dev Biol,2007，7:51.
    [28]
    Chen W H, Wang M, Yu S S, et al. Clioquinol and vitamin B12 (cobalamin) synergistically rescue the lead-induced impairments of synaptic plasticity in hippocampal dentate gyrus area of the anaesthetized rats in vivo[J]. Neuroscience, 2007,147:853-864.
    [29]
    Wang M, Chen W H, Zhu D M, et al. Effects of carbachol on lead-induced impairment of the long-term potentiation/depotentiation in rat dentate gyrus in vivo[J]. Food Chem Toxicol, 2007,45:412-418.
    [30]
    Li X M, Li C C, Yu S S, et al. JNK1 contributes to metabotropic glutamate receptor-dependent long-term depression and short-term synaptic plasticity in the mice area hippocampal CA1[J]. Eur J Neurosci, 2007, 25:391-396.
    [31]
    Li C C, Li X, Chen W, et al. The different roles of cyclinD1-CDK4 in STP and mGluR-LTD during the postnatal development in mice hippocampus area CA1[J]. BMC Dev Biol，2007，7:57.
    [32]
    Finkelstein Y, Markowitz M E, Rosen J F. Low-level lead-induced neurotoxicity in children: an update on central nervous system effects(Review)[J]. Brain Res Rev, 1998, 27: 168-176.
    [33]
    Brostrom C O, Wolff D J. Properties and functions of calmodulin(Review)[J]. Biochem Pharmacol, 1981, 30:1 395-1 405.
    [34]
    Alkondon M, Costa A C, Radhakrishnan V, et al. Selective blockade of NMDA-activated channel currents may be implicated in learning deficits caused by lead[J]. FEBS Lett, 1990, 261:124-130.
    [35]
    Goebel D J, Poosc M S. NMDA receptor subunit gene expression in the rat brain: a quantitative analysis of endogenous mRNA levels of NR1Com, NR2A, NR2B, NR2C, NR2D and NR3A[J]. Brain Res Mol Brain Res, 1999, 69:164-170.
    [36]
    Monyer H, Giffard R G, Hartley D M, et al. Oxygen or glucose deprivation-induced neuronal injury in cortical cell cultures is reduced by tetanus toxin[J]. Neuron, 1992,8:967-973.
    [37]
    Ujihara H, Albuguergue E X. Development change of the inhibition by lead of NMDA-activated currents in cultured hippocampal neurons[J]. J Pharmacol Exp Ther, 1992, 263: 868-875.
    [38]
    Uteshev V, Büsselberg D, Haas H L. Pb2+ modulates the NMDA-receptor-channel complex[J]. Naunyn Schmiedebergs Arch Pharmacol,1993,347:209-213.
    [39]
    Guilarte T R, Miceli R C. Age-dependent effects of lead on [3H]MK-801 binding to the NMDA receptor-gated ionophore: in vitro and in vivo studies[J]. Neurosci Lett, 1992, 148(1/2):27-30.
    [40]
    Lasley S M. Regulation of dopaminergic activity, but not tyrosine hydroxylase, is diminished after chronic inorganic lead exposure[J]. Neurotoxicology, 1992,13:625-635.
    [41]
    Shih T M, Hanin I. Effects of chronic lead exposure on levels of acetylcholine and choline and on acetylcholine turnover rate in rat brain areas in vivo[J]. Psychopharmacology(Berl), 1978, 58: 263-269.
    [42]
    Costa L G, Fox D A. A selective decrease of cholinergic muscarinic receptors in the visual cortex of adult rats following developmental lead exposure[J]. Brain Res, 1983, 276:259-266.
    [43]
    Sierra E M, Rowles T K, Martin J, et al. Low level lead neurotoxicity in a pregnant guinea pigs model: neuroglial enzyme activities and brain trace metal concentrations[J]. Toxicology, 1989, 59:81-96.
    [44]
    Tischmeyer W, Kaczmarek L, Strauss M, et al. Accumulation of c-fos mRNA in rat hippocampus during acquisition of a brightness discrimination[J]. Behav Neural Biol,1990, 54:165-171.
    [45]
    Frank D A, Greenberg M E. CREB: A mediator of long-term memory from mollusks to mammals(Review)[J]. Cell, 1994,79:5-8.
    [46]
    Finkelsyein Y. Mechanism of lead-induced neurotixicity [C]//96 International Symposium on Childhood Lead Poisoning Prevention. Shanghai, 1996: 78-82.
    [47]
    Gurer H, Ozgunes H, Oztezcan S, et al. Antioxidant role of alpha-lipoic acid in lead toxicity[J]. Free Radic Biol Med, 1999,27: 75-81.
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    [1]
    Pocock S J, Smith M, Baghurst P. Environmental lead and childrens intelligence: a systematic review of the epidemiological evidence[J]. BMJ,1994,309:1 189-1 197.
    [2]
    Shen X M, Rosen J F, Guo D, et al. Childhood lead poisoning in China[J]. Sci Total Environ, 1996,181:101-109.
    [3]
    Altmann L, Weinsberg F, Sveinsson K, et al. Impairment of long-term potentiation and learning following chronic lead exposure[J]. Toxicol Lett, 1993, 66:105-112.
    [4]
    Ruan D Y, Chen J T, Zhao C, et al. Impairment of long-term potentiation and paired-pulse facilitation in rat hippocampal dentate gyrus following developmental lead exposure in vivo[J]. Brain Res,1998, 806: 196-201.
    [5]
    Xu Y Z, Ruan D Y, Wu Y, et al. Nitric oxide affects LTP in area CA1 and CA3 of hippocampus in low-level lead-exposed rat[J]. Neurotoxicol Teratol, 1998,20: 69-73.
    [6]
    Zhao W F, Ruan D Y, Xu Y Z, et al. The effects of chronic lead exposure on long-term depression in area CA1 and dentate gyrus of rat hippocampus in vitro[J]. Brain Res,1999,818:153-159.
    [7]
    Sui L, Ge S Y, Ruan D Y, et al. Age-related impairment of long-term depression in area CA1 and dentate gyrus of rat hippocampus following developmental lead exposure in vitro[J]. Neurotoxicol Teratol,2000,22: 381-387.
    [8]
    Sui L, Ruan D Y, Ge SY, et al. Two components of long-term depression are impaired by chronic lead exposure in area CA1 and dentate gyrus of rat hippocampus in vitro[J]. Neurotoxicol Teratol, 2000,22：741-749.
    [9]
    Ge S Y, Ruan D Y, Yu K, et al. Effects of Fe2+ on ion channels: Na+ channel, delayed rectified and transient outward K+ channels[J]. Food Chem Toxicol, 2001, 39: 1 271-1 278.
    [10]
    Sui L, Ruan D Y. Impairment of the Ca2+-permeable AMPA/kainate receptors by lead exposure in organotypic rat hippocampal slice cultures[J]. Pharmacol Toxicol,2000,87: 204-210.
    [11]
    Zhang X Y, Liu A P, Ruan D Y, et al. Effect of developmental lead exposure on the expression of specific NMDA receptor subunit mRNAs in the hippocampus of neonatal rats by digoxigenin-labeled in situ hybridization histochemistry[J]. Neurotoxicol Teratol, 2002,24:149-160.
    [12]
    Wang M, Ruan D Y, Chen J T, et al. Lack of effects of vitamin E on aluminum-induced deficit of synaptic plasticity in rat dentate gyrus in vivo[J]. Food Chem Toxicol, 2002,40: 471-478.
    [13]
    Yu K, Ge S Y, Dai X Q, et al. Effects of Pb2+ on the transient outward potassium current in acutely dissociated rat hippocampal neurons[J]. Can J Physiol Pharmacol, 2003,81:825-833.
    [14]
    Meng X M, Ruan D Y, Kang L L, et al. Age-related morphological impairments in the rat hippocampus following developmental lead exposure: An MRI, LM and EM study[J]. Envir Toxicol Pharmacol, 2003,13:187-197.
    [15]
    Ruan D Y. The effects of developmental lead exposure on morphology and electrophysiology of rat hippocampus and brain function of children[J]. Toxicology, 2003,191:34-34.
    [16]
    Meng X M, Zhu D M, Ruan D Y, et al. Effects of chronic lead exposure on 1H MRS of hippocampus and frontal lobes in children[J]. Neurology,2005,64:1 644-1 647.
    [17]
    He S J, Xiao C, Wu Z Y, et al. Caffeine-dependent stimulus-triggered oscillations in the CA3 region of hippocampal slices from rats chronically exposed to lead[J]. Exp Neurol, 2004,190: 525-534.
    [18]
    Yu K, Yu S S, Ruan D Y. Opposite effects of lead exposure on taurine-and HFS-induced LTP in rat hippocampus[J]. Brain Res Bull,2005,64:525-531.
    [19]
    Zhu D M, Wang M, Ruan D Y. Protection by a taurine supplemented diet from lead-induced deficits of long-term potentiation/depotentiation in dentate gyrus of rats in vivo[J]. Neuroscience,2005,134: 215-224.
    [20]
    Gu Y, Wang L, Xiao C,et al. Effects of lead on voltage-gated sodium channels in rat hippocampal CA1 neurons[J]. Neuroscience, 2005,133:679-690.
    [21]
    Sheng W, Hang H W, Ruan D Y. In vivo microdialysis study of the relationship between lead-induced impairment of learning and neurotransmitter changes in the hippocampus[J]. Envir Toxicol Pharmacol, 2005,20,233-240.
    [22]
    Wang H L, Chen X T, Luo L,et al. Reparatory effects of nicotine on NMDA receptor-mediated synaptic plasticity in the hippocampal CA1 region of chronically lead-exposed rats[J]. Eur J Neurosci, 2006,23:1 111-1 119.
    [23]
    Li X M, Gu Y, She J Q, et al. Lead Inhibited N-methyl-D-aspartate receptor-independent long-term potentiation involved ryanodine-sensitive calcium stores in rat hippocampal area CA1[J]. Neuroscience,2006, 139:463-473.
    [24]
    Xiao C, Gu Y, Zhou C Y, et al. Pb2+ impairs GABAergic synaptic transmission in rat hippocampal slices: a possible involvement of presynaptic calcium channels[J]. Brain Res, 2006,1 088:93-100.
    [25]
    She J Q, Wang M, Zhu D M, et al. Effect of Ganglioside on synaptic plasticity of hippocampus in lead-exposed rats in vivo[J]. Brain Res, 2005, 1 060(1/2)：162-169.
    [26]
    Wang L, Luo L, Luo Y Y, et al. Effects of Pb2+ on muscarinic modulation of glutamatergic synaptic transmission in rat hippocampal CA1 area[J]. Neurotoxicology, 2007，28：499-507.
    [27]
    Yu S S, Wang M, Li X M, et al. Influences of different developmental periods of taurine supplements on synaptic plasticity in hippocampal CA1 area of rats following prenatal and perinatal lead exposure[J]. BMC Dev Biol,2007，7:51.
    [28]
    Chen W H, Wang M, Yu S S, et al. Clioquinol and vitamin B12 (cobalamin) synergistically rescue the lead-induced impairments of synaptic plasticity in hippocampal dentate gyrus area of the anaesthetized rats in vivo[J]. Neuroscience, 2007,147:853-864.
    [29]
    Wang M, Chen W H, Zhu D M, et al. Effects of carbachol on lead-induced impairment of the long-term potentiation/depotentiation in rat dentate gyrus in vivo[J]. Food Chem Toxicol, 2007,45:412-418.
    [30]
    Li X M, Li C C, Yu S S, et al. JNK1 contributes to metabotropic glutamate receptor-dependent long-term depression and short-term synaptic plasticity in the mice area hippocampal CA1[J]. Eur J Neurosci, 2007, 25:391-396.
    [31]
    Li C C, Li X, Chen W, et al. The different roles of cyclinD1-CDK4 in STP and mGluR-LTD during the postnatal development in mice hippocampus area CA1[J]. BMC Dev Biol，2007，7:57.
    [32]
    Finkelstein Y, Markowitz M E, Rosen J F. Low-level lead-induced neurotoxicity in children: an update on central nervous system effects(Review)[J]. Brain Res Rev, 1998, 27: 168-176.
    [33]
    Brostrom C O, Wolff D J. Properties and functions of calmodulin(Review)[J]. Biochem Pharmacol, 1981, 30:1 395-1 405.
    [34]
    Alkondon M, Costa A C, Radhakrishnan V, et al. Selective blockade of NMDA-activated channel currents may be implicated in learning deficits caused by lead[J]. FEBS Lett, 1990, 261:124-130.
    [35]
    Goebel D J, Poosc M S. NMDA receptor subunit gene expression in the rat brain: a quantitative analysis of endogenous mRNA levels of NR1Com, NR2A, NR2B, NR2C, NR2D and NR3A[J]. Brain Res Mol Brain Res, 1999, 69:164-170.
    [36]
    Monyer H, Giffard R G, Hartley D M, et al. Oxygen or glucose deprivation-induced neuronal injury in cortical cell cultures is reduced by tetanus toxin[J]. Neuron, 1992,8:967-973.
    [37]
    Ujihara H, Albuguergue E X. Development change of the inhibition by lead of NMDA-activated currents in cultured hippocampal neurons[J]. J Pharmacol Exp Ther, 1992, 263: 868-875.
    [38]
    Uteshev V, Büsselberg D, Haas H L. Pb2+ modulates the NMDA-receptor-channel complex[J]. Naunyn Schmiedebergs Arch Pharmacol,1993,347:209-213.
    [39]
    Guilarte T R, Miceli R C. Age-dependent effects of lead on [3H]MK-801 binding to the NMDA receptor-gated ionophore: in vitro and in vivo studies[J]. Neurosci Lett, 1992, 148(1/2):27-30.
    [40]
    Lasley S M. Regulation of dopaminergic activity, but not tyrosine hydroxylase, is diminished after chronic inorganic lead exposure[J]. Neurotoxicology, 1992,13:625-635.
    [41]
    Shih T M, Hanin I. Effects of chronic lead exposure on levels of acetylcholine and choline and on acetylcholine turnover rate in rat brain areas in vivo[J]. Psychopharmacology(Berl), 1978, 58: 263-269.
    [42]
    Costa L G, Fox D A. A selective decrease of cholinergic muscarinic receptors in the visual cortex of adult rats following developmental lead exposure[J]. Brain Res, 1983, 276:259-266.
    [43]
    Sierra E M, Rowles T K, Martin J, et al. Low level lead neurotoxicity in a pregnant guinea pigs model: neuroglial enzyme activities and brain trace metal concentrations[J]. Toxicology, 1989, 59:81-96.
    [44]
    Tischmeyer W, Kaczmarek L, Strauss M, et al. Accumulation of c-fos mRNA in rat hippocampus during acquisition of a brightness discrimination[J]. Behav Neural Biol,1990, 54:165-171.
    [45]
    Frank D A, Greenberg M E. CREB: A mediator of long-term memory from mollusks to mammals(Review)[J]. Cell, 1994,79:5-8.
    [46]
    Finkelsyein Y. Mechanism of lead-induced neurotixicity [C]//96 International Symposium on Childhood Lead Poisoning Prevention. Shanghai, 1996: 78-82.
    [47]
    Gurer H, Ozgunes H, Oztezcan S, et al. Antioxidant role of alpha-lipoic acid in lead toxicity[J]. Free Radic Biol Med, 1999,27: 75-81.
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