Chronic Developmental Lead Exposure Reduces Neurogenesis in Adult Rat Hippocampus but Does Not Impair Spatial Learning
The dentate granule cell (DG) layer of the hippocampal formation has the distinctive property of ongoing neurogenesis that continues throughout adult life. Although the function of these newly generated neurons and the mechanisms that control their birth are unknown, age, activity, diet and psychoso...
Saved in:
| Published in | Toxicological sciences Vol. 86; no. 2; pp. 365 - 374 |
|---|---|
| Main Authors | , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
Oxford University Press
01.08.2005
|
| Subjects | |
| Online Access | Get full text |
| ISSN | 1096-6080 1096-0929 |
| DOI | 10.1093/toxsci/kfi156 |
Cover
| Abstract | The dentate granule cell (DG) layer of the hippocampal formation has the distinctive property of ongoing neurogenesis that continues throughout adult life. Although the function of these newly generated neurons and the mechanisms that control their birth are unknown, age, activity, diet and psychosocial stress have all been demonstrated to regulate this type of neurogenesis. Little information on the impact of environmental insults on this process has appeared to date. Developmental lead (Pb) exposure has been well documented to impair cognitive function in children and animals and reduce activity-dependent synaptic plasticity in the hippocampus of rodents. Therefore, we examined the effects of this classic environmental neurotoxicant on hippocampal-dependent learning and adult neurogenesis in the hippocampus. Pregnant rats were exposed to a low level of Pb-acetate (0.2%) via the drinking water from late gestation (GD 16) until weaning on postnatal day 21 (PN 21). At weaning, half of the Pb-exposed animals were weaned to control drinking water and the remainder were maintained on Pb water until termination of the study. Animals were paired- housed and on PN 75 were administered a series of injections of a thymidine analog bromodeoxyuridine (BrdU), a marker of DNA synthesis that labels proliferating cells and their progeny. At 12-h intervals for 12 days, rats received an ip injection of BrdU (50 mg/kg). Subjects were sacrificed and perfused 24 h and 28 days after the last injection. Spatial learning was assessed in an independent group of animals beginning on PN 110 using a Morris water maze. No Pb-induced impairments were evident in water maze learning. Immunohistochemistry for the detection of BrdU-labeled cells was performed on 40-μm coronal sections throughout the hippocampus. Continuous exposure to Pb (Life) reduced the total number of BrdU-positive cells at 28 days without affecting the total number of labeled cells evident 24 h after the last injection. No differences in the number of progenitor cells labeled or surviving were seen between control and treated animals whose Pb exposure was terminated at weaning. Double labeling with BrdU and the glial specific marker, glial acidic fibrillary protein (GFAP) indicated that the bulk of the surviving cells were of a neuronal rather than a glial phenotype. These data reveal that chronic low-level Pb exposure reduces the capacity for neurogenesis in the adult hippocampus. Despite deficits in synaptic plasticity previously reported from our laboratory (e.g., Gilbert, M. E., Mack, C. M., and Lusley, S. M. Brain Res. 1996; 736, 118–124), and now structural plasticity, no significant impact on spatial learning was detected. |
|---|---|
| AbstractList | The dentate granule cell (DG) layer of the hippocampal formation has the distinctive property of ongoing neurogenesis that continues throughout adult life. Although the function of these newly generated neurons and the mechanisms that control their birth are unknown, age, activity, diet and psychosocial stress have all been demonstrated to regulate this type of neurogenesis. Little information on the impact of environmental insults on this process has appeared to date. Developmental lead (Pb) exposure has been well documented to impair cognitive function in children and animals and reduce activity-dependent synaptic plasticity in the hippocampus of rodents. Therefore, we examined the effects of this classic environmental neurotoxicant on hippocampal-dependent learning and adult neurogenesis in the hippocampus. Pregnant rats were exposed to a low level of Pb-acetate (0.2%) via the drinking water from late gestation (GD 16) until weaning on postnatal day 21 (PN 21). At weaning, half of the Pb-exposed animals were weaned to control drinking water and the remainder were maintained on Pb water until termination of the study. Animals were paired- housed and on PN 75 were administered a series of injections of a thymidine analog bromodeoxyuridine (BrdU), a marker of DNA synthesis that labels proliferating cells and their progeny. At 12-h intervals for 12 days, rats received an ip injection of BrdU (50 mg/kg). Subjects were sacrificed and perfused 24 h and 28 days after the last injection. Spatial learning was assessed in an independent group of animals beginning on PN 110 using a Morris water maze. No Pb-induced impairments were evident in water maze learning. Immunohistochemistry for the detection of BrdU-labeled cells was performed on 40-μm coronal sections throughout the hippocampus. Continuous exposure to Pb (Life) reduced the total number of BrdU-positive cells at 28 days without affecting the total number of labeled cells evident 24 h after the last injection. No differences in the number of progenitor cells labeled or surviving were seen between control and treated animals whose Pb exposure was terminated at weaning. Double labeling with BrdU and the glial specific marker, glial acidic fibrillary protein (GFAP) indicated that the bulk of the surviving cells were of a neuronal rather than a glial phenotype. These data reveal that chronic low-level Pb exposure reduces the capacity for neurogenesis in the adult hippocampus. Despite deficits in synaptic plasticity previously reported from our laboratory (e.g., Gilbert, M. E., Mack, C. M., and Lusley, S. M. Brain Res. 1996; 736, 118–124), and now structural plasticity, no significant impact on spatial learning was detected. The dentate granule cell (DG) layer of the hippocampal formation has the distinctive property of ongoing neurogenesis that continues throughout adult life. Although the function of these newly generated neurons and the mechanisms that control their birth are unknown, age, activity, diet and psychosocial stress have all been demonstrated to regulate this type of neurogenesis. Little information on the impact of environmental insults on this process has appeared to date. Developmental lead (Pb) exposure has been well documented to impair cognitive function in children and animals and reduce activity-dependent synaptic plasticity in the hippocampus of rodents. Therefore, we examined the effects of this classic environmental neurotoxicant on hippocampal-dependent learning and adult neurogenesis in the hippocampus. Pregnant rats were exposed to a low level of Pb-acetate (0.2%) via the drinking water from late gestation (GD 16) until weaning on postnatal day 21 (PN 21). At weaning, half of the Pb-exposed animals were weaned to control drinking water and the remainder were maintained on Pb water until termination of the study. Animals were paired- housed and on PN 75 were administered a series of injections of a thymidine analog bromodeoxyuridine (BrdU), a marker of DNA synthesis that labels proliferating cells and their progeny. At 12-h intervals for 12 days, rats received an ip injection of BrdU (50 mg/kg). Subjects were sacrificed and perfused 24 h and 28 days after the last injection. Spatial learning was assessed in an independent group of animals beginning on PN 110 using a Morris water maze. No Pb-induced impairments were evident in water maze learning. Immunohistochemistry for the detection of BrdU-labeled cells was performed on 40-microm coronal sections throughout the hippocampus. Continuous exposure to Pb (Life) reduced the total number of BrdU-positive cells at 28 days without affecting the total number of labeled cells evident 24 h after the last injection. No differences in the number of progenitor cells labeled or surviving were seen between control and treated animals whose Pb exposure was terminated at weaning. Double labeling with BrdU and the glial specific marker, glial acidic fibrillary protein (GFAP) indicated that the bulk of the surviving cells were of a neuronal rather than a glial phenotype. These data reveal that chronic low-level Pb exposure reduces the capacity for neurogenesis in the adult hippocampus. Despite deficits in synaptic plasticity previously reported from our laboratory, and now structural plasticity, no significant impact on spatial learning was detected.The dentate granule cell (DG) layer of the hippocampal formation has the distinctive property of ongoing neurogenesis that continues throughout adult life. Although the function of these newly generated neurons and the mechanisms that control their birth are unknown, age, activity, diet and psychosocial stress have all been demonstrated to regulate this type of neurogenesis. Little information on the impact of environmental insults on this process has appeared to date. Developmental lead (Pb) exposure has been well documented to impair cognitive function in children and animals and reduce activity-dependent synaptic plasticity in the hippocampus of rodents. Therefore, we examined the effects of this classic environmental neurotoxicant on hippocampal-dependent learning and adult neurogenesis in the hippocampus. Pregnant rats were exposed to a low level of Pb-acetate (0.2%) via the drinking water from late gestation (GD 16) until weaning on postnatal day 21 (PN 21). At weaning, half of the Pb-exposed animals were weaned to control drinking water and the remainder were maintained on Pb water until termination of the study. Animals were paired- housed and on PN 75 were administered a series of injections of a thymidine analog bromodeoxyuridine (BrdU), a marker of DNA synthesis that labels proliferating cells and their progeny. At 12-h intervals for 12 days, rats received an ip injection of BrdU (50 mg/kg). Subjects were sacrificed and perfused 24 h and 28 days after the last injection. Spatial learning was assessed in an independent group of animals beginning on PN 110 using a Morris water maze. No Pb-induced impairments were evident in water maze learning. Immunohistochemistry for the detection of BrdU-labeled cells was performed on 40-microm coronal sections throughout the hippocampus. Continuous exposure to Pb (Life) reduced the total number of BrdU-positive cells at 28 days without affecting the total number of labeled cells evident 24 h after the last injection. No differences in the number of progenitor cells labeled or surviving were seen between control and treated animals whose Pb exposure was terminated at weaning. Double labeling with BrdU and the glial specific marker, glial acidic fibrillary protein (GFAP) indicated that the bulk of the surviving cells were of a neuronal rather than a glial phenotype. These data reveal that chronic low-level Pb exposure reduces the capacity for neurogenesis in the adult hippocampus. Despite deficits in synaptic plasticity previously reported from our laboratory, and now structural plasticity, no significant impact on spatial learning was detected. The dentate granule cell (DG) layer of the hippocampal formation has the distinctive property of ongoing neurogenesis that continues throughout adult life. Although the function of these newly generated neurons and the mechanisms that control their birth are unknown, age, activity, diet and psychosocial stress have all been demonstrated to regulate this type of neurogenesis. Little information on the impact of environmental insults on this process has appeared to date. Developmental lead (Pb) exposure has been well documented to impair cognitive function in children and animals and reduce activity-dependent synaptic plasticity in the hippocampus of rodents. Therefore, we examined the effects of this classic environmental neurotoxicant on hippocampal-dependent learning and adult neurogenesis in the hippocampus. Pregnant rats were exposed to a low level of Pb-acetate (0.2%) via the drinking water from late gestation (GD 16) until weaning on postnatal day 21 (PN 21). At weaning, half of the Pb-exposed animals were weaned to control drinking water and the remainder were maintained on Pb water until termination of the study. Animals were paired-housed and on PN 75 were administered a series of injections of a thymidine analog bromodeoxyuridine (BrdU), a marker of DNA synthesis that labels proliferating cells and their progeny. At 12-h intervals for 12 days, rats received an ip injection of BrdU (50 mg/kg). Subjects were sacrificed and perfused 24 h and 28 days after the last injection. Spatial learning was assessed in an independent group of animals beginning on PN 110 using a Morris water maze. No Pb-induced impairments were evident in water maze learning. Immunohistochemistry for the detection of BrdU-labeled cells was performed on 40- mu m coronal sections throughout the hippocampus. Continuous exposure to Pb (Life) reduced the total number of BrdU-positive cells at 28 days without affecting the total number of labeled cells evident 24 h after the last injection. No differences in the number of progenitor cells labeled or surviving were seen between control and treated animals whose Pb exposure was terminated at weaning. Double labeling with BrdU and the glial specific marker, glial acidic fibrillary protein (GFAP) indicated that the bulk of the surviving cells were of a neuronal rather than a glial phenotype. These data reveal that chronic low-level Pb exposure reduces the capacity for neurogenesis in the adult hippocampus. Despite deficits in synaptic plasticity previously reported from our laboratory (e.g., Gilbert, M. E., Mack, C. M., and Lusley, S. M. Brain Res. 1996; 736, 118-124), and now structural plasticity, no significant impact on spatial learning was detected. The dentate granule cell (DG) layer of the hippocampal formation has the distinctive property of ongoing neurogenesis that continues throughout adult life. Although the function of these newly generated neurons and the mechanisms that control their birth are unknown, age, activity, diet and psychosocial stress have all been demonstrated to regulate this type of neurogenesis. Little information on the impact of environmental insults on this process has appeared to date. Developmental lead (Pb) exposure has been well documented to impair cognitive function in children and animals and reduce activity-dependent synaptic plasticity in the hippocampus of rodents. Therefore, we examined the effects of this classic environmental neurotoxicant on hippocampal-dependent learning and adult neurogenesis in the hippocampus. Pregnant rats were exposed to a low level of Pb-acetate (0.2%) via the drinking water from late gestation (GD 16) until weaning on postnatal day 21 (PN 21). At weaning, half of the Pb-exposed animals were weaned to control drinking water and the remainder were maintained on Pb water until termination of the study. Animals were paired- housed and on PN 75 were administered a series of injections of a thymidine analog bromodeoxyuridine (BrdU), a marker of DNA synthesis that labels proliferating cells and their progeny. At 12-h intervals for 12 days, rats received an ip injection of BrdU (50 mg/kg). Subjects were sacrificed and perfused 24 h and 28 days after the last injection. Spatial learning was assessed in an independent group of animals beginning on PN 110 using a Morris water maze. No Pb-induced impairments were evident in water maze learning. Immunohistochemistry for the detection of BrdU-labeled cells was performed on 40-microm coronal sections throughout the hippocampus. Continuous exposure to Pb (Life) reduced the total number of BrdU-positive cells at 28 days without affecting the total number of labeled cells evident 24 h after the last injection. No differences in the number of progenitor cells labeled or surviving were seen between control and treated animals whose Pb exposure was terminated at weaning. Double labeling with BrdU and the glial specific marker, glial acidic fibrillary protein (GFAP) indicated that the bulk of the surviving cells were of a neuronal rather than a glial phenotype. These data reveal that chronic low-level Pb exposure reduces the capacity for neurogenesis in the adult hippocampus. Despite deficits in synaptic plasticity previously reported from our laboratory, and now structural plasticity, no significant impact on spatial learning was detected. |
| Author | Goodman, J. H. Samsam, T. E. Kelly, M. E. Gilbert, M. E. |
| Author_xml | – sequence: 1 givenname: M. E. surname: Gilbert fullname: Gilbert, M. E. email: To whom correspondence should be addressed at Neurotoxicology Division (MD B105–05), National Health and Environmental Effects Research Laboratory, U.S. Environmental Protection Agency, Research Triangle Park, NC 27711. Fax: (919) 541-4849. gilbert.mary@epa.gov. organization: Neurotoxicology Division, U.S. Environmental Protection Agency, Research Triangle Park, North Carolina – sequence: 2 givenname: M. E. surname: Kelly fullname: Kelly, M. E. organization: Children's Hospital of Philadelphia, Philadelphia, Pennsylvania; and – sequence: 3 givenname: T. E. surname: Samsam fullname: Samsam, T. E. organization: Neurotoxicology Division, U.S. Environmental Protection Agency, Research Triangle Park, North Carolina – sequence: 4 givenname: J. H. surname: Goodman fullname: Goodman, J. H. organization: Center for Neural Recovery & Rehabilitation Research, Helen Hayes Hospital, West Haverstraw, New York |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/15788721$$D View this record in MEDLINE/PubMed |
| BookMark | eNqFkU1v1DAQhi3Uin7AkSvyiVuoHSdxcqy2ha1YtVIpAnGxJs6kmCa2sZ1q---bKksPHOhpPvTMq5l5j8iedRYJecfZR84acZLcNmpzctcbXlavyOHcrDLW5M3eLq9YzQ7IUYy_GeO8Ys1rcsBLWdcy54fkfvUrOGs0PcN7HJwf0SYY6Aaho-db7-IUkF5jN2mM9BKn4G7RYjSRGktPu2lI9BoSXRvvnYbRT5G2U6Jn7gl3iV6MHkygXz0ks-gGa-ztG7LfwxDx7S4ek2-fzm9W62xz9flidbrJtKhYynrRtoDFfAKA7LHrWcubosplXjLgWAgJTd6DbKUGoUuYK8jbEmTR9jIXTByTD4uuD-7PhDGp0USNwwAW3RRVVTMmKyZfBLkUshasnMH3O3BqR-yUD2aE8KD-vnQGxALo4GIM2Ctt0ny9symAGRRn6sk4tRinFuPmqeyfqWfh__MmJtw-wxDuVDWvWqr1j5-qLG7kl3X5XeXiEd3BriI |
| CitedBy_id | crossref_primary_10_3390_biology11081164 crossref_primary_10_1016_j_neuro_2009_08_011 crossref_primary_10_1371_journal_pone_0115556 crossref_primary_10_1016_j_neuro_2012_04_016 crossref_primary_10_1007_s12640_009_9126_x crossref_primary_10_1016_j_tox_2021_152782 crossref_primary_10_1186_1471_2202_13_82 crossref_primary_10_1016_j_envres_2025_120830 crossref_primary_10_1007_s00244_009_9307_x crossref_primary_10_1016_j_neuro_2010_03_007 crossref_primary_10_1016_j_ntt_2012_09_001 crossref_primary_10_1111_j_1474_9726_2007_00363_x crossref_primary_10_1007_s11064_010_0235_y crossref_primary_10_1016_j_neuro_2017_01_008 crossref_primary_10_1016_j_ntt_2014_09_001 crossref_primary_10_1080_09540260701797936 crossref_primary_10_1038_nrn1867 crossref_primary_10_1016_j_ijdevneu_2005_07_005 crossref_primary_10_3390_toxics9020023 crossref_primary_10_1016_j_neuro_2007_01_012 crossref_primary_10_1095_biolreprod_108_075341 crossref_primary_10_1289_ehp_1002524 crossref_primary_10_1016_j_neuro_2012_02_014 crossref_primary_10_1016_S0895_3988_09_60025_8 crossref_primary_10_1111_j_1600_0404_2009_01155_x crossref_primary_10_1016_j_tiv_2015_05_001 crossref_primary_10_1016_j_ntt_2019_01_005 crossref_primary_10_1007_s12640_021_00355_9 crossref_primary_10_14202_vetworld_2016_133_141 crossref_primary_10_1007_s00580_014_1895_9 crossref_primary_10_1155_2014_235941 crossref_primary_10_3389_fcell_2021_648261 crossref_primary_10_1177_1073858408317008 crossref_primary_10_1016_j_bbr_2014_12_036 crossref_primary_10_1039_C5TX00071H crossref_primary_10_1080_09603123_2024_2307344 crossref_primary_10_1007_s11064_010_0300_6 crossref_primary_10_1007_s13530_020_00059_1 crossref_primary_10_1016_j_cotox_2021_03_006 crossref_primary_10_1093_toxsci_kfaa144 crossref_primary_10_1089_ars_2022_0076 crossref_primary_10_3945_ajcn_2009_28839 crossref_primary_10_1007_s00441_013_1631_9 crossref_primary_10_1515_REVEH_2006_21_2_105 crossref_primary_10_1016_j_ntt_2014_12_001 crossref_primary_10_1016_j_envres_2021_111908 crossref_primary_10_1093_ilar_ilaa012 crossref_primary_10_1007_s11356_014_3498_z crossref_primary_10_1016_j_ntt_2018_04_001 crossref_primary_10_1371_journal_pone_0073720 crossref_primary_10_1016_j_ntt_2013_04_003 crossref_primary_10_1093_toxsci_kfu028 crossref_primary_10_3109_01480545_2014_907578 crossref_primary_10_1080_02772248_2011_585744 crossref_primary_10_1016_j_jhazmat_2023_132906 crossref_primary_10_1016_j_neuro_2016_12_009 crossref_primary_10_1016_j_jchemneu_2018_03_005 crossref_primary_10_1016_j_brainres_2018_02_014 crossref_primary_10_1016_j_neuroscience_2015_06_010 crossref_primary_10_4236_jbbs_2012_22021 crossref_primary_10_1016_j_neulet_2017_09_060 crossref_primary_10_1016_j_neuro_2018_08_001 crossref_primary_10_1289_EHP265 crossref_primary_10_1016_j_ijdevneu_2010_09_008 crossref_primary_10_1016_j_ecoenv_2020_111850 crossref_primary_10_1289_ehp_11268 crossref_primary_10_3109_15622975_2013_797104 crossref_primary_10_1016_j_ntt_2020_106865 crossref_primary_10_2478_10004_1254_62_2011_2070 crossref_primary_10_1016_j_toxlet_2015_09_015 crossref_primary_10_1016_j_toxlet_2012_07_002 crossref_primary_10_1038_nm1619 crossref_primary_10_1093_cercor_bhab431 crossref_primary_10_1007_s12640_020_00162_8 |
| Cites_doi | 10.1016/0306-4522(93)90335-D 10.1146/annurev.pa.35.040195.002135 10.1073/pnas.94.19.10409 10.1038/35066584 10.1038/6365 10.1016/S0091-3057(96)00350-4 10.1002/cne.901240303 10.1016/S0014-4886(03)00272-3 10.1016/S0006-8993(97)01517-5 10.1037/0735-7044.111.3.532 10.1002/ana.10262 10.1523/JNEUROSCI.13-07-02930.1993 10.1016/S0006-8993(99)02464-6 10.1016/S0197-4580(02)00096-9 10.1006/taap.1999.8743 10.1542/peds.87.2.219 10.1016/j.neuroscience.2003.09.029 10.1046/j.1471-4159.2002.01085.x 10.1289/ehp.9086177 10.1016/j.brainres.2003.10.068 10.1016/0892-0362(88)90024-4 10.1523/JNEUROSCI.22-07-02679.2002 10.1073/pnas.120552597 10.1006/nbdi.2002.0531 10.1002/hipo.10103 10.1016/0378-4274(93)90085-C 10.1523/JNEUROSCI.18-19-07768.1998 10.1016/S0006-8993(00)03249-2 10.1007/978-1-4615-3330-6_7 10.1523/JNEUROSCI.20-16-06144.2000 10.1016/S0006-8993(98)00739-2 10.1523/JNEUROSCI.17-07-02492.1997 10.1038/4151030a 10.1523/JNEUROSCI.18-09-03206.1998 10.1002/ana.10399 10.1523/JNEUROSCI.0204-04.2004 10.1016/0892-0362(95)02026-8 10.1073/pnas.1230907100 10.1002/cne.1040 10.1016/S0304-3940(97)00633-2 10.1016/S0378-4274(98)00388-9 10.1016/0006-8993(96)00665-8 10.1016/0006-8993(96)00666-X 10.1016/S0169-328X(00)00010-3 10.1046/j.1471-4159.2002.01214.x 10.1016/S0006-8993(00)02790-6 10.1002/(SICI)1097-4695(19980615)35:4<395::AID-NEU7>3.0.CO;2-U 10.1523/JNEUROSCI.16-06-02027.1996 10.1016/S0378-4274(01)00450-7 10.1002/(SICI)1097-4695(20000205)42:2<248::AID-NEU8>3.0.CO;2-J 10.1523/JNEUROSCI.17-10-03727.1997 10.1016/j.ntt.2004.01.010 10.1016/j.neuroscience.2004.10.009 10.1016/0006-8993(93)90217-B 10.1093/toxsci/66.1.139 10.1016/S0892-0362(01)00116-7 |
| ContentType | Journal Article |
| DBID | BSCLL AAYXX CITATION CGR CUY CVF ECM EIF NPM 7TK 7U7 C1K 7X8 |
| DOI | 10.1093/toxsci/kfi156 |
| DatabaseName | Istex CrossRef Medline MEDLINE MEDLINE (Ovid) MEDLINE MEDLINE PubMed Neurosciences Abstracts Toxicology Abstracts Environmental Sciences and Pollution Management MEDLINE - Academic |
| DatabaseTitle | CrossRef MEDLINE Medline Complete MEDLINE with Full Text PubMed MEDLINE (Ovid) Toxicology Abstracts Neurosciences Abstracts Environmental Sciences and Pollution Management MEDLINE - Academic |
| DatabaseTitleList | MEDLINE - Academic Toxicology Abstracts MEDLINE |
| Database_xml | – sequence: 1 dbid: NPM name: PubMed url: https://proxy.k.utb.cz/login?url=http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed sourceTypes: Index Database – sequence: 2 dbid: EIF name: MEDLINE url: https://proxy.k.utb.cz/login?url=https://www.webofscience.com/wos/medline/basic-search sourceTypes: Index Database |
| DeliveryMethod | fulltext_linktorsrc |
| Discipline | Medicine Public Health Pharmacy, Therapeutics, & Pharmacology |
| EISSN | 1096-0929 |
| EndPage | 374 |
| ExternalDocumentID | 15788721 10_1093_toxsci_kfi156 ark_67375_HXZ_54T7KH5W_2 |
| Genre | Journal Article |
| GroupedDBID | --- --K -E4 .2P .I3 .ZR 0R~ 123 18M 1B1 1~5 29Q 2WC 4.4 48X 4G. 53G 5RE 5VS 5WA 5WD 7-5 70D A8Z AABZA AACZT AAEDT AAHBH AAIMJ AAJKP AAJQQ AALRI AAMDB AAMVS AAOGV AAPNW AAPQZ AAPXW AAQXK AARHZ AAUAY AAUQX AAVAP AAVLN AAWDT AAXUO AAYWO ABDFA ABEJV ABEUO ABGNP ABIME ABIXL ABJNI ABKDP ABMAC ABMNT ABNGD ABNHQ ABNKS ABPQP ABPTD ABQLI ABVGC ABWST ABWVN ABXVV ABXZS ABZBJ ACFRR ACGFO ACGFS ACRPL ACUFI ACUKT ACUTJ ACUTO ADBBV ADEYI ADEZT ADGKP ADGZP ADHKW ADHZD ADIPN ADMUD ADNBA ADNMO ADOCK ADQBN ADRTK ADVEK ADYVW ADZTZ ADZXQ AEGPL AEGXH AEHUL AEJOX AEKSI AELWJ AEMDU AENEX AENZO AEPUE AETBJ AEWNT AFFZL AFGWE AFIYH AFOFC AGINJ AGKEF AGORE AGQPQ AGQXC AGSYK AHGBF AHMMS AHXPO AIJHB AJBYB AJEEA AJNCP AKHUL AKRWK AKWXX ALMA_UNASSIGNED_HOLDINGS ALUQC ALXQX ANFBD APIBT APWMN AQDSO ARIXL ASPBG ATGXG ATTQO AVWKF AXUDD AYOIW AZFZN BAWUL BAYMD BCRHZ BEYMZ BHONS BQDIO BSCLL BSWAC BTRTY BVRKM CAG CDBKE COF CS3 CZ4 DAKXR DIK DILTD DM4 DU5 D~K E3Z EBD EBS EDH EE~ EJD ELUNK EMOBN F5P F9B FDB FEDTE FGOYB FHSFR FIRID FLUFQ FOEOM FOTVD FQBLK GAUVT GJXCC GX1 H13 H5~ HAR HH5 HVGLF HW0 HZ~ I-F IHE IOX JXSIZ KAQDR KBUDW KOP KQ8 KSI KSN LG5 M-Z N9A NGC NLBLG NOMLY NOYVH NQ- NTWIH NU- NVLIB O-L O0~ O9- OAWHX OBOKY OCZFY ODMLO OHT OJQWA OJZSN OPAEJ OWPYF O~Y P2P PAFKI PB- PEELM Q1. Q5Y R2- R44 RD5 RIG RNI ROL ROX RPZ RUSNO RW1 RXO RZO SSZ SV3 TJX TLC TR2 UHS W8F WOQ X7H XPP YAYTL YKOAZ YXANX ZGI ZKX ZMT ZXP ~02 ~91 AAYXX CITATION 1TH AACTN ABQTQ ADJQC ADRIX AFXEN CGR CUY CVF ECM EIF J21 M49 NPM OK1 YCJ 7TK 7U7 C1K ESTFP 7X8 |
| ID | FETCH-LOGICAL-c360t-f3bbae4608aa7fedf0b194627250a1e437a92fa7b7ca3c5aa92a2b5a74bf72303 |
| ISSN | 1096-6080 |
| IngestDate | Mon Sep 08 13:17:09 EDT 2025 Mon Sep 08 15:09:41 EDT 2025 Wed Feb 19 01:40:15 EST 2025 Thu Apr 24 23:05:00 EDT 2025 Tue Jul 01 02:57:05 EDT 2025 Tue Aug 05 16:49:34 EDT 2025 |
| IsPeerReviewed | true |
| IsScholarly | true |
| Issue | 2 |
| Language | English |
| LinkModel | OpenURL |
| MergedId | FETCHMERGED-LOGICAL-c360t-f3bbae4608aa7fedf0b194627250a1e437a92fa7b7ca3c5aa92a2b5a74bf72303 |
| Notes | ark:/67375/HXZ-54T7KH5W-2 istex:0AD31B20609644354E4D4CEC6F6008E4084A1E75 1To whom correspondence should be addressed at Neurotoxicology Division (MD B105–05), National Health and Environmental Effects Research Laboratory, U.S. Environmental Protection Agency, Research Triangle Park, NC 27711. Fax: (919) 541-4849. E-mail: gilbert.mary@epa.gov. local:kfi156 ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
| PMID | 15788721 |
| PQID | 17378305 |
| PQPubID | 23462 |
| PageCount | 10 |
| ParticipantIDs | proquest_miscellaneous_68007607 proquest_miscellaneous_17378305 pubmed_primary_15788721 crossref_citationtrail_10_1093_toxsci_kfi156 crossref_primary_10_1093_toxsci_kfi156 istex_primary_ark_67375_HXZ_54T7KH5W_2 |
| ProviderPackageCode | CITATION AAYXX |
| PublicationCentury | 2000 |
| PublicationDate | 2005-08 2005-08-01 2005-Aug 20050801 |
| PublicationDateYYYYMMDD | 2005-08-01 |
| PublicationDate_xml | – month: 08 year: 2005 text: 2005-08 |
| PublicationDecade | 2000 |
| PublicationPlace | United States |
| PublicationPlace_xml | – name: United States |
| PublicationTitle | Toxicological sciences |
| PublicationTitleAlternate | Toxicol. Sci |
| PublicationYear | 2005 |
| Publisher | Oxford University Press |
| Publisher_xml | – name: Oxford University Press |
| References | key 20171013203358_BIB41 key 20171013203358_BIB42 key 20171013203358_BIB43 key 20171013203358_BIB44 key 20171013203358_BIB45 key 20171013203358_BIB46 key 20171013203358_BIB47 key 20171013203358_BIB48 key 20171013203358_BIB49 key 20171013203358_BIB50 key 20171013203358_BIB51 key 20171013203358_BIB30 key 20171013203358_BIB31 key 20171013203358_BIB32 key 20171013203358_BIB33 key 20171013203358_BIB34 key 20171013203358_BIB35 key 20171013203358_BIB36 key 20171013203358_BIB37 key 20171013203358_BIB38 key 20171013203358_BIB39 key 20171013203358_BIB40 key 20171013203358_BIB7 key 20171013203358_BIB63 key 20171013203358_BIB8 key 20171013203358_BIB20 key 20171013203358_BIB64 key 20171013203358_BIB9 key 20171013203358_BIB21 key 20171013203358_BIB65 key 20171013203358_BIB22 key 20171013203358_BIB3 key 20171013203358_BIB23 key 20171013203358_BIB4 key 20171013203358_BIB24 key 20171013203358_BIB5 key 20171013203358_BIB25 key 20171013203358_BIB6 key 20171013203358_BIB26 key 20171013203358_BIB27 key 20171013203358_BIB28 key 20171013203358_BIB29 key 20171013203358_BIB1 key 20171013203358_BIB2 key 20171013203358_BIB52 key 20171013203358_BIB53 key 20171013203358_BIB10 key 20171013203358_BIB54 key 20171013203358_BIB11 key 20171013203358_BIB55 key 20171013203358_BIB12 key 20171013203358_BIB56 key 20171013203358_BIB13 key 20171013203358_BIB57 key 20171013203358_BIB14 key 20171013203358_BIB58 key 20171013203358_BIB15 key 20171013203358_BIB59 key 20171013203358_BIB16 key 20171013203358_BIB17 key 20171013203358_BIB18 key 20171013203358_BIB19 key 20171013203358_BIB60 key 20171013203358_BIB61 key 20171013203358_BIB62 16044537 - Toxicol Sci. 2005 Aug;86(2):211-3 |
| References_xml | – ident: key 20171013203358_BIB17 – ident: key 20171013203358_BIB6 doi: 10.1016/0306-4522(93)90335-D – ident: key 20171013203358_BIB8 doi: 10.1146/annurev.pa.35.040195.002135 – ident: key 20171013203358_BIB28 doi: 10.1073/pnas.94.19.10409 – ident: key 20171013203358_BIB59 doi: 10.1038/35066584 – ident: key 20171013203358_BIB19 doi: 10.1038/6365 – ident: key 20171013203358_BIB26 doi: 10.1016/S0091-3057(96)00350-4 – ident: key 20171013203358_BIB51 – ident: key 20171013203358_BIB3 doi: 10.1002/cne.901240303 – ident: key 20171013203358_BIB64 doi: 10.1016/S0014-4886(03)00272-3 – ident: key 20171013203358_BIB14 doi: 10.1016/S0006-8993(97)01517-5 – ident: key 20171013203358_BIB25 doi: 10.1037/0735-7044.111.3.532 – ident: key 20171013203358_BIB27 doi: 10.1002/ana.10262 – ident: key 20171013203358_BIB49 doi: 10.1523/JNEUROSCI.13-07-02930.1993 – ident: key 20171013203358_BIB9 doi: 10.1016/S0006-8993(99)02464-6 – ident: key 20171013203358_BIB45 doi: 10.1016/S0197-4580(02)00096-9 – ident: key 20171013203358_BIB34 doi: 10.1006/taap.1999.8743 – ident: key 20171013203358_BIB4 doi: 10.1542/peds.87.2.219 – ident: key 20171013203358_BIB13 doi: 10.1016/j.neuroscience.2003.09.029 – ident: key 20171013203358_BIB38 doi: 10.1046/j.1471-4159.2002.01085.x – ident: key 20171013203358_BIB21 doi: 10.1289/ehp.9086177 – ident: key 20171013203358_BIB65 doi: 10.1016/j.brainres.2003.10.068 – ident: key 20171013203358_BIB44 doi: 10.1016/0892-0362(88)90024-4 – ident: key 20171013203358_BIB53 doi: 10.1523/JNEUROSCI.22-07-02679.2002 – ident: key 20171013203358_BIB11 doi: 10.1073/pnas.120552597 – ident: key 20171013203358_BIB57 doi: 10.1006/nbdi.2002.0531 – ident: key 20171013203358_BIB60 doi: 10.1002/hipo.10103 – ident: key 20171013203358_BIB2 doi: 10.1016/0378-4274(93)90085-C – ident: key 20171013203358_BIB41 doi: 10.1523/JNEUROSCI.18-19-07768.1998 – ident: key 20171013203358_BIB56 doi: 10.1016/S0006-8993(00)03249-2 – ident: key 20171013203358_BIB10 – ident: key 20171013203358_BIB52 doi: 10.1007/978-1-4615-3330-6_7 – ident: key 20171013203358_BIB35 – ident: key 20171013203358_BIB55 doi: 10.1523/JNEUROSCI.20-16-06144.2000 – ident: key 20171013203358_BIB54 doi: 10.1016/S0006-8993(98)00739-2 – ident: key 20171013203358_BIB20 doi: 10.1523/JNEUROSCI.17-07-02492.1997 – ident: key 20171013203358_BIB40 – ident: key 20171013203358_BIB62 doi: 10.1038/4151030a – ident: key 20171013203358_BIB29 doi: 10.1523/JNEUROSCI.18-09-03206.1998 – ident: key 20171013203358_BIB23 doi: 10.1002/ana.10399 – ident: key 20171013203358_BIB39 doi: 10.1523/JNEUROSCI.0204-04.2004 – ident: key 20171013203358_BIB1 doi: 10.1016/0892-0362(95)02026-8 – ident: key 20171013203358_BIB24 doi: 10.1073/pnas.1230907100 – ident: key 20171013203358_BIB5 doi: 10.1002/cne.1040 – ident: key 20171013203358_BIB30 doi: 10.1016/S0304-3940(97)00633-2 – ident: key 20171013203358_BIB42 doi: 10.1016/S0378-4274(98)00388-9 – ident: key 20171013203358_BIB15 doi: 10.1016/0006-8993(96)00665-8 – ident: key 20171013203358_BIB32 doi: 10.1016/0006-8993(96)00666-X – ident: key 20171013203358_BIB22 doi: 10.1016/S0169-328X(00)00010-3 – ident: key 20171013203358_BIB48 doi: 10.1046/j.1471-4159.2002.01214.x – ident: key 20171013203358_BIB16 – ident: key 20171013203358_BIB43 doi: 10.1016/S0006-8993(00)02790-6 – ident: key 20171013203358_BIB58 doi: 10.1002/(SICI)1097-4695(19980615)35:4<395::AID-NEU7>3.0.CO;2-U – ident: key 20171013203358_BIB31 doi: 10.1523/JNEUROSCI.16-06-02027.1996 – ident: key 20171013203358_BIB46 doi: 10.1016/S0378-4274(01)00450-7 – ident: key 20171013203358_BIB63 doi: 10.1002/(SICI)1097-4695(20000205)42:2<248::AID-NEU8>3.0.CO;2-J – ident: key 20171013203358_BIB50 doi: 10.1523/JNEUROSCI.17-10-03727.1997 – ident: key 20171013203358_BIB7 doi: 10.1016/j.ntt.2004.01.010 – ident: key 20171013203358_BIB61 doi: 10.1016/j.neuroscience.2004.10.009 – ident: key 20171013203358_BIB18 doi: 10.1016/0006-8993(93)90217-B – ident: key 20171013203358_BIB36 doi: 10.1093/toxsci/66.1.139 – ident: key 20171013203358_BIB47 – ident: key 20171013203358_BIB33 – ident: key 20171013203358_BIB37 doi: 10.1016/S0892-0362(01)00116-7 – ident: key 20171013203358_BIB12 – reference: 16044537 - Toxicol Sci. 2005 Aug;86(2):211-3 |
| SSID | ssj0011609 |
| Score | 2.13012 |
| Snippet | The dentate granule cell (DG) layer of the hippocampal formation has the distinctive property of ongoing neurogenesis that continues throughout adult life.... |
| SourceID | proquest pubmed crossref istex |
| SourceType | Aggregation Database Index Database Enrichment Source Publisher |
| StartPage | 365 |
| SubjectTerms | adult neurogenesis Aging - physiology Animals Bromodeoxyuridine - administration & dosage Bromodeoxyuridine - analysis Cell Proliferation - drug effects Cell Survival - drug effects dentate gyrus Dentate Gyrus - drug effects Dentate Gyrus - embryology Dentate Gyrus - growth & development Dentate Gyrus - physiopathology Female Glial Fibrillary Acidic Protein - analysis hippocampus Hippocampus - drug effects Hippocampus - embryology Hippocampus - growth & development Hippocampus - physiopathology Immunohistochemistry in vivo lead Lead - administration & dosage Lead - blood Lead - toxicity learning and memory Long-Term Potentiation - drug effects Male Maze Learning - drug effects Morris water maze Neurons - classification Neurons - drug effects Neurons - physiology neurotoxicity Pregnancy Prenatal Exposure Delayed Effects rat Rats Rats, Long-Evans spatial learning Time Factors |
| Title | Chronic Developmental Lead Exposure Reduces Neurogenesis in Adult Rat Hippocampus but Does Not Impair Spatial Learning |
| URI | https://api.istex.fr/ark:/67375/HXZ-54T7KH5W-2/fulltext.pdf https://www.ncbi.nlm.nih.gov/pubmed/15788721 https://www.proquest.com/docview/17378305 https://www.proquest.com/docview/68007607 |
| Volume | 86 |
| hasFullText | 1 |
| inHoldings | 1 |
| isFullTextHit | |
| isPrint | |
| link | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwnV1ba9swFBahhTEYY8tu2VUPIy-OXd_lPJbR1XR0lM1lYS9Gsq1iusYhsUe6f7d_tqNLbGdrRrcX4whhFJ3P5-aj7yD0VpioIooC0-d-ZsKbGJpTn0PMk4c2c72cOzKVffoxjM_9k1kwGwx-9qqWmppZ2Y8bz5X8j1RhDOQqTsn-g2Tbh8IA3IN84QoShuutZKyZbfuVPyIvDWITFMaVSP7B_uWNqLqSLBwXQrOVsgT2UBBvGJ9obcTlYgEW7WrRrAzW1OBTi-lVLZiDabk0RNfiUj1XZlH6_mxSrcus1Z_anLZu-nEpGLRUQYhlHFmddtcNrrdGP9OrlYJn0h8-rqpcp2lPLCO2tvIUQVslV__t_GNP9UIwZYa26utkFd2YPdU5Ea2vNXV22QublfL1VNcJbcc91f3nDxOh6LPqag17AjeXvHSCG8i4fzOSbekiXV6KWjgSpPHsaxr4CfkQB19S8AL2XUJkpUActxGY44Syyqj9c5rmFRZxoJZwoBaw5Rbtizd8vTvmkb5P8gDd10ELPlQIfIgGxXyI7pzqsowhGp8pAvTrCU6683yrCR7js44a_XqI7qksMVaH3x6h7xrBeAvBWCAYbxCMNYJxH8G4nGOJYAwIxj0EY0AwFgjGgGCsEIw1gvEGwY_R-fuj5F1s6k4gZuaFdm1yjzFa-LCBlBJe5NxmztQPXQIOPHUK3yN06nJKGMmolwUUflGXBZT4jBMIsr0naG9ezYtnCHPX4xFY1igPwXnlEaM5dQI2ZVlBI5Y5IzTZCCLNNE2-6NbyLVXlGl6q5JYquY3QuJ2-UPwwOydKqbazdgFphN5sxJ6Cqhff7-i8qJpV6sDsCOzz7hlhJL-0kxF6qvDSrSkQZcOu8_y2y3iB7nZv8Uu0Vy-b4hX43zV7LRH-CzlL4QQ |
| linkProvider | ABC ChemistRy |
| openUrl | ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fsummon.serialssolutions.com&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.atitle=Chronic+Developmental+Lead+Exposure+Reduces+Neurogenesis+in+Adult+Rat+Hippocampus+but+Does+Not+Impair+Spatial+Learning&rft.jtitle=Toxicological+sciences&rft.au=Gilbert%2C+M.+E.&rft.au=Kelly%2C+M.+E.&rft.au=Samsam%2C+T.+E.&rft.au=Goodman%2C+J.+H.&rft.date=2005-08-01&rft.pub=Oxford+University+Press&rft.issn=1096-6080&rft.eissn=1096-0929&rft.volume=86&rft.issue=2&rft.spage=365&rft.epage=374&rft_id=info:doi/10.1093%2Ftoxsci%2Fkfi156&rft.externalDBID=n%2Fa&rft.externalDocID=ark_67375_HXZ_54T7KH5W_2 |
| thumbnail_l | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=1096-6080&client=summon |
| thumbnail_m | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=1096-6080&client=summon |
| thumbnail_s | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=1096-6080&client=summon |