17β-Estradiol Treatment Attenuates Neurogenesis Damage and Improves Behavior Performance After Ketamine Exposure in Neonatal Rats
Ketamine exposure disturbed normal neurogenesis in the developing brain and resulted in subsequent neurocognitive deficits. 17β-estradiol provides robust neuroprotection in a variety of brain injury models in animals of both sexes and attenuates neurodegeneration induced by anesthesia agents. In the...
Saved in:
| Published in | Frontiers in cellular neuroscience Vol. 13; p. 251 |
|---|---|
| Main Authors | , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Switzerland
Frontiers Research Foundation
13.06.2019
Frontiers Media S.A |
| Subjects | |
| Online Access | Get full text |
| ISSN | 1662-5102 1662-5102 |
| DOI | 10.3389/fncel.2019.00251 |
Cover
| Abstract | Ketamine exposure disturbed normal neurogenesis in the developing brain and resulted in subsequent neurocognitive deficits. 17β-estradiol provides robust neuroprotection in a variety of brain injury models in animals of both sexes and attenuates neurodegeneration induced by anesthesia agents. In the present study, we aimed to investigate whether 17β-estradiol could attenuate neonatal ketamine exposure-disturbed neurogenesis and behavioral performance. We treated 7-day-old (Postnatal day 7, PND 7) Sprague-Dawley rats and neural stem cells (NSCs) with either normal saline, ketamine, or 17β-estradiol before/after ketamine exposure, respectively. At PND 14, the rats were decapitated to detect neurogenesis in the subventricular zone (SVZ) and subgranular zone (SGZ) of the hippocampus by immunofluorescence staining. The proliferation, neuronal differentiation, and apoptosis of NSCs were assessed by immunohistochemistry method and TUNEL assay, respectively. The protein levels of cleaved caspase-3
in addition to GSK-3β and p-GSK-3β
were examined by western blotting. Spatial learning and memory abilities were assessed by Morris water maze (MWM) test at PND 42-47. Ketamine exposure decreased cell proliferation in the SVZ and SGZ, inhibited NSC proliferation and neuronal differentiation, promoted NSC apoptosis and led to adult cognitive deficits. Furthermore, ketamine increased cleaved caspase-3
and decreased the expression of p-GSK-3β
. Treatment with 17β-estradiol could attenuate ketamine-induced changes both
and
. For the first time we showed that 17β-estradiol alleviated ketamine-induced neurogenesis inhibition and cognitive dysfunction in the developing rat brain. Moreover, the protection of 17β-estradiol was associated with GSK-3β. |
|---|---|
| AbstractList | Ketamine exposure disturbed normal neurogenesis in the developing brain and resulted in subsequent neurocognitive deficits. 17β-estradiol provides robust neuroprotection in a variety of brain injury models in animals of both sexes and attenuates neurodegeneration induced by anesthesia agents. In the present study, we aimed to investigate whether 17β-estradiol could attenuate neonatal ketamine exposure-disturbed neurogenesis and behavioral performance. We treated 7-day-old (Postnatal day 7, PND 7) Sprague-Dawley rats and neural stem cells (NSCs) with either normal saline, ketamine, or 17β-estradiol before/after ketamine exposure, respectively. At PND 14, the rats were decapitated to detect neurogenesis in the subventricular zone (SVZ) and subgranular zone (SGZ) of the hippocampus by immunofluorescence staining. The proliferation, neuronal differentiation, and apoptosis of NSCs were assessed by immunohistochemistry method and TUNEL assay, respectively. The protein levels of cleaved caspase-3
in addition to GSK-3β and p-GSK-3β
were examined by western blotting. Spatial learning and memory abilities were assessed by Morris water maze (MWM) test at PND 42-47. Ketamine exposure decreased cell proliferation in the SVZ and SGZ, inhibited NSC proliferation and neuronal differentiation, promoted NSC apoptosis and led to adult cognitive deficits. Furthermore, ketamine increased cleaved caspase-3
and decreased the expression of p-GSK-3β
. Treatment with 17β-estradiol could attenuate ketamine-induced changes both
and
. For the first time we showed that 17β-estradiol alleviated ketamine-induced neurogenesis inhibition and cognitive dysfunction in the developing rat brain. Moreover, the protection of 17β-estradiol was associated with GSK-3β. Ketamine exposure disturbed normal neurogenesis in the developing brain and resulted in subsequent neurocognitive deficits. 17β-estradiol provides robust neuroprotection in a variety of brain injury models in animals of both sexes and attenuates neurodegeneration induced by anesthesia agents. In the present study, we aimed to investigate whether 17β-estradiol could attenuate neonatal ketamine exposure-disturbed neurogenesis and behavioral performance. We treated 7-day-old (Postnatal day 7, PND 7) Sprague-Dawley rats and neural stem cells (NSCs) with either normal saline, ketamine, or 17β-estradiol before/after ketamine exposure, respectively. At PND 14, the rats were decapitated to detect neurogenesis in the subventricular zone (SVZ) and subgranular zone (SGZ) of the hippocampus by immunofluorescence staining. The proliferation, neuronal differentiation, and apoptosis of NSCs were assessed by immunohistochemistry method and TUNEL assay, respectively. The protein levels of cleaved caspase-3 in vivo in addition to GSK-3β and p-GSK-3β in vitro were examined by western blotting. Spatial learning and memory abilities were assessed by Morris water maze (MWM) test at PND 42–47. Ketamine exposure decreased cell proliferation in the SVZ and SGZ, inhibited NSC proliferation and neuronal differentiation, promoted NSC apoptosis and led to adult cognitive deficits. Furthermore, ketamine increased cleaved caspase-3 in vivo and decreased the expression of p-GSK-3β in vitro . Treatment with 17β-estradiol could attenuate ketamine-induced changes both in vivo and in vitro . For the first time we showed that 17β-estradiol alleviated ketamine-induced neurogenesis inhibition and cognitive dysfunction in the developing rat brain. Moreover, the protection of 17β-estradiol was associated with GSK-3β. Ketamine exposure disturbed normal neurogenesis in the developing brain and resulted in subsequent neurocognitive deficits. 17β-estradiol provides robust neuroprotection in a variety of brain injury models in animals of both sexes and attenuates neurodegeneration induced by anesthesia agents. In the present study, we aimed to investigate whether 17β-estradiol could attenuate neonatal ketamine exposure-disturbed neurogenesis and behavioral performance. We treated 7-day-old (Postnatal day 7, PND 7) Sprague-Dawley rats and neural stem cells (NSCs) with either normal saline, ketamine, or 17β-estradiol before/after ketamine exposure, respectively. At PND 14, the rats were decapitated to detect neurogenesis in the subventricular zone (SVZ) and subgranular zone (SGZ) of the hippocampus by immunofluorescence staining. The proliferation, neuronal differentiation, and apoptosis of NSCs were assessed by immunohistochemistry method and TUNEL assay, respectively. The protein levels of cleaved caspase-3 in vivo in addition to GSK-3β and p-GSK-3β in vitro were examined by western blotting. Spatial learning and memory abilities were assessed by Morris water maze (MWM) test at PND 42–47. Ketamine exposure decreased cell proliferation in the SVZ and SGZ, inhibited NSC proliferation and neuronal differentiation, promoted NSC apoptosis and led to adult cognitive deficits. Furthermore, ketamine increased cleaved caspase-3 in vivo and decreased the expression of p-GSK-3β in vitro. Treatment with 17β-estradiol could attenuate ketamine-induced changes both in vivo and in vitro. For the first time we showed that 17β-estradiol alleviated ketamine-induced neurogenesis inhibition and cognitive dysfunction in the developing rat brain. Moreover, the protection of 17β-estradiol was associated with GSK-3β. Ketamine exposure disturbed normal neurogenesis in the developing brain and resulted in subsequent neurocognitive deficits. 17β-estradiol provides robust neuroprotection in a variety of brain injury models in animals of both sexes and attenuates neurodegeneration induced by anesthesia agents. In the present study, we aimed to investigate whether 17β-estradiol could attenuate neonatal ketamine exposure-disturbed neurogenesis and behavioral performance. We treated 7-day-old (Postnatal day 7, PND 7) Sprague-Dawley rats and neural stem cells (NSCs) with either normal saline, ketamine, or 17β-estradiol before/after ketamine exposure, respectively. At PND 14, the rats were decapitated to detect neurogenesis in the subventricular zone (SVZ) and subgranular zone (SGZ) of the hippocampus by immunofluorescence staining. The proliferation, neuronal differentiation, and apoptosis of NSCs were assessed by immunohistochemistry method and TUNEL assay, respectively. The protein levels of cleaved caspase-3 in vivo in addition to GSK-3β and p-GSK-3β in vitro were examined by western blotting. Spatial learning and memory abilities were assessed by Morris water maze (MWM) test at PND 42-47. Ketamine exposure decreased cell proliferation in the SVZ and SGZ, inhibited NSC proliferation and neuronal differentiation, promoted NSC apoptosis and led to adult cognitive deficits. Furthermore, ketamine increased cleaved caspase-3 in vivo and decreased the expression of p-GSK-3β in vitro. Treatment with 17β-estradiol could attenuate ketamine-induced changes both in vivo and in vitro. For the first time we showed that 17β-estradiol alleviated ketamine-induced neurogenesis inhibition and cognitive dysfunction in the developing rat brain. Moreover, the protection of 17β-estradiol was associated with GSK-3β.Ketamine exposure disturbed normal neurogenesis in the developing brain and resulted in subsequent neurocognitive deficits. 17β-estradiol provides robust neuroprotection in a variety of brain injury models in animals of both sexes and attenuates neurodegeneration induced by anesthesia agents. In the present study, we aimed to investigate whether 17β-estradiol could attenuate neonatal ketamine exposure-disturbed neurogenesis and behavioral performance. We treated 7-day-old (Postnatal day 7, PND 7) Sprague-Dawley rats and neural stem cells (NSCs) with either normal saline, ketamine, or 17β-estradiol before/after ketamine exposure, respectively. At PND 14, the rats were decapitated to detect neurogenesis in the subventricular zone (SVZ) and subgranular zone (SGZ) of the hippocampus by immunofluorescence staining. The proliferation, neuronal differentiation, and apoptosis of NSCs were assessed by immunohistochemistry method and TUNEL assay, respectively. The protein levels of cleaved caspase-3 in vivo in addition to GSK-3β and p-GSK-3β in vitro were examined by western blotting. Spatial learning and memory abilities were assessed by Morris water maze (MWM) test at PND 42-47. Ketamine exposure decreased cell proliferation in the SVZ and SGZ, inhibited NSC proliferation and neuronal differentiation, promoted NSC apoptosis and led to adult cognitive deficits. Furthermore, ketamine increased cleaved caspase-3 in vivo and decreased the expression of p-GSK-3β in vitro. Treatment with 17β-estradiol could attenuate ketamine-induced changes both in vivo and in vitro. For the first time we showed that 17β-estradiol alleviated ketamine-induced neurogenesis inhibition and cognitive dysfunction in the developing rat brain. Moreover, the protection of 17β-estradiol was associated with GSK-3β. Ketamine exposure in the developing brain disturbed normal neurogenesis and resulted in subsequent neurocognitive deficits. 17β-estradiol provides robust neuroprotection in a variety of brain injury models in animals of both sexes and attenuates neurodegeneration induced by anesthesia agents. In the present study, we investigated whether 17β-estradiol could attenuate disturbed neurogenesis and behavioural deficits induced by ketamine exposure in neonatal rats. Sprague-Dawley rats at postnatal day (PND) 7 and neural stem cells (NSCs) were treated with either normal saline, ketamine, or 17β-estradiol prior/after ketamine exposure, respectively. The rats were decapitated at PND14 for detection of neurogenesis in the subventricular zone (SVZ) and subgranular zone (SGZ) of the hippocampus by immunostaining. NSC proliferation, neuronal differentiation, and apoptosis were assessed by immunohistochemistry and TUNEL, respectively. The protein expressions of caspase-3 in vivo and GSK-3β, p-GSK-3β in vitro were assessed by western blotting. Spatial learning and memory abilities were measured by the Morris water maze test at PND 42-47. Ketamine exposure decreased cell proliferation in the SVZ and SGZ, inhibited NSC proliferation and neuronal differentiation, promoted NSC apoptosis and led to late cognitive deficits. Furthermore, ketamine increased caspase-3 expression in vivo and decreased protein expressions of p-GSK-3β in vitro. Treatment with 17β-estradiol attenuated ketamine-elicited changes both in vivo and in vitro. We for the first time showed that 17β-estradiol alleviated ketamine-induced neurogenesis damage and neurocognitive deficits in developing rat brain. Moreover, the protection of17β-estradiol is associated with the GSK-3β. |
| Author | Lei, Shan Zheng, Juan Zhang, Pengbo Lu, Haixia Wei, Haidong Lu, Yang Liu, Yong Li, Weisong Li, Huixian Chen, Xinlin |
| AuthorAffiliation | 2 Institute of Neurobiology, National Key Academic Subject, Physiology of Xi’an Jiaotong University , Xi’an , China 1 Department of Anesthesiology, The Second Affiliated Hospital of Xi’an Jiaotong University , Xi’an , China |
| AuthorAffiliation_xml | – name: 1 Department of Anesthesiology, The Second Affiliated Hospital of Xi’an Jiaotong University , Xi’an , China – name: 2 Institute of Neurobiology, National Key Academic Subject, Physiology of Xi’an Jiaotong University , Xi’an , China |
| Author_xml | – sequence: 1 givenname: Weisong surname: Li fullname: Li, Weisong – sequence: 2 givenname: Huixian surname: Li fullname: Li, Huixian – sequence: 3 givenname: Haidong surname: Wei fullname: Wei, Haidong – sequence: 4 givenname: Yang surname: Lu fullname: Lu, Yang – sequence: 5 givenname: Shan surname: Lei fullname: Lei, Shan – sequence: 6 givenname: Juan surname: Zheng fullname: Zheng, Juan – sequence: 7 givenname: Haixia surname: Lu fullname: Lu, Haixia – sequence: 8 givenname: Xinlin surname: Chen fullname: Chen, Xinlin – sequence: 9 givenname: Yong surname: Liu fullname: Liu, Yong – sequence: 10 givenname: Pengbo surname: Zhang fullname: Zhang, Pengbo |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/31263401$$D View this record in MEDLINE/PubMed |
| BookMark | eNp1ks1u1DAUhSNURH9gzwpZYsNmBttxnGSDNJQBRlSAUFlbN_HN1KPEntrOCLY8Eg_CM-HMtKitxMqWfe6no3PPaXZkncUse87oPM-r-nVnW-znnLJ6Tikv2KPshEnJZwWj_OjO_Tg7DWFDqeRSVE-y45xxmQvKTrJfrPzze7YM0YM2rieXHiEOaCNZxIh2hIiBfMbRuzVaDCaQdzDAGglYTVbD1rtdErzFK9gZ58lX9J3zAyRfZNFF9OQTRhiMRbL8sXVh9EiMTUBnIUJPvkEMT7PHHfQBn92cZ9n398vL84-ziy8fVueLi1kraMFmotQ5sKJtmqLsKo2sLCRvhABdtw2ghkYXdaU5SIEoUhyM58gEo2VTUWhlfpatDlztYKO23gzgfyoHRu0fnF8r8NG0PSpaNXJKq6nqSgiuQcoGKNRYFgXKLk-sNwfWdmwG1G0KzEN_D3r_x5ortXY7JYuqYHICvLoBeHc9YohqMCEtsweLbgyKp20yLsqaJ-nLB9KNG71NUSVVledJIuqkenHX0T8rt6tOAnkQtN6F4LFTrYkQjZsMml4xqqZOqX2n1NQpte9UGqQPBm_Z_x35Cwo60ZE |
| CitedBy_id | crossref_primary_10_1016_j_lfs_2019_116931 crossref_primary_10_1002_ibra_12071 crossref_primary_10_1111_cns_14604 crossref_primary_10_1016_j_ynstr_2019_100208 crossref_primary_10_3390_ijms23031128 crossref_primary_10_1097_FBP_0000000000000689 crossref_primary_10_1111_jcmm_17816 crossref_primary_10_1007_s12640_022_00511_9 crossref_primary_10_1186_s12974_021_02295_9 crossref_primary_10_3390_cells12091285 crossref_primary_10_1007_s12264_024_01265_4 crossref_primary_10_1111_bcp_15467 crossref_primary_10_3389_fnins_2019_01205 crossref_primary_10_1186_s12868_019_0534_4 crossref_primary_10_1016_j_biopha_2022_113229 crossref_primary_10_1007_s11010_021_04339_3 crossref_primary_10_3390_molecules27154753 crossref_primary_10_1007_s10571_019_00733_0 crossref_primary_10_1016_j_toxlet_2025_02_012 crossref_primary_10_1038_s41598_020_62192_8 crossref_primary_10_3389_fgene_2021_677935 crossref_primary_10_1016_j_ibneur_2024_01_005 crossref_primary_10_1016_j_mce_2021_111394 crossref_primary_10_1021_acsabm_0c00934 |
| Cites_doi | 10.1016/j.brainres.2012.07.059 10.1016/j.neuroscience.2017.03.057 10.1159/000369698 10.1006/mcne.2002.1194 10.1097/ALN.0b013e3182834d77 10.1016/j.yexcr.2014.08.030 10.1213/ANE.0b013e3182860fc9 10.1038/nrn2870 10.1111/aas.12689 10.1016/s1043-2760(03)00076-6 10.1097/ALN.0000000000001735 10.1111/j.1399-6576.2009.02024.x 10.1002/dneu.22119 10.1016/j.neuroscience.2012.11.042 10.1093/toxsci/kfh224 10.1016/j.ntt.2011.01.001 10.1016/j.ydbio.2018.02.004 10.1002/jnr.20362 10.1523/jneurosci.12-11-04565.1992 10.1016/j.neuroscience.2007.06.040 10.1016/s0301-0082(00)00025-3 10.1016/j.brainres.2014.09.013 10.1093/bja/aet057 10.1097/01.anes.0000278892.62305.9c 10.1016/j.neulet.2007.01.074 10.1016/j.bbadis.2016.08.018 10.1159/000490823 10.1016/s0006-8993(99)02231-3 10.1016/j.nbd.2014.02.009 10.1007/s12640-016-9615-9617 10.1016/j.neuroscience.2005.05.008 10.1016/j.ejphar.2011.12.021 10.1111/j.1399-6576.2012.02722.x 10.1016/j.physbeh.2012.08.007 10.1016/j.bbagen.2012.12.012 10.1016/j.ntt.2016.10.001 10.1073/pnas.242735799 |
| ContentType | Journal Article |
| Copyright | 2019. This work is licensed under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. Copyright © 2019 Li, Li, Wei, Lu, Lei, Zheng, Lu, Chen, Liu and Zhang. 2019 Li, Li, Wei, Lu, Lei, Zheng, Lu, Chen, Liu and Zhang |
| Copyright_xml | – notice: 2019. This work is licensed under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. – notice: Copyright © 2019 Li, Li, Wei, Lu, Lei, Zheng, Lu, Chen, Liu and Zhang. 2019 Li, Li, Wei, Lu, Lei, Zheng, Lu, Chen, Liu and Zhang |
| DBID | AAYXX CITATION NPM 3V. 7XB 88I 8FE 8FH 8FK ABUWG AFKRA AZQEC BBNVY BENPR BHPHI CCPQU DWQXO GNUQQ HCIFZ LK8 M2P M7P PHGZM PHGZT PIMPY PKEHL PQEST PQGLB PQQKQ PQUKI PRINS Q9U 7X8 5PM DOA |
| DOI | 10.3389/fncel.2019.00251 |
| DatabaseName | CrossRef PubMed ProQuest Central (Corporate) ProQuest Central (purchase pre-March 2016) Science Database (Alumni Edition) ProQuest SciTech Collection ProQuest Natural Science Collection ProQuest Central (Alumni) (purchase pre-March 2016) ProQuest Central (Alumni) ProQuest Central UK/Ireland ProQuest Central Essentials Biological Science Collection ProQuest Central Natural Science Collection ProQuest One ProQuest Central Korea ProQuest Central Student SciTech Premium Collection Biological Sciences Science Database Biological Science Database ProQuest Central Premium ProQuest One Academic (New) ProQuest Publicly Available Content Database ProQuest One Academic Middle East (New) ProQuest One Academic Eastern Edition (DO NOT USE) ProQuest One Applied & Life Sciences ProQuest One Academic ProQuest One Academic UKI Edition ProQuest Central China ProQuest Central Basic MEDLINE - Academic PubMed Central (Full Participant titles) DOAJ Directory of Open Access Journals |
| DatabaseTitle | CrossRef PubMed Publicly Available Content Database ProQuest Central Student ProQuest One Academic Middle East (New) ProQuest Central Essentials ProQuest Central (Alumni Edition) SciTech Premium Collection ProQuest One Community College ProQuest Natural Science Collection ProQuest Central China ProQuest Central ProQuest One Applied & Life Sciences Natural Science Collection ProQuest Central Korea Biological Science Collection ProQuest Central (New) ProQuest Science Journals (Alumni Edition) ProQuest Biological Science Collection ProQuest Central Basic ProQuest Science Journals ProQuest One Academic Eastern Edition Biological Science Database ProQuest SciTech Collection ProQuest One Academic UKI Edition ProQuest One Academic ProQuest One Academic (New) ProQuest Central (Alumni) MEDLINE - Academic |
| DatabaseTitleList | PubMed MEDLINE - Academic Publicly Available Content Database |
| Database_xml | – sequence: 1 dbid: DOA name: DOAJ Directory of Open Access Journals url: https://www.doaj.org/ sourceTypes: Open Website – sequence: 2 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: 3 dbid: BENPR name: ProQuest Central url: https://www.proquest.com/central sourceTypes: Aggregation Database |
| DeliveryMethod | fulltext_linktorsrc |
| Discipline | Medicine |
| EISSN | 1662-5102 |
| ExternalDocumentID | oai_doaj_org_article_08b60062b898442da66ba0a9e755e6f3 PMC6585163 31263401 10_3389_fncel_2019_00251 |
| Genre | Journal Article |
| GeographicLocations | China |
| GeographicLocations_xml | – name: China |
| GrantInformation_xml | – fundername: National Natural Science Foundation of China |
| GroupedDBID | --- 29H 2WC 53G 5GY 5VS 88I 8FE 8FH 9T4 AAFWJ AAYXX ABUWG ACGFO ACGFS ACXDI ADBBV ADRAZ AEGXH AENEX AFKRA AFPKN AIAGR ALMA_UNASSIGNED_HOLDINGS AOIJS AZQEC BAWUL BBNVY BCNDV BENPR BHPHI BPHCQ CCPQU CITATION CS3 DIK DWQXO E3Z EMOBN F5P GNUQQ GROUPED_DOAJ GX1 HCIFZ HYE KQ8 LK8 M2P M48 M7P M~E O5R O5S OK1 OVT PGMZT PHGZM PHGZT PIMPY PQQKQ PROAC RNS RPM TR2 C1A IAO IEA IHR IHW IPNFZ ISR NPM RIG 3V. 7XB 8FK PKEHL PQEST PQGLB PQUKI PRINS Q9U 7X8 PUEGO 5PM |
| ID | FETCH-LOGICAL-c4051-47d3a15cbb57f8de17562b44ad9cbaedabd598d2a64ee4002123e14107b80ac63 |
| IEDL.DBID | M48 |
| ISSN | 1662-5102 |
| IngestDate | Wed Aug 27 01:26:40 EDT 2025 Thu Aug 21 14:24:30 EDT 2025 Thu Sep 04 23:56:08 EDT 2025 Fri Jul 25 11:34:33 EDT 2025 Thu Jan 02 23:00:17 EST 2025 Tue Jul 01 03:30:15 EDT 2025 Thu Apr 24 23:02:54 EDT 2025 |
| IsDoiOpenAccess | true |
| IsOpenAccess | true |
| IsPeerReviewed | true |
| IsScholarly | true |
| Keywords | p-GSK-3β 17β-estradiol neurotoxicity ketamine neural stem cells |
| Language | English |
| License | This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
| LinkModel | DirectLink |
| MergedId | FETCHMERGED-LOGICAL-c4051-47d3a15cbb57f8de17562b44ad9cbaedabd598d2a64ee4002123e14107b80ac63 |
| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 Edited by: Hung-Ming Chang, Taipei Medical University, Taiwan This article was submitted to Cellular Neurophysiology, a section of the journal Frontiers in Cellular Neuroscience Reviewed by: Yuriko Iwakura, Niigata University, Japan; Hari Prasad Osuru, University of Virginia, United States |
| OpenAccessLink | http://journals.scholarsportal.info/openUrl.xqy?doi=10.3389/fncel.2019.00251 |
| PMID | 31263401 |
| PQID | 2283392349 |
| PQPubID | 4424410 |
| ParticipantIDs | doaj_primary_oai_doaj_org_article_08b60062b898442da66ba0a9e755e6f3 pubmedcentral_primary_oai_pubmedcentral_nih_gov_6585163 proquest_miscellaneous_2251124792 proquest_journals_2283392349 pubmed_primary_31263401 crossref_citationtrail_10_3389_fncel_2019_00251 crossref_primary_10_3389_fncel_2019_00251 |
| ProviderPackageCode | CITATION AAYXX |
| PublicationCentury | 2000 |
| PublicationDate | 20190613 |
| PublicationDateYYYYMMDD | 2019-06-13 |
| PublicationDate_xml | – month: 6 year: 2019 text: 20190613 day: 13 |
| PublicationDecade | 2010 |
| PublicationPlace | Switzerland |
| PublicationPlace_xml | – name: Switzerland – name: Lausanne |
| PublicationTitle | Frontiers in cellular neuroscience |
| PublicationTitleAlternate | Front Cell Neurosci |
| PublicationYear | 2019 |
| Publisher | Frontiers Research Foundation Frontiers Media S.A |
| Publisher_xml | – name: Frontiers Research Foundation – name: Frontiers Media S.A |
| References | Wang (B34) 2003; 100 Fredriksson (B6) 2007; 107 Zheng (B38) 2012; 231 Dong (B3) 2016; 60 Lu (B21) 2018; 47 Reynolds (B28) 1992; 12 Liu (B19) 2013; 110 Liu (B20) 2007; 415 Paule (B26) 2011; 33 Ponten (B27) 2012; 56 Zhao (B37) 2014; 68 Eriksson (B4) 1997; 18 Huang (B11) 2015; 35 Hara (B8) 2018; 436 Muramatsu (B25) 2007; 148 Scallet (B30) 2004; 81 Huang (B12) 2012; 1476 McCullough (B23) 2003; 14 Brännvall (B2) 2002; 21 Shi (B32) 2013; 1830 Kandimalla (B15) 2016; 1863 Kishi (B17) 2005; 79 Li (B18) 2014; 1593 Sabbagh (B29) 2012; 107 Isgor (B14) 2005; 134 Sokolowski (B33) 2013; 73 Eriksson (B5) 2000; 853 Garcia-Segura (B7) 2001; 63 Bai (B1) 2013; 116 Hur (B13) 2010; 11 Hu (B9) 2017; 127 Moosavi (B24) 2012; 677 Lu (B22) 2017; 352 Wu (B35) 2014; 328 Huang (B10) 2016; 30 Shen (B31) 2013; 118 Kang (B16) 2017; 60 Zhang (B36) 2009; 53 |
| References_xml | – volume: 1476 start-page: 164 year: 2012 ident: B12 article-title: Ketamine potentiates hippocampal neurodegeneration and persistent learning and memory impairment through the PKC gamma-ERK signaling pathway in the developing brain. publication-title: Brain Res. doi: 10.1016/j.brainres.2012.07.059 – volume: 352 start-page: 144 year: 2017 ident: B22 article-title: Pretreatment with minocycline restores neurogenesis in the subventricular zone and subgranular zone of the hippocampus after ketamine exposure in neonatal rats. publication-title: Neuroscience doi: 10.1016/j.neuroscience.2017.03.057 – volume: 35 start-page: 315 year: 2015 ident: B11 article-title: Ketamine interferes with the proliferation and differentiation of neural stem cells in the subventricular zone of neonatal rats. publication-title: Cell Physiol. Biochem. doi: 10.1159/000369698 – volume: 21 start-page: 512 year: 2002 ident: B2 article-title: Estrogen-receptor-dependent regulation of neural stem cell proliferation and differentiation. publication-title: Mol. Cell Neurosci. doi: 10.1006/mcne.2002.1194 – volume: 118 start-page: 502 year: 2013 ident: B31 article-title: Selective anesthesia-induced neuroinflammation in developing mouse brain and cognitive impairment. publication-title: Anesthesiology doi: 10.1097/ALN.0b013e3182834d77 – volume: 328 start-page: 351 year: 2014 ident: B35 article-title: Estrogen increases Nrf2 activity through activation of the PI3K pathway in MCF-7 breast cancer cells. publication-title: Exp. Cell Res. doi: 10.1016/j.yexcr.2014.08.030 – volume: 116 start-page: 869 year: 2013 ident: B1 article-title: Ketamine enhances human neural stem cell proliferation and induces neuronal apoptosis via reactive oxygen species-mediated mitochondrial pathway. publication-title: Anesth. Analg. doi: 10.1213/ANE.0b013e3182860fc9 – volume: 11 start-page: 539 year: 2010 ident: B13 article-title: GSK3 signalling in neural development. publication-title: Nat. Rev. Neurosci. doi: 10.1038/nrn2870 – volume: 60 start-page: 579 year: 2016 ident: B3 article-title: Ketamine exposure during embryogenesis inhibits cellular proliferation in rat fetal cortical neurogenic regions. publication-title: Acta Anaesthesiol. Scand. doi: 10.1111/aas.12689 – volume: 14 start-page: 228 year: 2003 ident: B23 article-title: Estrogen and ischemic neuroprotection: an integrated view. publication-title: Trends Endocrinol. Metab. doi: 10.1016/s1043-2760(03)00076-6 – volume: 127 start-page: 227 year: 2017 ident: B9 article-title: Association between exposure of young children to procedures requiring general anesthesia and learning and behavioral outcomes in a population-based birth cohort. publication-title: Anesthesiology doi: 10.1097/ALN.0000000000001735 – volume: 53 start-page: 1184 year: 2009 ident: B36 article-title: Human neural stem cell transplantation attenuates apoptosis and improves neurological functions after cerebral ischemia in rats. publication-title: Acta Anaesthesiol. Scand. doi: 10.1111/j.1399-6576.2009.02024.x – volume: 73 start-page: 936 year: 2013 ident: B33 article-title: Neural stem cell apoptosis after low-methylmercury exposures in postnatal hippocampus produce persistent cell loss and adolescent memory deficits. publication-title: Dev. Neurobiol. doi: 10.1002/dneu.22119 – volume: 231 start-page: 82 year: 2012 ident: B38 article-title: Post-stroke estradiol treatment enhances neurogenesis in the subventricular zone of rats after permanent focal cerebral ischemia. publication-title: Neuroscience doi: 10.1016/j.neuroscience.2012.11.042 – volume: 81 start-page: 364 year: 2004 ident: B30 article-title: Developmental neurotoxicity of ketamine: morphometric confirmation, exposure parameters, and multiple fluorescent labeling of apoptotic neurons. publication-title: Toxicol. Sci. doi: 10.1093/toxsci/kfh224 – volume: 18 start-page: 719 year: 1997 ident: B4 article-title: Developmental neurotoxicity of environmental agents in the neonate. publication-title: Neurotoxicology – volume: 33 start-page: 220 year: 2011 ident: B26 article-title: Ketamine anesthesia during the first week of life can cause long-lasting cognitive deficits in rhesus monkeys. publication-title: Neurotoxicol. Teratol. doi: 10.1016/j.ntt.2011.01.001 – volume: 436 start-page: 28 year: 2018 ident: B8 article-title: Cell death in neural precursor cells and neurons before neurite formation prevents the emergence of abnormal neural structures in the Drosophila optic lobe. publication-title: Dev. Biol. doi: 10.1016/j.ydbio.2018.02.004 – volume: 79 start-page: 279 year: 2005 ident: B17 article-title: Estrogen promotes differentiation and survival of dopaminergic neurons derived from human neural stem cells. publication-title: J. Neurosci. Res. doi: 10.1002/jnr.20362 – volume: 12 start-page: 4565 year: 1992 ident: B28 article-title: A multipotent EGF-responsive striatal embryonic progenitor cell produces neurons and astrocytes. publication-title: J. Neurosci. doi: 10.1523/jneurosci.12-11-04565.1992 – volume: 148 start-page: 593 year: 2007 ident: B25 article-title: Neonatally born granule cells numerically dominate adult mice dentate gyrus. publication-title: Neuroscience doi: 10.1016/j.neuroscience.2007.06.040 – volume: 63 start-page: 29 year: 2001 ident: B7 article-title: Neuroprotection by estradiol. publication-title: Prog. Neurobiol. doi: 10.1016/s0301-0082(00)00025-3 – volume: 1593 start-page: 30 year: 2014 ident: B18 article-title: 17beta-estradiol attenuates ketamine-induced neuroapoptosis and persistent cognitive deficits in the developing brain. publication-title: Brain Res. doi: 10.1016/j.brainres.2014.09.013 – volume: 110 start-page: i3 year: 2013 ident: B19 article-title: Role of glycogen synthase kinase-3beta in ketamine-induced developmental neuroapoptosis in rats. publication-title: Br. J. Anaesth. doi: 10.1093/bja/aet057 – volume: 107 start-page: 427 year: 2007 ident: B6 article-title: Neonatal exposure to a combination of N-methyl-D-aspartate and gamma-aminobutyric acid type a receptor anesthetic agents potentiates apoptotic neurodegeneration and persistent behavioral deficits. publication-title: Anesthesiology doi: 10.1097/01.anes.0000278892.62305.9c – volume: 415 start-page: 237 year: 2007 ident: B20 article-title: Dose dependence and therapeutic window for the neuroprotective effects of 17beta-estradiolwhen administered after cerebral ischemia. publication-title: Neurosci. Lett. doi: 10.1016/j.neulet.2007.01.074 – volume: 1863 start-page: 1078 year: 2016 ident: B15 article-title: Is Alzheimer’s disease a type 3 diabetes? a critical appraisal. publication-title: Biochim. Biophys. Acta doi: 10.1016/j.bbadis.2016.08.018 – volume: 47 start-page: 1377 year: 2018 ident: B21 article-title: Dexmedetomidine protects neural stem cells from ketamine-induced injury. publication-title: Cell Physiol. Biochem. doi: 10.1159/000490823 – volume: 853 start-page: 41 year: 2000 ident: B5 article-title: Exposure to nicotine during a defined period in neonatal life induces permanent changes in brain nicotinic receptors and in behaviour of adult mice. publication-title: Brain Res. doi: 10.1016/s0006-8993(99)02231-3 – volume: 68 start-page: 145 year: 2014 ident: B37 article-title: Ketamine administered to pregnant rats in the second trimester causes long-lasting behavioral disorders in offspring. publication-title: Neurobiol. Dis. doi: 10.1016/j.nbd.2014.02.009 – volume: 30 start-page: 185 year: 2016 ident: B10 article-title: Ketamine affects the neurogenesis of the hippocampal dentate gyrus in 7-day-old Rats. publication-title: Neurotox. Res. doi: 10.1007/s12640-016-9615-9617 – volume: 134 start-page: 847 year: 2005 ident: B14 article-title: Estrogen receptor alpha and beta mRNA expressions by proliferating and differentiating cells in the adult rat dentate gyrus and subventricular zone. publication-title: Neuroscience doi: 10.1016/j.neuroscience.2005.05.008 – volume: 677 start-page: 107 year: 2012 ident: B24 article-title: The effect of sub-anesthetic and anesthetic ketamine on water maze memory acquisition, consolidation and retrieval. publication-title: Eur. J. Pharmacol. doi: 10.1016/j.ejphar.2011.12.021 – volume: 56 start-page: 1058 year: 2012 ident: B27 article-title: Clonidine abolishes the adverse effects on apoptosis and behaviour after neonatal ketamine exposure in mice. publication-title: Acta Anaesth. Scand. doi: 10.1111/j.1399-6576.2012.02722.x – volume: 107 start-page: 355 year: 2012 ident: B29 article-title: Examination of ketamine-induced deficits in sensorimotor gating and spatial learning. publication-title: Physiol. Behav. doi: 10.1016/j.physbeh.2012.08.007 – volume: 1830 start-page: 2538 year: 2013 ident: B32 article-title: Incorporation of beta-sitosterol into the membrane increases resistance to oxidative stress and lipid peroxidation via estrogen receptor-mediated PI3K/GSK3beta signaling. publication-title: Biochim. Biophys. Acta doi: 10.1016/j.bbagen.2012.12.012 – volume: 60 start-page: 33 year: 2017 ident: B16 article-title: Neurogenesis and developmental anesthetic neurotoxicity. publication-title: Neurotoxicol. Teratol. doi: 10.1016/j.ntt.2016.10.001 – volume: 100 start-page: 703 year: 2003 ident: B34 article-title: Estrogen receptor (ER)beta knockout mice reveal a role for ERbeta in migration of cortical neurons in the developing brain. publication-title: Proc. Natl. Acad. Sci. U.S.A. doi: 10.1073/pnas.242735799 |
| SSID | ssj0062648 |
| Score | 2.316783 |
| Snippet | Ketamine exposure disturbed normal neurogenesis in the developing brain and resulted in subsequent neurocognitive deficits. 17β-estradiol provides robust... Ketamine exposure in the developing brain disturbed normal neurogenesis and resulted in subsequent neurocognitive deficits. 17β-estradiol provides robust... |
| SourceID | doaj pubmedcentral proquest pubmed crossref |
| SourceType | Open Website Open Access Repository Aggregation Database Index Database Enrichment Source |
| StartPage | 251 |
| SubjectTerms | 17β-Estradiol Anesthesia Anesthesiology Animal models Apoptosis Brain Brain injury Caspase Caspase-3 Cell cycle Cell proliferation Cognition Cognitive ability Immunohistochemistry Ischemia Ketamine Kinases Laboratory animals Memory Neonates Neural stem cells Neurodegeneration Neurogenesis Neuroprotection Neuroscience Neurosciences Neurotoxicity p-GSK-3β Phosphorylation Rodents Spatial discrimination learning Spatial memory Stem cell transplantation Stem cells Subventricular zone Swimming Western blotting |
| SummonAdditionalLinks | – databaseName: DOAJ Directory of Open Access Journals dbid: DOA link: http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwrV3NbtQwEB6hHiouiH8CBRmJC4dok9ix4-NCt6pARQi1Um-W_wIrtdmqm5U495H6IH2mzjjZpYsQXLjGjuPMjO1vPOPPAO-idQhDrUDjVSEXVQh547XMvXBN6XFGDJrOOx99kYcn4tNpfXrnqi_KCRvogQfBTYrGSTro5xrdCGzLSulsYXVUdR1lm3g-C12snalhDpaUtzUEJdEF05MWBUhxhpLIKau63FqEElf_nwDm73mSdxaeg4fwYESMbDr09BHci91j2D0aY-JP4KpUN9f5jLYswnxxxo7XqeNs2iMgXhGYZImD4zvNa_Ml27fnOIsw2wU27ClghZEn8ZJ9_XWSgE3pAnH2Ofb2HD_FZj8vFrShyOYdNkjb7tivb7ZfPoWTg9nxx8N8vFkBdYCjMBcqcFvW3rlatU2IiCFQwkLYoL2zMVgXat2EykoRo0g08DxSRqhyTWG95M9gp1t08QWwGLiTDv0gH4NoY225jzpUXrRECaxVBpO1qI0facfp9oszg-4HKcck5RhSjknKyeD95o2LgXLjL3U_kPY29YgsOz1AEzKjCZl_mVAGe2vdm3EELw3RAiF25EJn8HZTjGOPAiq2i4sV1SG4KpSuMng-mMqmJ7ysJEfnNQO1ZURbXd0u6eY_Er-3pFCt5C__x7-9gvskLUpuK_ke7PSXq_gaYVTv3qQRcwsaKx4v priority: 102 providerName: Directory of Open Access Journals – databaseName: ProQuest Central dbid: BENPR link: http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwfV1La9wwEBZtAqWX0nfdpEWFXnowu7ZkWTqFTbshtCSEkEBuQi8nC4m93fVCz_1J-SH5TZ2x5U23lFytsS00D41mRt8Q8jkYC26o4SC8pU957n0qnRKp41ZmDiyiV3jf-ehYHJ7z7xfFRQy4LWNZ5WATO0PtG4cx8hHCtMBezrjam_9MsWsUZldjC43HZBtMsAQ5396fHp-cDrZYYP1Wn5yEo5gaVbCQmG_IEKQyL7KNzajD7P-fo_lvveRfG9DBc_Iseo500rP6BXkU6pfkyVHMjb8iv7Py7jadYujCz5prejaUkNNJC47xCp1K2mFxXKJ9my3pN3MD1oSa2tM-tgAEES9xQU_ubxTQCTYSpz9Ca27gV3T6a95gYJHOavgght9hXqemXb4m5wfTs6-HaeywALwAbUx56ZnJCmdtUVbSB_AlRG45N145a4I31hdK-twIHgLv4OBZwMrQ0sqxcYK9IVt1U4d3hAbPrLBwHnLB8yoUhrmgfO54hdDAqkzIaFhq7SL8OHbBuNZwDEHm6I45GpmjO-Yk5Mv6jXkPvfEA7T5yb02HoNndg2ZxqaMO6rG0AmXCSiU5iKURwpqxUaEsiiAqlpDdgfc6avJS38tdQj6th0EHMbFi6tCskAbdVl6qPCFve1FZz4RluWBwiE1IuSFEG1PdHKlnVx3Ot8CUrWDvH57WDnmK64DlaxnbJVvtYhU-gKPU2o9RG_4AbPUXuQ priority: 102 providerName: ProQuest |
| Title | 17β-Estradiol Treatment Attenuates Neurogenesis Damage and Improves Behavior Performance After Ketamine Exposure in Neonatal Rats |
| URI | https://www.ncbi.nlm.nih.gov/pubmed/31263401 https://www.proquest.com/docview/2283392349 https://www.proquest.com/docview/2251124792 https://pubmed.ncbi.nlm.nih.gov/PMC6585163 https://doaj.org/article/08b60062b898442da66ba0a9e755e6f3 |
| Volume | 13 |
| hasFullText | 1 |
| inHoldings | 1 |
| isFullTextHit | |
| isPrint | |
| link | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwnV1Lb9QwELZQK1W9IN4EyspIXDiEbmLHiQ8IbWFLBdqqqrrS3iK_0q60TcpuVipXfhI_hN_EjPMoi1YcuOQQ24nlmbHn5W8IeeOUBjVUcWDe1IY8tjbMjBSh4TqLDOyIVuJ958mpOJnyL7Nkdnc9ul3A1VbTDutJTZeLd7ffvn8AgX-PFiect4cFLA9GESKEnozxPvUunEsCTbEJ72MKAnO5mkDl1lH7ZI9FsWC8rQ_TnVEeyn-b_vl3GuUf59LxA3K_VSjpqOGAh-SeKx-RvUkbMn9MfkTpr5_hGD0adl4t6EWXWU5HNejLa9Q1qYfouMRtb76in9Q1bDJUlZY2Lgfo0MIoLunZ3UUDOsL64vSrq9U1_IqOb28q9DfSeQkfRK88zOtc1asnZHo8vvh4EraFF4BEIKQhTy1TUWK0TtIisw5UDBFrzpWVRitnlbaJzGysBHeOe5R45jBhNNXZUBnBnpKdsirdc0KdZVpoMJOMs7xwiWLGSRsbXiBisEwDctgtdW5aVHIsjrHIwTpBOuWeTjnSKfd0CsjbfsRNg8jxj75HSL2-H2Jp-xfV8jJvRTMfZloge-hMZhy4VQmh1VBJlyaJEwULyEFH-7zjzxxRg0C1ZFwG5HXfDKKJ8RZVumqNfVCb5amMA_KsYZV-Jh2rBSTdYKKNqW62lPMrD_8tMJIr2Iv_HvmS7OMSYcJbxA7ITr1cu1egWtV6QHaPxqdn5wPvmoDn51k08FL0GwGtKq8 |
| linkProvider | Scholars Portal |
| linkToHtml | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwtV1Lb9NAEB6VVAIuiDeGAosEBw5WYu967T0glNJUKWmiqkql3syud1MitXbIQ8CVH8SBH8JvYsaPlCDUW6_etb3aeey89huA104bNEO1QOaNrS9Ca_0kU9LPhEmCDDWiVXTfeTiS_RPx8TQ63YKfzV0YKqtsdGKpqG2RUYy8TTAteJZzod7PvvjUNYqyq00LjYotBu77V3TZFu8O9pC-b8Jwvzf-0PfrrgL4f-RAX8SW6yDKjIniSWIdnp8yNEJoqzKjndXGRiqxoZbCOVFCoHNH1ZCxSTo6kxy_ewO2Bd1obcH2bm90dNzofkn1YlUyFF0_1Z4g4Si_ERAoZhgFG4df2SPgf4btv_WZfx14-3fhTm2psm7FWvdgy-X34eawzsU_gB9B_PuX36NQiZ0W52zclKyz7hIN8RUZsazE_jgjfTpdsD19gdqL6dyyKpaBE2p8xjk7urzBwLrUuJwN3FJf4K9Y79usoEAmm-b4QQr347qO9XLxEE6uZe8fQSsvcvcEmLPcSIP-V-asmLhI88wpG2ZiQlDEKvag3Wx1mtVw59R14zxFt4eIk5bESYk4aUkcD96u35hVUB9XzN0l6q3nEUh3-aCYn6W1zKedxEjiCZOoRKAYaCmN7mjl4ihycsI92Glon9aaY5Fe8rkHr9bDKPOUyNG5K1Y0h8xkEavQg8cVq6xXwoNQcnSaPYg3mGhjqZsj-fRziSsuKUUs-dOrl_USbvXHw8P08GA0eAa3aU-odC7gO9BazlfuORppS_OilgwGn65bGP8ALiZUyA |
| linkToPdf | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwtV1Lb9NAEB6VVKq4IN41FFgkOHCwEnvXa_uAUEoStYRGUdVKvZl9pURq7ZCHgCs_iSM_gt_EjB8pQai3XuO1M9p57szsNwCvnNIYhiqBwhtbX4TW-olJpW-ETgKDFtGmdN_5aCQPTsWHs-hsC341d2GorbKxiaWhtoWhHHmbYFrQl3ORtid1W8S4N3g3--LTBCmqtDbjNCoRGbrvX_H4tnh72ENevw7DQf_k_YFfTxhAWlAafRFbroLIaB3Fk8Q69KUy1EIomxqtnFXaRmliQyWFc6KEQ-eOOiNjnXSUkRy_ewu2Y_SKogXb-_3R-LjxA5J6x6rCKB4DkWpkItU6AgLIDKNgwxGW8wL-F-T-26v5l_Mb3IU7ddTKupWY3YMtl9-HnaO6Lv8AfgTx759-n9ImdlpcsJOmfZ11lxiUryigZSUOyDnZ1umC9dQlWjKmcsuqvAYuqLEa52x8dZuBdWmIORu6pbrEv2L9b7OCkppsmuMHKfWPdB2r5eIhnN7I3j-CVl7kbheYs1xLjWcx46yYuEhx41IbGjEhWOI09qDdbHVmauhzmsBxkeERiJiTlczJiDlZyRwP3qzfmFWwH9es3SfurdcRYHf5QzE_z2r9zzqJliQTOkkTgSqhpNSqo1IXR5GTE-7BXsP7rLYii-xK5j14uX6M-k9FHZW7YkVrKGQWcRp68LgSlTUlPAglxwO0B_GGEG2Quvkkn34uMcYllYslf3I9WS9gB5Uw-3g4Gj6F27Ql1EUX8D1oLecr9wzjtaV-XisGg083rYt_AKKUWPQ |
| 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=17%CE%B2-Estradiol+Treatment+Attenuates+Neurogenesis+Damage+and+Improves+Behavior+Performance+After+Ketamine+Exposure+in+Neonatal+Rats&rft.jtitle=Frontiers+in+cellular+neuroscience&rft.au=Li%2C+Weisong&rft.au=Li%2C+Huixian&rft.au=Wei%2C+Haidong&rft.au=Lu%2C+Yang&rft.date=2019-06-13&rft.pub=Frontiers+Media+S.A&rft.eissn=1662-5102&rft.volume=13&rft_id=info:doi/10.3389%2Ffncel.2019.00251&rft_id=info%3Apmid%2F31263401&rft.externalDocID=PMC6585163 |
| thumbnail_l | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=1662-5102&client=summon |
| thumbnail_m | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=1662-5102&client=summon |
| thumbnail_s | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=1662-5102&client=summon |