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Article: Long-term increase of Sp-1 transcription factors in the hippocampus after kainic acid treatment

TitleLong-term increase of Sp-1 transcription factors in the hippocampus after kainic acid treatment
Authors
Issue Date1999
PublisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/molbrainres
Citation
Molecular Brain Research, 1999, v. 69 n. 1, p. 144-148 How to Cite?
AbstractSystemic administration of kainic acid (KA), a glutamate receptor agonist, causes robust seizures and has been used as an excellent rodent model for human temporal lobe epilepsy. Recently, we have demonstrated that a single injection of KA increases the steady-state levels of proenkephalin (PENK) mRNA in the rat hippocampus for at least one year. However, the molecular mechanisms underlying this long-term increase in PENK mRNA levels have not been clearly defined. To determine the possible involvement of the Sp-1 transcription factors in this regulation, electrophoresis mobility-shift assays were used to study the expression of Sp-1 factors in the hippocampus after KA treatment. The results showed that there are long-lasting increases in Sp-1 DNA-binding activity. The Sp-1 DNA-binding complexes were only competed by the non-radioactive Sp-1 element and not by ENKCRE2, AP-1 or CRE elements, indicating the specificity of Sp-1 DNA-binding activity. Since the expression of Sp-1 parallels the time course of long-lasting increase in the expression of PENK mRNA and mossy fiber sprouting after KA treatment, we hypothesize that the increase in Sp-1 activity may be associated with the long-term changes in the plasticity of hippocampal function after KA-induced seizures. Copyright (C) 1999 Elsevier Science B.V.
Persistent Identifierhttp://hdl.handle.net/10722/149579
ISSN
2007 Impact Factor: 1.997
2008 SCImago Journal Rankings: 1.457
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorFeng, Zen_US
dc.contributor.authorChang, RCCen_US
dc.contributor.authorBing, Gen_US
dc.contributor.authorHudson, Pen_US
dc.contributor.authorTiao, Nen_US
dc.contributor.authorJin, Len_US
dc.contributor.authorHong, JSen_US
dc.date.accessioned2012-06-26T05:55:32Z-
dc.date.available2012-06-26T05:55:32Z-
dc.date.issued1999en_US
dc.identifier.citationMolecular Brain Research, 1999, v. 69 n. 1, p. 144-148en_US
dc.identifier.issn0169-328Xen_US
dc.identifier.urihttp://hdl.handle.net/10722/149579-
dc.description.abstractSystemic administration of kainic acid (KA), a glutamate receptor agonist, causes robust seizures and has been used as an excellent rodent model for human temporal lobe epilepsy. Recently, we have demonstrated that a single injection of KA increases the steady-state levels of proenkephalin (PENK) mRNA in the rat hippocampus for at least one year. However, the molecular mechanisms underlying this long-term increase in PENK mRNA levels have not been clearly defined. To determine the possible involvement of the Sp-1 transcription factors in this regulation, electrophoresis mobility-shift assays were used to study the expression of Sp-1 factors in the hippocampus after KA treatment. The results showed that there are long-lasting increases in Sp-1 DNA-binding activity. The Sp-1 DNA-binding complexes were only competed by the non-radioactive Sp-1 element and not by ENKCRE2, AP-1 or CRE elements, indicating the specificity of Sp-1 DNA-binding activity. Since the expression of Sp-1 parallels the time course of long-lasting increase in the expression of PENK mRNA and mossy fiber sprouting after KA treatment, we hypothesize that the increase in Sp-1 activity may be associated with the long-term changes in the plasticity of hippocampal function after KA-induced seizures. Copyright (C) 1999 Elsevier Science B.V.en_US
dc.languageengen_US
dc.publisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/molbrainresen_US
dc.relation.ispartofMolecular Brain Researchen_US
dc.subject.meshAnimalsen_US
dc.subject.meshAntibodiesen_US
dc.subject.meshBrain Chemistry - Geneticsen_US
dc.subject.meshDna Primersen_US
dc.subject.meshDisease Models, Animalen_US
dc.subject.meshEpilepsy, Temporal Lobe - Physiopathologyen_US
dc.subject.meshExcitatory Amino Acid Agonists - Pharmacologyen_US
dc.subject.meshGene Expression - Drug Effectsen_US
dc.subject.meshKainic Acid - Pharmacologyen_US
dc.subject.meshMaleen_US
dc.subject.meshMossy Fibers, Hippocampal - Chemistry - Drug Effects - Physiologyen_US
dc.subject.meshNerve Degeneration - Chemically Induced - Physiopathologyen_US
dc.subject.meshProtein Binding - Physiologyen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Inbred F344en_US
dc.subject.meshSp1 Transcription Factor - Genetics - Immunology - Metabolismen_US
dc.titleLong-term increase of Sp-1 transcription factors in the hippocampus after kainic acid treatmenten_US
dc.typeArticleen_US
dc.identifier.emailChang, RCC:rccchang@hkucc.hku.hken_US
dc.identifier.authorityChang, RCC=rp00470en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/S0169-328X(99)00099-6en_US
dc.identifier.pmid10350646-
dc.identifier.scopuseid_2-s2.0-0032942218en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0032942218&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume69en_US
dc.identifier.issue1en_US
dc.identifier.spage144en_US
dc.identifier.epage148en_US
dc.identifier.isiWOS:000080577100015-
dc.publisher.placeNetherlandsen_US
dc.identifier.scopusauthoridFeng, Z=7403442974en_US
dc.identifier.scopusauthoridChang, RCC=7403713410en_US
dc.identifier.scopusauthoridBing, G=7004276368en_US
dc.identifier.scopusauthoridHudson, P=35566903000en_US
dc.identifier.scopusauthoridTiao, N=7801575007en_US
dc.identifier.scopusauthoridJin, L=55231952700en_US
dc.identifier.scopusauthoridHong, JS=7404117981en_US

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