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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
KeywordsHippocampus
Kainic acid
Mossy fiber sprouting
Temporal lobe epilepsy
Transcription factor
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
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.subjectHippocampus-
dc.subjectKainic acid-
dc.subjectMossy fiber sprouting-
dc.subjectTemporal lobe epilepsy-
dc.subjectTranscription factor-
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
dc.identifier.issnl0169-328X-

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