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Early Maintenance of Hippocampal Mossy Fiber–Long-Term Potentiation Depends on Protein and RNA Synthesis and Presynaptic Granule Cell Integrity

dc.creatorCalixto, Eduardo
dc.creatorThiels, Edda
dc.creatorKlann, Eric
dc.creatorBarrionuevo, Germán
dc.date.accessioned2017-06-29T03:46:20Z
dc.date.available2017-06-29T03:46:20Z
dc.date.issued2003es_ES
dc.identifier2658es_ES
dc.identifier.issn0270-6474es_ES
dc.identifier.urihttp://repositorio.inprf.gob.mx/handle/123456789/4507
dc.identifier.urihttps://doi.org/10.1523/JNEUROSCI.23-12-04842.2003es_ES
dc.identifier.urihttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6741163/es_ES
dc.description.abstractes_ES
dc.language.isoenges_ES
dc.publisheres_ES
dc.relation23(12) 4842-4849p.es_ES
dc.relationversión del editores_ES
dc.rightsacceso cerradoes_ES
dc.subject.meshAnimalses_ES
dc.subject.meshColforsin/pharmacologyes_ES
dc.subject.meshElectric Stimulationes_ES
dc.subject.meshExcitatory Amino Acid Antagonists/pharmacologyes_ES
dc.subject.meshExcitatory Postsynaptic Potentials/drug effectses_ES
dc.subject.meshExcitatory Postsynaptic Potentials/physiologyes_ES
dc.subject.meshHippocampus/cytologyes_ES
dc.subject.meshHippocampus/drug effectses_ES
dc.subject.meshHippocampus/physiologyes_ES
dc.subject.meshIn Vitro Techniqueses_ES
dc.subject.meshLong-Term Potentiation/drug effectses_ES
dc.subject.meshLong-Term Potentiation/physiologyes_ES
dc.subject.meshMalees_ES
dc.subject.meshMossy Fibers, Hippocampal/drug effectses_ES
dc.subject.meshMossy Fibers, Hippocampal/physiologyes_ES
dc.subject.meshNeurons/drug effectses_ES
dc.subject.meshNeurons/physiologyes_ES
dc.subject.meshNucleic Acid Synthesis Inhibitors/pharmacologyes_ES
dc.subject.meshPresynaptic Terminals/physiologyes_ES
dc.subject.meshProtein Biosynthesises_ES
dc.subject.meshProtein Synthesis Inhibitors/pharmacologyes_ES
dc.subject.meshPyramidal Cells/drug effectses_ES
dc.subject.meshPyramidal Cells/physiologyes_ES
dc.subject.meshRNA/biosynthesises_ES
dc.subject.meshRatses_ES
dc.subject.meshRats, Sprague-Dawleyes_ES
dc.titleEarly Maintenance of Hippocampal Mossy Fiber–Long-Term Potentiation Depends on Protein and RNA Synthesis and Presynaptic Granule Cell Integrityes_ES
dc.title.alternativees_ES
dc.typeartículoes_ES
dc.contributor.affiliationDepartment of Neuroscience and Center for the Neural Basis of Cognition, University of Pittsburgh, Pittsburgh, Pennsylvania 15260es_ES
dc.contributor.emailgerman@bns.pitt.edues_ES
dc.relation.jnabreviadoJ NEUROSCIes_ES
dc.relation.journalThe Journal of Neurosciencees_ES
dc.identifier.placeEstados Unidoses_ES
dc.date.published2003es_ES
dc.identifier.organizacionInstituto Nacional de Psiquiatría Ramón de la Fuente Muñizes_ES
dc.identifier.eissnes_ES
dc.identifier.doies_ES
dc.description.monthJunes_ES
dc.description.abstractotrodiomaThe neural substrates of memory likely include long-term potentiation (LTP) of synaptic strength that results from high-frequency stimulation (HFS) of the afferent pathway. The mechanisms that underlie the maintenance of LTP include RNA and protein synthesis, although the contribution of these molecular events typically does not become essential until several hours after LTP induction. We here show that, different from this pattern, (1) LTP maintenance at the mossy fiber (MF) input to CA3 pyramidal cells in the hippocampus depends on protein and RNA synthesis soon after LTP induction, and (2) some of these molecular events are controlled by signaling from the presynaptic granule cell soma. Bath application of the protein synthesis inhibitor emetine or cycloheximide 1 hr after MF LTP induction in hippocampal slices caused loss of MF potentiation. In contrast, application of emetine 1 hr after LTP induction at the commissural–associational input to CA3 pyramidal cells had no effect on this form of LTP. Administration of emetine or the RNA synthesis inhibitor actinomycin-D before delivery of HFS to MF input also caused a rapid decay of MF potentiation, although neither drug had an effect on the amplitude or the time-constant of decay of post-tetanic potentiation (PTP). Similarly, transection of MF axons near granule cell somas had no effect on baseline or PTP parameters but caused loss of potentiation at a rate comparable with that after actinomycin-D application. These results indicate that the mechanisms that underlie MF LTP maintenance differ from those involved in LTP maintenance at other glutamatergic synapses.es_ES
dc.subject.meshmes_ES
dc.subject.kwes_ES
dc.subject.koMossy fiberes_ES
dc.subject.koLTPes_ES
dc.subject.koCA3es_ES
dc.subject.koDentate gyruses_ES
dc.subject.koProtein synthesises_ES
dc.subject.koRNA synthesises_ES


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