title: Dysfunctional regulation of alphaCaMKII and syntaxin 1B transcription after induction of LTP in the aged rat.
abstract: Syntaxin 1B and alphaCaMKII are two genes that are upregulated after the induction of LTP and appear to underlie different mechanisms of synaptic plasticity. alphaCaMKII is directly implicated in strengthening the synapses that have been modified, whereas syntaxin 1B has been implicated in a mechanism for the propagation of synaptic plasticity within neural circuits. In these experiments we have investigated whether the regulation of these genes is altered after the induction of LTP in aged rats. We found, three hours after the induction of LTP in the dentate gyrus, that aged rats could be subgrouped into those in which LTP was maintained and those in which LTP had decayed back to basal levels. Both genes were upregulated in young adult rats, whereas there was a differential pattern of LTP-induced expression in the aged rats. Dendritic alphaCaMKII was upregulated in aged rats only when LTP was maintained. In contrast, regulation of syntaxin 1B and alphaCaMKII was absent in the granule cell bodies of the aged rats regardless of whether LTP was maintained or not. These results suggest that molecular mechanisms implicated in two aspects of hippocampal synaptic plasticity malfunction during normal ageing and therefore may have some contributory role in the decline in memory function routinely observed in ageing.
authors.affiliation: Laboratoire de Neurobiologie de l'Apprentissage, de la Mémoire et de la Communication, CNRS UMR 8620, Bât 446, Université Paris Sud, 91405 Orsay, France. sabrina.davis@ibaic.u-psud.fr
authors.forename: S
authors.initials: S
authors.lastname: Davis
authors.forename: H
authors.initials: H
authors.lastname: Salin
authors.forename: A
authors.initials: A
authors.lastname: Helme-Guizon
authors.forename: S
authors.initials: S
authors.lastname: Dumas
authors.forename: A
authors.initials: A
authors.lastname: Stéphan
authors.forename: M
authors.initials: M
authors.lastname: Corbex
authors.forename: J
authors.initials: J
authors.lastname: Mallet
authors.forename: S
authors.initials: S
authors.lastname: Laroche
mesh_terms: D000375:Aging / Q000378:metabolism*; D000818:Animals; D000954:Antigens, Surface / Q000235:genetics* / Q000378:metabolism; D054732:Calcium-Calmodulin-Dependent Protein Kinase Type 2; D017871:Calcium-Calmodulin-Dependent Protein Kinases / Q000235:genetics* / Q000378:metabolism; D003712:Dendrites / Q000201:enzymology; D004789:Enzyme Activation / Q000502:physiology; D015971:Gene Expression Regulation, Enzymologic; D006624:Hippocampus / Q000166:cytology / Q000378:metabolism; D017774:Long-Term Potentiation / Q000235:genetics*; D008297:Male; D009419:Nerve Tissue Proteins / Q000235:genetics* / Q000378:metabolism; D009473:Neuronal Plasticity / Q000235:genetics; D009474:Neurons / Q000201:enzymology / Q000648:ultrastructure; D012333:RNA, Messenger / Q000032:analysis; D051381:Rats; D017208:Rats, Wistar; D013572:Synaptic Vesicles / Q000201:enzymology; D050827:Syntaxin 1; D014158:Transcription, Genetic / Q000502:physiology*
chemical_list: D000954:Antigens, Surface; D009419:Nerve Tissue Proteins; D012333:RNA, Messenger; D050827:Syntaxin 1; D054732:Calcium-Calmodulin-Dependent Protein Kinase Type 2; D017871:Calcium-Calmodulin-Dependent Protein Kinases