Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
6809523 | Neurobiology of Aging | 2012 | 14 Pages |
Abstract
Aging increases the likelihood of cognitive decline after negative life events such as infection or injury. We have modeled this increased vulnerability in aged (24-month-old), but otherwise unimpaired F344xBN rats. In these animals, but not in younger (3-month-old) counterparts, a single intraperitoneal injection of E. coli leads to specific deficits in long-term memory and long-lasting synaptic plasticity in hippocampal area CA1-processes strongly dependent on brain-derived neurotrophic factor (BDNF). Here we have investigated the effects of age and infection on basal and fear-conditioning-stimulated expression of Bdnf in hippocampus. We performed in situ hybridization with 6 probes recognizing: total (pan-)BDNF mRNA, the 4 predominant 5â² exon-specific transcripts (I, II, IV, and VI), and BDNF mRNAs with a long 3â² untranslated region (3â² UTR). In CA1, aging reduced basal levels and fear-conditioning-induced expression of total BDNF mRNA, exon IV-specific transcripts, and transcripts with long 3â² UTRs; effects of infection were similar and sometimes compounded the effects of aging. In CA3, aging reduced all of the transcripts to some degree; infection had no effect. Effects in dentate were minimal. Northern blot analysis confirmed an aging-associated loss of total BDNF mRNA in areas CA1 and CA3, and revealed a parallel, preferential loss of BDNF mRNA transcripts with long 3â² UTRs.
Keywords
Related Topics
Life Sciences
Biochemistry, Genetics and Molecular Biology
Ageing
Authors
Timothy R. Chapman, Ruth M. Barrientos, Jared T. Ahrendsen, Jennifer M. Hoover, Steven F. Maier, Susan L. Patterson,