Aging and infection reduce expression of specific brain-derived neurotrophic factor mRNAs in hippocampus.

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 5' exon-specific transcripts (I, II, IV, and VI), and BDNF mRNAs with a long 3' untranslated region (3' UTR). In CA1, aging reduced basal levels and fear-conditioning-induced expression of total BDNF mRNA, exon IV-specific transcripts, and transcripts with long 3' 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 3' UTRs.

journal_name

Neurobiol Aging

journal_title

Neurobiology of aging

authors

Chapman TR,Barrientos RM,Ahrendsen JT,Hoover JM,Maier SF,Patterson SL

doi

10.1016/j.neurobiolaging.2011.07.015

subject

Has Abstract

pub_date

2012-04-01 00:00:00

pages

832.e1-14

issue

4

eissn

0197-4580

issn

1558-1497

pii

S0197-4580(11)00300-9

journal_volume

33

pub_type

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