Article Figures & Data
Figures
- Figure 1.
Stimulus–response curves are not altered by age or a history of infection. Plots of fEPSP slopes (in millivolts per millisecond) at various stimulation intensities for hippocampal slices from young and aged rats with and without a recent history of infection show no significant differences in basal synaptic transmission in area CA1. Input-output curves are shown for slice collected 8 d (A) and 14 d (B) after injection of E. coli or saline.
- Figure 2.
Aging and a peripheral immune challenge interact to produce prolonged, but temporary, reductions in L-LTP. Hippocampal slices were collected from young (3 mo) and aged (24 mo) rats 8, 14, or 21 d after injection of E. coli or saline (vehicle). L-LTP was induced in Schaffer collateral-CA1 synapses using theta-burst stimulation (12 bursts of 4 pulses at 100 Hz, delivered 200 ms apart). fEPSP slopes were normalized to pretetanus baselines, averaged, and plotted for each group. Error bars indicate SEM. Insets show representative traces before and 3 h after tetanus. A, L-LTP is severely impaired in slices from aged, but not young, rats 8 d after E. coli injection. B, L-LTP is still reduced but recovering in aged rats at 14 d. C, The L-LTP is back to baselines at 21 d.
- Figure 3.
Levels of the mature BDNF protein isoform and activation of TrkB and downstream signaling are reduced in aged rats 8 d after infection. Western blot analysis was conducted using hippocampal synaptoneurosomes prepared from young and aged rats 8 d after injection of E. coli or vehicle; representative examples are shown. A, levels of mBDNF, but not proBDNF, are diminished in the aged animals 8 d after infection. B–D, Graphs present the ratio of phosphorylated TrkB (pTrkB), PLCγ1 (pPLCγ), or ERK (pERK) to total expression of TrkB (tTrkB), PLCγ1 (tPLCγ), or ERK (tERK). Levels of phosphorylated TrkB (B), PLC γ1 (C), and ERK (D) are significantly lower in the aged animals 8 d after infection. Protein bands were quantified using ImageJ, normalized to their actin controls, and expressed as percentages of mean protein levels from young vehicle-injected animals. Error bars represent SEM. All graphs here and below represent at least three independent experiments, with 1–2 animals per group in each experiment.
- Figure 4.
Levels of mBDNF and activation of TrkB, PLCγ1, and ERK in aged rats have returned to normal 14 d after E. coli injection. Western blot analysis of hippocampal synaptoneurosomes prepared from young and aged rats 14 d after injection of E. coli or vehicle; representative examples are shown. A–D, Aged E. coli animals show no significant difference in levels of mBDNF (A) or activation of TrkB (B), PLC γ1 (C), or ERK (D). Quantification was as described in the legend for Fig. 3.
- Figure 5.
A summary of the effects of age and infection at multiple time points after injection of E. coli or saline. Memory = hippocampus-dependent long-term memory; IL-1β = levels of proinflammatory cytokine interleukin-1β in hippocampal synaptoneurosomes; L-LTP = theta burst–evoked L-LTP in the hippocampal CA1 area; and BDNF = levels of mature BDNF and activity of related proteins in hippocampal synaptoneurosomes. Upward arrows indicate an increase, and downward arrows show a reduction. Three arrows represent severe deficits, and one arrow means impairments to a lesser degree. Horizontal lines indicate baseline values. Data summarized for day 4 are drawn from earlier publications: Memory and IL-1β (Barrientos et al., 2006, 2009), L-LTP (Chapman et al., 2010), and BDNF (Cortese et al., 2011).
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