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1.
Figure 1

Figure 1. From: CX3CR1 deficiency leads to impairment of hippocampal cognitive function and synaptic plasticity.

CX3CR1−/− mice show decreased hippocampal neurogenesis in a gene-dose dependent manner (a, b). Unbiased stereology revealed a significant decrease in the number of DCX+ cells in the SGZ of adult male CX3CR1−/− and CX3CR1+/− mice compared to wild-type mice (p< 0.001). CX3CR1−/− were also significantly different from CX3CR1+/− (p<0.05) (a). Quantification of the number of cells that were proliferating during the preceeding 24 hours as determined by the incorporation of BrdU, was significantly fewer in the CX3CR1−/− and CX3CR1+/− mice compared to wild-type (p<0.001). CX3CR1−/− were also significantly different from CX3CR1+/− (p<0.05) (b). Wild-type (WT, white bar), CX3CR1+/− (gray bar), CX3CR1−/− (black bar). All data are presented as mean ± SEM p < 0.01

T. Rogers Justin, et al. J Neurosci. ;31(45):16241-16250.
2.
Figure 6

Figure 6. From: CX3CR1 deficiency leads to impairment of hippocampal cognitive function and synaptic plasticity.

CX3CR1 deficiency leads to impairments in synaptic plasticity which are rescued through IL-1β antagonism. PTP was induced with HFS (1 sec, 100 Hz bursts; arrow) after 1 min of baseline recording. LTP was induced with HFS (2, 1 sec, 100 Hz bursts separated by 20 s; arrow) after 20 min of baseline recording. Changes in fEPSP slope are expressed as a percentage of baseline (a). The IL-1β antagonist, IL-1ra (100 μg/ml) rescues the PTP deficit (red, n=7) in hippocampi taken from CX3CR1−/− (black, n=8) in area CA1 to levels seen in wild-type (white, n=9). (b.) The LTP deficit seen in hippocampi taken from CX3CR1−/− (black, n=10) mice is rescued with the IL-1β antagonist IL-1ra (100 μg/ml) (red, n=11).

T. Rogers Justin, et al. J Neurosci. ;31(45):16241-16250.
3.
Figure 5

Figure 5. From: CX3CR1 deficiency leads to impairment of hippocampal cognitive function and synaptic plasticity.

CX3CR1 −/− and CX3CR1+/− show increased hippocampal protein levels of IL-1β compared to littermate wild-type (WT) as measured by ELISA (a). Western blot analysis of hippocampi from wild-type , CX3CR1−/− and CX3CR1+/− mice shows an increase in phospho (p) p-38 protein in CX3CR1−/− and CX3CR1+/− mice compared to that of wild-type (right blot in b; near-infrared image displayed in gray scale). Relative p p-38 expression normalized to β-actin, shows the highest expression in CX3CR1−/− and CX3CR1+/− (b). TNFα cerebellar protein levels are significantly increased in CX3CR1−/− and CX3CR1+/− mice as compared to wild-type mice as measured by ELISA (c). The area of Iba-1 staining is significant higher in CX3CR1−/− when compared to wild-type and CX3CR1+/− as measured by immunohistochemistry (d). Wild-type (WT, white bar), CX3CR1+/− (gray bar), CX3CR1−/− (black bar). Representative photomicrographs of the Iba-1+ cells in the dentate gyrus of wild-type (e) and CX3CR1 deficient mice (f). All data are presented as mean ± SEM p < 0.01. Asterisk represents p < 0.05

T. Rogers Justin, et al. J Neurosci. ;31(45):16241-16250.
4.
Figure 2

Figure 2. From: CX3CR1 deficiency leads to impairment of hippocampal cognitive function and synaptic plasticity.

CX3CR1−/− and CX3CR1+/− mice show motor learning impairment but normal spontaneous activity (a, b, c). On the first day of training (trial 1-4) no difference between genotypes was observed in the learning ability in the rotarod task (a). On the second day of training (trials 5-8) as expected, wild-type mice learned the rotarod task as demonstrated by their ability to remain on the rod for longer periods. Neither the CX3CR1−/− nor the CX3CR1+/− mice showed significant improvement in motor coordination with training when compared to wild-type (a; Repeated Measure ANOVA, p<0.0001.). Wild-type (WT, white circles), CX3CR1+/− (gray circles), CX3CR1−/− (black circles). All data are presented as mean ± SEM p < 0.01. Comparison of the motor performance of each group of mice on trial 1 versus trial 8, show that wild-type performed significantly better than CX3CR1−/− and CX3CR1+/− (b; linear regression, p<0.001). CX3CR1 −/− and CX3CR1+/− mice show normal spontaneous locomotor activity (c). Wild-type, CX3CR1−/− and CX3CR1+/− mice do not show any difference in total distance traveled in the open field (c). Wild-type (WT, white bar), CX3CR1+/− (gray bar), CX3CR1−/− (black bar). All data are presented as mean ± SEM p < 0.01

T. Rogers Justin, et al. J Neurosci. ;31(45):16241-16250.
5.
Figure 4

Figure 4. From: CX3CR1 deficiency leads to impairment of hippocampal cognitive function and synaptic plasticity.

CX3CR1 deficiency leads to impairments in LTP. LTP was induced with HFS (2, 1 sec, 100 Hz bursts separated by 20 s; arrow) after 20 min of baseline recording and changes in fEPSP slope are expressed as a percentage of baseline (a). Representative fEPSP traces taken from hippocampal slices of (left to right) wild-type, CX3CR1+/− and CX3CR1−/− mice (b). Both CX3CR1−/− (black) and CX3CR1+/− (red) have deficiencies in LTP of area CA1 compared to wild-type controls (white) (c). The last 5 min of fEPSPs slope recordings were averaged for wild-type (n=12), CX3CR1−/− (n=10) and CX3CR1+/− (n=9) mice (Asterisks represent p<0.05.) (d). Paired-pulse facilitation (PPF) was induced with the use of paired- pulses given with an initial delay of 20 ms and the time to the second pulse was increased 20 ms incrementally until a final delay of 300 ms was reached. There was no significant PPF differences between experimental groups. All data are presented as mean ± S.E p < 0.01

T. Rogers Justin, et al. J Neurosci. ;31(45):16241-16250.
6.
Figure 3

Figure 3. From: CX3CR1 deficiency leads to impairment of hippocampal cognitive function and synaptic plasticity.

CX3CR1−/− mice show impairment in contextual fear conditioning and Morris water maze memory function. CX3CR1−/− (black circles) and CX3CR1+/− (gray circles) are compared to littermate wild-type mice (white circles). In panel A, a tone (solid bar) was paired with a foot shock (arrowhead) at 2 and 4 minutes. Freezing behavior is shown on the day of training for CX3CR1−/−, CX3CR1+/− and wild-type (a) and is comparable in all groups. CX3CR1−/−, CX3CR1+/− showed significant reduced freezing response compared to wild-type, when tested 24 h following training (b). CX3CR1−/−, CX3CR1+/− showed normal freezing to cue component compared to controls (c). Asterisks represent p<0.01. Panels d and e show the hidden platform version of Morris water maze task. Mean latency to escape from a pool to hidden platform across training days (d). A first probe test was performed on day 7 and a second probe test was performed on day 11 (e) to determine the number of pseudo platform crossings in the target quadrant (TQ) compared to the opposite quadrant (OP), the left quadrant (LQ) and the right quadrant (RQ). Wild type (WT, white bar), CX3CR1+/− (gray bar), CX3CR1−/− (black bar). All data are presented as mean ± SEM p < 0.01. All data are presented as mean ± SEM p < 0.01

T. Rogers Justin, et al. J Neurosci. ;31(45):16241-16250.
7.
Figure 7

Figure 7. From: CX3CR1 deficiency leads to impairment of hippocampal cognitive function and synaptic plasticity.

IL-1ra reversed the deficit in contextual fear conditioning and Morris water maze memory function induced by the loss of CX3CR1 but not the deficit in motor learning.
CX3CR1−/− ACSF(blue square) and CX3CR1−/− IL-1ra - treated mice (red square) are compared to wild-type ACSF (open circles), wild-type treated with heat-inactivated IL-1ra (black square), and wild-type IL-1ra-treated mice (green squares). Panel A shows that on the first day of training (trial 1-4) no difference between groups was observed in the learning ability on the rotarod task (a). On the second day of training (trials 5-8) all wild-type mice groups learned the rotarod task as demonstrated by their ability to remain on the rod for longer periods. Neither the CX3CR1−/− ACSF nor the CX3CR1−/− IL-1ra treated mice showed significant improvement in motor coordination with training when compared to wild-type (a);. In panel B, a tone (solid bar) was paired with a foot shock (arrowhead) at 2 and 4 minutes. Freezing behavior is shown on the day of training for CX3CR1−/− ACSF (blue square), CX3CR1−/− IL-1ra – treated mice (red square), wild-type ACSF (white circles), wild-type treated with heat-inactivated IL-1ra (black square), and wild-type IL-1ra treated mice (green square) and is comparable in all groups. CX3CR1−/− control mice showed significantly reduced freezing compared to all wild-type groups, when tested 24 h following training (c). CX3CR1−/− treated with IL-1ra (red square) showed a freezing response similar to wild type groups. Panels d and e and f show the hidden platform version of Morris water maze task. Mean latency to escape from a pool to hidden platform across training days (d). A probe test was performed on day 10 to determine the number of pseudo platform crossings in the target quadrant (TQ) compared to the opposite quadrant (OP) (e). Wild type ACSF (WT, white bar), wild-type treated with heat-inactivated IL-1ra (light gray bar), wild-type treated with IL-1ra (dark gray bar), CX3CR1−/− ACSF (black bar), CX3CR1−/− IL-1ra – treated mice (black/white grid bar). Panel F shows the time spent in the target platform zone. CX3CR1−/− ACSF (black bar) mice spent significantly less time in the target zone compared to wild-type controls (wild-type ACSF (white bar), wild-type heat-inactivated IL-1ra (light gray bar), wild-type IL-1ra (dark gray bar). CX3CR1−/− mice treated with IL-1ra spent the same amount of time in the target quadrant when compared to wild-type controls. All data are presented as mean ± SEM p < 0.01. All data are presented as mean ± SEM p < 0.01 Asterisk represents p < 0.05: CX3CR1−/− control vs wild-type controls; ## represents p<0.001: CX3CR1−/− IL-1ra vs CX3CR1 −/−.

T. Rogers Justin, et al. J Neurosci. ;31(45):16241-16250.

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