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CX(3)CR1 deficiency alters hippocampal-dependent plasticity phenomena blunting the effects of enriched environment.

Maggi L, Scianni M, Branchi I, D'Andrea I, Lauro C, Limatola C - Front Cell Neurosci (2011)

Bottom Line: At this aim wt and CX(3)CR1(GFP/GFP) mice were exposed to long-lasting-enriched environment (EE) and the effects on hippocampal functions were studied by electrophysiological recordings of long-term potentiation of synaptic activity, behavioral tests of learning and memory in the Morris water maze paradigm and analysis of neurogenesis in the subgranular zone of the dentate gyrus (DG).We found that CX(3)CR1 deficiency increases hippocampal plasticity and spatial memory, blunting the potentiating effects of EE.These data indicate that CX(3)CL1/CX(3)CR1-mediated signaling is crucial for a normal experience-dependent modulation of hippocampal functions.

View Article: PubMed Central - PubMed

Affiliation: Department of Physiology and Pharmacology, Istituto Pasteur Fondazione Cenci Bolognetti, Università di Roma Rome Italy.

ABSTRACT
In recent years several evidence demonstrated that some features of hippocampal biology, like neurogenesis, synaptic transmission, learning, and memory performances are deeply modulated by social, motor, and sensorial experiences. Fractalkine/CX(3)CL1 is a transmembrane chemokine abundantly expressed in the brain by neurons, where it modulates glutamatergic transmission and long-term plasticity processes regulating the intercellular communication between glia and neurons, being its specific receptor CX(3)CR1 expressed by microglia. In this paper we investigated the role of CX(3)CL1/CX(3)CR1 signaling on experience-dependent hippocampal plasticity processes. At this aim wt and CX(3)CR1(GFP/GFP) mice were exposed to long-lasting-enriched environment (EE) and the effects on hippocampal functions were studied by electrophysiological recordings of long-term potentiation of synaptic activity, behavioral tests of learning and memory in the Morris water maze paradigm and analysis of neurogenesis in the subgranular zone of the dentate gyrus (DG). We found that CX(3)CR1 deficiency increases hippocampal plasticity and spatial memory, blunting the potentiating effects of EE. In contrast, exposure to EE increased the number and migration of neural progenitors in the DG of both wt and CX(3)CR1(GFP/GFP) mice. These data indicate that CX(3)CL1/CX(3)CR1-mediated signaling is crucial for a normal experience-dependent modulation of hippocampal functions.

No MeSH data available.


Related in: MedlinePlus

Morris water maze in wt and CX3CR1GFP/GFP mice exposed to either SE or EE condition. (A) Acquisition. Left: latency to find the platform. All subjects learnt to find the platform. However, EE mice, independently from their genotype, showed a significant reduction in escape latency compared with SE mice. Right: path length to find the platform. A main effect of genotype was found for path length, CX3CR1GFP/GFP swimming longer paths than wt during the acquisition phase. (B) Probe on the fourth day. SE CX3CR1GFP/GFP mice spent an amount of time similar to that spent by EE CX3CR1GFP/GFP mice and significantly longer than that spent by SE wt mice. (C) Probe on the sixth day. All experimental groups spent significantly more time in the quadrant where the platform had been located during training than in the other quadrants. The EE mice showed a better learning performance than SE mice, independently from their genotype. *p < 0.05 vs. both EE wt and SE CX3CR1GFP/GFP mice. #p < 0.05 vs. the other quadrants for each experimental group. Data are mean ± SEM.
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Figure 3: Morris water maze in wt and CX3CR1GFP/GFP mice exposed to either SE or EE condition. (A) Acquisition. Left: latency to find the platform. All subjects learnt to find the platform. However, EE mice, independently from their genotype, showed a significant reduction in escape latency compared with SE mice. Right: path length to find the platform. A main effect of genotype was found for path length, CX3CR1GFP/GFP swimming longer paths than wt during the acquisition phase. (B) Probe on the fourth day. SE CX3CR1GFP/GFP mice spent an amount of time similar to that spent by EE CX3CR1GFP/GFP mice and significantly longer than that spent by SE wt mice. (C) Probe on the sixth day. All experimental groups spent significantly more time in the quadrant where the platform had been located during training than in the other quadrants. The EE mice showed a better learning performance than SE mice, independently from their genotype. *p < 0.05 vs. both EE wt and SE CX3CR1GFP/GFP mice. #p < 0.05 vs. the other quadrants for each experimental group. Data are mean ± SEM.

Mentions: In the acquisition phase, all mice significantly reduced the latency to find the platform day after day [F(2,48) = 22.379, p < 0.0001]. However, the experimental subjects exposed to EE condition displayed better learning and memory abilities than those exposed to SE, as shown by the significant main effect of the environment [F(1,24) = 9.001, p = 0.0062; Figure 3A, left]. In line with the literature (Tremml et al., 2002; Harris et al., 2009), a reduced thigmotactic behavior in EE compared to SE mice was found [F(1,24) = 6.864, p = 0.0150; data not shown]. This may, at least in part, explain the difference in learning performances among groups shown during acquisition (Wolfer et al., 1998).


CX(3)CR1 deficiency alters hippocampal-dependent plasticity phenomena blunting the effects of enriched environment.

Maggi L, Scianni M, Branchi I, D'Andrea I, Lauro C, Limatola C - Front Cell Neurosci (2011)

Morris water maze in wt and CX3CR1GFP/GFP mice exposed to either SE or EE condition. (A) Acquisition. Left: latency to find the platform. All subjects learnt to find the platform. However, EE mice, independently from their genotype, showed a significant reduction in escape latency compared with SE mice. Right: path length to find the platform. A main effect of genotype was found for path length, CX3CR1GFP/GFP swimming longer paths than wt during the acquisition phase. (B) Probe on the fourth day. SE CX3CR1GFP/GFP mice spent an amount of time similar to that spent by EE CX3CR1GFP/GFP mice and significantly longer than that spent by SE wt mice. (C) Probe on the sixth day. All experimental groups spent significantly more time in the quadrant where the platform had been located during training than in the other quadrants. The EE mice showed a better learning performance than SE mice, independently from their genotype. *p < 0.05 vs. both EE wt and SE CX3CR1GFP/GFP mice. #p < 0.05 vs. the other quadrants for each experimental group. Data are mean ± SEM.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
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Figure 3: Morris water maze in wt and CX3CR1GFP/GFP mice exposed to either SE or EE condition. (A) Acquisition. Left: latency to find the platform. All subjects learnt to find the platform. However, EE mice, independently from their genotype, showed a significant reduction in escape latency compared with SE mice. Right: path length to find the platform. A main effect of genotype was found for path length, CX3CR1GFP/GFP swimming longer paths than wt during the acquisition phase. (B) Probe on the fourth day. SE CX3CR1GFP/GFP mice spent an amount of time similar to that spent by EE CX3CR1GFP/GFP mice and significantly longer than that spent by SE wt mice. (C) Probe on the sixth day. All experimental groups spent significantly more time in the quadrant where the platform had been located during training than in the other quadrants. The EE mice showed a better learning performance than SE mice, independently from their genotype. *p < 0.05 vs. both EE wt and SE CX3CR1GFP/GFP mice. #p < 0.05 vs. the other quadrants for each experimental group. Data are mean ± SEM.
Mentions: In the acquisition phase, all mice significantly reduced the latency to find the platform day after day [F(2,48) = 22.379, p < 0.0001]. However, the experimental subjects exposed to EE condition displayed better learning and memory abilities than those exposed to SE, as shown by the significant main effect of the environment [F(1,24) = 9.001, p = 0.0062; Figure 3A, left]. In line with the literature (Tremml et al., 2002; Harris et al., 2009), a reduced thigmotactic behavior in EE compared to SE mice was found [F(1,24) = 6.864, p = 0.0150; data not shown]. This may, at least in part, explain the difference in learning performances among groups shown during acquisition (Wolfer et al., 1998).

Bottom Line: At this aim wt and CX(3)CR1(GFP/GFP) mice were exposed to long-lasting-enriched environment (EE) and the effects on hippocampal functions were studied by electrophysiological recordings of long-term potentiation of synaptic activity, behavioral tests of learning and memory in the Morris water maze paradigm and analysis of neurogenesis in the subgranular zone of the dentate gyrus (DG).We found that CX(3)CR1 deficiency increases hippocampal plasticity and spatial memory, blunting the potentiating effects of EE.These data indicate that CX(3)CL1/CX(3)CR1-mediated signaling is crucial for a normal experience-dependent modulation of hippocampal functions.

View Article: PubMed Central - PubMed

Affiliation: Department of Physiology and Pharmacology, Istituto Pasteur Fondazione Cenci Bolognetti, Università di Roma Rome Italy.

ABSTRACT
In recent years several evidence demonstrated that some features of hippocampal biology, like neurogenesis, synaptic transmission, learning, and memory performances are deeply modulated by social, motor, and sensorial experiences. Fractalkine/CX(3)CL1 is a transmembrane chemokine abundantly expressed in the brain by neurons, where it modulates glutamatergic transmission and long-term plasticity processes regulating the intercellular communication between glia and neurons, being its specific receptor CX(3)CR1 expressed by microglia. In this paper we investigated the role of CX(3)CL1/CX(3)CR1 signaling on experience-dependent hippocampal plasticity processes. At this aim wt and CX(3)CR1(GFP/GFP) mice were exposed to long-lasting-enriched environment (EE) and the effects on hippocampal functions were studied by electrophysiological recordings of long-term potentiation of synaptic activity, behavioral tests of learning and memory in the Morris water maze paradigm and analysis of neurogenesis in the subgranular zone of the dentate gyrus (DG). We found that CX(3)CR1 deficiency increases hippocampal plasticity and spatial memory, blunting the potentiating effects of EE. In contrast, exposure to EE increased the number and migration of neural progenitors in the DG of both wt and CX(3)CR1(GFP/GFP) mice. These data indicate that CX(3)CL1/CX(3)CR1-mediated signaling is crucial for a normal experience-dependent modulation of hippocampal functions.

No MeSH data available.


Related in: MedlinePlus