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Learning-Induced Gene Expression in the Hippocampus Reveals a Role of Neuron -Astrocyte Metabolic Coupling in Long Term Memory.

Tadi M, Allaman I, Lengacher S, Grenningloh G, Magistretti PJ - PLoS ONE (2015)

Bottom Line: The quantitative determination of mRNA levels revealed learning-induced changes in the expression of genes thought to be involved in astrocyte-neuron metabolic coupling in a time dependent manner.Twenty four hours following IA training, an enhanced gene expression was seen, particularly for genes encoding monocarboxylate transporters 1 and 4 (MCT1, MCT4), alpha2 subunit of the Na/K-ATPase and glucose transporter type 1.Together, these observations indicate that neuron-glia metabolic coupling undergoes metabolic adaptations following learning as indicated by the change in expression of key metabolic genes.

View Article: PubMed Central - PubMed

Affiliation: Brain Mind Institute, Ecole Polytechnique Fédérale de Lausanne (EPFL), Lausanne, Switzerland.

ABSTRACT
We examined the expression of genes related to brain energy metabolism and particularly those encoding glia (astrocyte)-specific functions in the dorsal hippocampus subsequent to learning. Context-dependent avoidance behavior was tested in mice using the step-through Inhibitory Avoidance (IA) paradigm. Animals were sacrificed 3, 9, 24, or 72 hours after training or 3 hours after retention testing. The quantitative determination of mRNA levels revealed learning-induced changes in the expression of genes thought to be involved in astrocyte-neuron metabolic coupling in a time dependent manner. Twenty four hours following IA training, an enhanced gene expression was seen, particularly for genes encoding monocarboxylate transporters 1 and 4 (MCT1, MCT4), alpha2 subunit of the Na/K-ATPase and glucose transporter type 1. To assess the functional role for one of these genes in learning, we studied MCT1 deficient mice and found that they exhibit impaired memory in the inhibitory avoidance task. Together, these observations indicate that neuron-glia metabolic coupling undergoes metabolic adaptations following learning as indicated by the change in expression of key metabolic genes.

No MeSH data available.


Related in: MedlinePlus

Down regulation of MCT1 impairs long term memory in MCT1 +/- heterozygous mice.Step-through latencies were measured during IA training and retention testing (24 hours after the foot shock). Results are shown as mean ± SEM transfer latency responses. Baseline latency did not differ significantly across the two groups (p>0.05). MCT1+/- mice depicted a significantly reduced transfer latency time for the retention trial than the wild-type (WT) littermates (Two-way ANOVA followed by Bonferroni post hoc test; ***P < 0.001, MCT1+/-: n = 14; WT littermates: n = 14).
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pone.0141568.g007: Down regulation of MCT1 impairs long term memory in MCT1 +/- heterozygous mice.Step-through latencies were measured during IA training and retention testing (24 hours after the foot shock). Results are shown as mean ± SEM transfer latency responses. Baseline latency did not differ significantly across the two groups (p>0.05). MCT1+/- mice depicted a significantly reduced transfer latency time for the retention trial than the wild-type (WT) littermates (Two-way ANOVA followed by Bonferroni post hoc test; ***P < 0.001, MCT1+/-: n = 14; WT littermates: n = 14).

Mentions: When tested for context-dependent avoidance behavior, MCT1+/- mice exhibited 4 times lower transfer latencies (19.9 ± 2.3 vs 79.3± 14.3 sec) for retention trial than the controls indicating impairment of long term memory (Fig 7). Two-way ANOVA followed by Bonferroni post hoc test revealed that MCT1+/- mice have significantly lower transfer latency on the retention testing day (P < 0.001) whereas baseline latency to enter the dark chamber did not differ between the two groups (p > 0.05). The above results point to a critical role of MCT1 for long term memory formation.


Learning-Induced Gene Expression in the Hippocampus Reveals a Role of Neuron -Astrocyte Metabolic Coupling in Long Term Memory.

Tadi M, Allaman I, Lengacher S, Grenningloh G, Magistretti PJ - PLoS ONE (2015)

Down regulation of MCT1 impairs long term memory in MCT1 +/- heterozygous mice.Step-through latencies were measured during IA training and retention testing (24 hours after the foot shock). Results are shown as mean ± SEM transfer latency responses. Baseline latency did not differ significantly across the two groups (p>0.05). MCT1+/- mice depicted a significantly reduced transfer latency time for the retention trial than the wild-type (WT) littermates (Two-way ANOVA followed by Bonferroni post hoc test; ***P < 0.001, MCT1+/-: n = 14; WT littermates: n = 14).
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Related In: Results  -  Collection

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getmorefigures.php?uid=PMC4625956&req=5

pone.0141568.g007: Down regulation of MCT1 impairs long term memory in MCT1 +/- heterozygous mice.Step-through latencies were measured during IA training and retention testing (24 hours after the foot shock). Results are shown as mean ± SEM transfer latency responses. Baseline latency did not differ significantly across the two groups (p>0.05). MCT1+/- mice depicted a significantly reduced transfer latency time for the retention trial than the wild-type (WT) littermates (Two-way ANOVA followed by Bonferroni post hoc test; ***P < 0.001, MCT1+/-: n = 14; WT littermates: n = 14).
Mentions: When tested for context-dependent avoidance behavior, MCT1+/- mice exhibited 4 times lower transfer latencies (19.9 ± 2.3 vs 79.3± 14.3 sec) for retention trial than the controls indicating impairment of long term memory (Fig 7). Two-way ANOVA followed by Bonferroni post hoc test revealed that MCT1+/- mice have significantly lower transfer latency on the retention testing day (P < 0.001) whereas baseline latency to enter the dark chamber did not differ between the two groups (p > 0.05). The above results point to a critical role of MCT1 for long term memory formation.

Bottom Line: The quantitative determination of mRNA levels revealed learning-induced changes in the expression of genes thought to be involved in astrocyte-neuron metabolic coupling in a time dependent manner.Twenty four hours following IA training, an enhanced gene expression was seen, particularly for genes encoding monocarboxylate transporters 1 and 4 (MCT1, MCT4), alpha2 subunit of the Na/K-ATPase and glucose transporter type 1.Together, these observations indicate that neuron-glia metabolic coupling undergoes metabolic adaptations following learning as indicated by the change in expression of key metabolic genes.

View Article: PubMed Central - PubMed

Affiliation: Brain Mind Institute, Ecole Polytechnique Fédérale de Lausanne (EPFL), Lausanne, Switzerland.

ABSTRACT
We examined the expression of genes related to brain energy metabolism and particularly those encoding glia (astrocyte)-specific functions in the dorsal hippocampus subsequent to learning. Context-dependent avoidance behavior was tested in mice using the step-through Inhibitory Avoidance (IA) paradigm. Animals were sacrificed 3, 9, 24, or 72 hours after training or 3 hours after retention testing. The quantitative determination of mRNA levels revealed learning-induced changes in the expression of genes thought to be involved in astrocyte-neuron metabolic coupling in a time dependent manner. Twenty four hours following IA training, an enhanced gene expression was seen, particularly for genes encoding monocarboxylate transporters 1 and 4 (MCT1, MCT4), alpha2 subunit of the Na/K-ATPase and glucose transporter type 1. To assess the functional role for one of these genes in learning, we studied MCT1 deficient mice and found that they exhibit impaired memory in the inhibitory avoidance task. Together, these observations indicate that neuron-glia metabolic coupling undergoes metabolic adaptations following learning as indicated by the change in expression of key metabolic genes.

No MeSH data available.


Related in: MedlinePlus