Abstract
There is increasing evidence that GABAergic system plays an important role in the neural control of learning and memory processes. GAT1 over-expressing mice (NA) were generated, in which GAT1 is under the control of a neuron-specific enolase (NSE) promoter, to investigate effects of GABA transporter on cognitive function. Our results revealed that NA mice displayed cognitive deterioration in associative learning ability and new object recognition retention, compared with the wild-type littermates (WT2). However, the impaired cognitive function of transgenic mice could be rescued after chronic administration of GAT1 selective inhibitor for 6 days. In addition, there was no change of the expression of NMDA receptors in NA mice. Taken together, we show a potentially important role for GAT1 in the neural control of cognitive processes, and indicate great potential for GAT1 as a clinical target of cognitive disorders.
Publication types
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Comparative Study
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Avoidance Learning / physiology
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Carrier Proteins / biosynthesis*
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Carrier Proteins / genetics*
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Cerebral Cortex / metabolism
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Cognition Disorders / genetics
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Cognition Disorders / metabolism*
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GABA Plasma Membrane Transport Proteins
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Gene Expression Regulation / physiology*
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Hippocampus / metabolism
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Membrane Proteins / biosynthesis*
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Membrane Proteins / genetics*
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Membrane Transport Proteins*
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Mice
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Mice, Inbred C57BL
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Mice, Transgenic
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Organic Anion Transporters*
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Phosphopyruvate Hydratase / biosynthesis
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Phosphopyruvate Hydratase / genetics
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Receptors, N-Methyl-D-Aspartate / biosynthesis
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Receptors, N-Methyl-D-Aspartate / genetics
Substances
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Carrier Proteins
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GABA Plasma Membrane Transport Proteins
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Membrane Proteins
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Membrane Transport Proteins
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Organic Anion Transporters
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Receptors, N-Methyl-D-Aspartate
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Slc6a1 protein, mouse
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Phosphopyruvate Hydratase