Abstract
GABA uptake is crucial for the termination of inhibitory synaptic events. In addition, GABA transporters may also control the level of diffusely distributed GABA in the extracellular space. We analysed this function by superfusing rat hippocampal slices with different concentrations of GABA. Whole-cell patch clamp recordings of CA1 pyramidal cells revealed small increases in chloride conductance at 5-10 microM GABA which increased dramatically upon addition of the GABA uptake blocker tiagabine. Tiagabine alone induced a significant chloride conductance indicating that spontaneous release of GABA in hippocampal slices is neutralized by GAT-1, the main hippocampal GABA transporter. Thus, GAT-1 clears the extracellular space in the hippocampus from diffusely distributed GABA with high efficacy.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Carrier Proteins
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Electric Conductivity
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GABA Plasma Membrane Transport Proteins
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Hippocampus / cytology
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Hippocampus / drug effects
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Hippocampus / metabolism*
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Hippocampus / physiology
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In Vitro Techniques
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Membrane Proteins
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Membrane Transport Proteins*
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Neurotransmitter Uptake Inhibitors / pharmacology
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Nipecotic Acids / pharmacology
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Organic Anion Transporters*
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Patch-Clamp Techniques
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Pyramidal Cells / metabolism
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Rats
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Tiagabine
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gamma-Aminobutyric Acid / metabolism*
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gamma-Aminobutyric Acid / pharmacology
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gamma-Aminobutyric Acid / physiology
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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Neurotransmitter Uptake Inhibitors
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Nipecotic Acids
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Organic Anion Transporters
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Slc6a1 protein, rat
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gamma-Aminobutyric Acid
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Tiagabine