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CGP 56999A

Known as: CGP-56999A, CGP56999A 
 
National Institutes of Health

Papers overview

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2012
2012
In a previous study, we reported a rat model of early-life limbic seizures which resulted in a loss of GABA(B) receptor… Expand
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2010
2010
Whether seizures in the developing brain cause long-term changes in the mature brain has been debated. We tested the hypothesis… Expand
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2008
2008
Paired-pulse depression (PPD), a short-term neural plasticity, was studied in hippocampal CA1 of urethane-anesthetized rats in… Expand
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2006
2006
Spike backpropagation has been proposed to enhance dendritic depolarization and synaptic plasticity. However, relatively little… Expand
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2003
2003
γ-Hydroxybutyrate (GHB) naturally occurs in the brain, but its exogenous administration induces profound effects on the central… Expand
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2003
2003
gamma-Hydroxybutyrate (GHB) naturally occurs in the brain, but its exogenous administration induces profound effects on the… Expand
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2002
2002
The expression of secretogranin-II and its major proteolytic product secretoneurin (SN) is under the control of neuronal… Expand
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2000
2000
In this study we show that single, physiologically-active and non-convulsive doses of the three GABA(B) receptor antagonists CGP… Expand
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1997
1997
CGP 56999A ([3-[1-(R)-[(3-cyclohexylmethyl)hydroxyphosphinyl]-2-(S)- hydroxy-propyl] amino]ethyl]-benzoic acid) is a potent GABAB… Expand
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1996
1996
1. The effects of various GABA receptor ligands on the electrically-evoked release of endogenous GABA, glutamate and substance P… Expand
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