G119

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关键词:'G119'

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29th Colloquium, Protides of Biological Fluids null

Allosteric regulation of alpha-amino-3-hydroxy-5-methyl-4-isoxazole-propionate receptors by thiocyanate and cyclothiazide at a common modulatory site distinct from that of 2,3-benzodiazepines.

S D Donevan et al.

Neuroscience, 87(3), 615-629 (1998-10-03)

Allosteric regulators of alpha-amino-3-hydroxy-5-methyl-4-isoxazole-propionate (AMPA) receptors include 2,3-benzodiazepines such as GYKI 52466 and GYKI 53655 and the chaotropic anion thiocyanate that inhibit, and benzothiadiazines such as cyclothiazide that potentiate AMPA receptor currents. Here we sought to determine whether the allosteric

Differential antagonism of alpha-amino-3-hydroxy-5-methyl-4- isoxazolepropionic acid-preferring and kainate-preferring receptors by 2,3-benzodiazepines.

T J Wilding et al.

Molecular pharmacology, 47(3), 582-587 (1995-03-01)

Whole-cell recordings were used to study the antagonism of alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)-preferring and kainate-preferring receptors by 2,3-benzodiazepines. Current through kainate-preferring receptors was recorded in rat dorsal root ganglion (DRG) neuron-s, whereas AMPA receptor current was measured in cultured neurons from

GYKI 52466, a 2,3-benzodiazepine, is a highly selective, noncompetitive antagonist of AMPA/kainate receptor responses.

S D Donevan et al.

Neuron, 10(1), 51-59 (1993-01-01)

In whole-cell voltage-clamp recordings from cultured rat hippocampal neurons, the 2,3-benzodiazepine GYKI 52466 was a potent antagonist of kainate- and AMPA-activated currents (IC50 values, 7.5 and 11 microM, respectively), but was inactive against N-methyl-D-aspartate (NMDA) or gamma-aminobutyric acid responses. The

2013 IEEE International Conference on Solid Dielectrics (ICSD) IEEE null

Glutamatergic mechanisms for speed control and network operation in the rodent locomotor CpG.

Adolfo E Talpalar et al.

Frontiers in neural circuits, 4 (2010-09-17)

Locomotion is a fundamental motor act that, to a large degree, is controlled by central pattern-generating (CPG) networks in the spinal cord. Glutamate is thought to be responsible for most of the excitatory input to and the excitatory activity within

53rd National Meeting of the Italian Society of Biochemistry and Molecular Biology (SIB) and National Meeting of Chemistry of Biological Systems ? Italian Chemical Society (SCI - Section CSB) null

Activation of GluR6-containing kainate receptors induces ubiquitin-dependent Bcl-2 degradation via denitrosylation in the rat hippocampus after kainate treatment.

Jia Zhang et al.

The Journal of biological chemistry, 286(9), 7669-7680 (2010-12-15)

We previously showed that Bcl-2 (B-cell lymphoma 2) is down-regulated in a kainate (KA)-induced rat epileptic seizure model. The underlying mechanism had remained largely unknown, but we here report for the first time that denitrosylation and ubiquitination are involved. Our

Molecular and pharmacological evidence for a facilitatory functional role of pre-synaptic GLUK2/3 kainate receptors on GABA release in rat trigeminal caudal nucleus.

I Samengo et al.

European journal of pain (London, England), 16(8), 1148-1157 (2012-03-07)

Gamma-aminobutyric acid (GABA) and glutamate (GLU) are involved in nociceptive signals processing in the trigeminal system. In this study, we investigated the influence of excitatory transmission on GABA release in nerve terminals isolated from the rat trigeminal caudal nucleus (TCN).

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