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QX 314 chloride
Membrane impermeable quaternary derivative of lidocaine, a blocker of voltage-activated Na+ channels.
|Storage||Store at RT|
The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis.
Tocris products are intended for laboratory research use only, unless stated otherwise.
|Solvent||Max Conc. mg/mL||Max Conc. mM|
Preparing Stock Solutions
The following data is based on the product molecular weight 298.85. Batch specific molecular weights may vary from batch to batch due to the degree of hydration, which will affect the solvent volumes required to prepare stock solutions.
|Concentration / Solvent Volume / Mass||1 mg||5 mg||10 mg|
|1 mM||3.35 mL||16.73 mL||33.46 mL|
|5 mM||0.67 mL||3.35 mL||6.69 mL|
|10 mM||0.33 mL||1.67 mL||3.35 mL|
|50 mM||0.07 mL||0.33 mL||0.67 mL|
References are publications that support the biological activity of the product.
Stichartz et al (1973) The inhibition of sodium currents in myelinated nerve by quaternary derivatives of lidocaine. J.Gen.Physiol. 62 37 PMID: 4541340
Alreja and Aghajanian (1994) QX-314 blocks the potassium but not the sodium dependent components of the opiate response in locus coeruleus neurons. Brain Res. 639 320 PMID: 8205485
Perkins and Wong (1995) Intracellular QX-314 blocks the hyperpolarization activated inward current Iq in hippocampal CA1 pyramidal cells. J.Neurophysiol. 72 911 PMID: 7760149
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Keywords: QX 314 chloride, QX 314 chloride supplier, Na+, channel, blockers, Sodium, NaV, Channels, voltage-gated, voltage-dependent, QX314, chloride, Voltage-gated, 2313, Tocris Bioscience
9 Citations for QX 314 chloride
Citations are publications that use Tocris products. Selected citations for QX 314 chloride include:
Dong et al (2018) CAST/ELKS Proteins Control Voltage-Gated Ca2+ Channel Density and Synaptic Release Probability at a Mammalian Central Synapse. Cell Rep 24 284 PMID: 29996090
Collins et al (2018) Reciprocal Circuits Linking the Prefrontal Cortex with Dorsal and Ventral Thalamic Nuclei. Neuron 98 366 PMID: 29628187
Bell et al (2015) Acetylcholine release in mouse hippocampal CA1 preferentially activates inhibitory-selective interneurons via α4β2* nicotinic receptor activation. Mol Pain 9 115 PMID: 25918499
Birdsong et al (2019) Synapse-specific opioid modulation of thalamo-cortico-striatal circuits. Elife 8 PMID: 31099753
Wang et al (2006) DArgic control of corticostriatal long-term synaptic depression in medium spiny neurons is mediated by cholinergic interneurons. Neuron 50 443 PMID: 16675398
Arvin et al (2019) Probing nicotinic acetylcholine receptor function in mouse brain slices via laser flash photolysis of photoactivatable nicotine. J Vis Exp 143 e58873 PMID: 30735191
Hull (2017) Measuring Feedforward Inhibition and Its Impact on Local Circuit Function. Cold Spring Harb Protoc 2017 PMID: 28461661
Wood et al (2009) Synaptic circuit abnormalities of motor-frontal layer 2/3 pyramidal neurons in an RNA interference model of methyl-CpG-binding protein 2 deficiency. Front Cell Neurosci 29 12440 PMID: 19812320
Cunningham et al (2014) hPSC-derived maturing GABAergic interneurons ameliorate seizures and abnormal behavior in epileptic mice. Cell Stem Cell 15 559 PMID: 25517465
Do you know of a great paper that uses QX 314 chloride from Tocris? Please let us know.
Reviews for QX 314 chloride
Average Rating: 4.5 (Based on 2 Reviews.)
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In whole cell electrophysiology experiments, we include this in our internal solution to block voltage gated sodium channels. Typically, we use 5-30 mM. Blockade is use-dependent. Drug needs some time and activity to be more effective. Picture is of a putative evoked EPSC in a cell held at +40mV with Qx-314 in internal solution.
Literature in this Area
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Epilepsy is a brain disease that affects 60 million people globally. More than 20 anti-seizure drugs are currently available, but these do not address the underlying causes of the condition. This poster summarizes current knowledge about the development of the condition and highlights some approaches that have disease-modifying effects in proof-of-concept studies.