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QX 314 bromide is a membrane impermeable quaternary derivative of lidocaine, a blocker of voltage-activated Na+ channels. Intracellular QX 314 bromide also inhibits calcium currents in hippocampal CA1 pyramidal neurons.
|Storage||Desiccate 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|
The following data is based on the product molecular weight 343.31. 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||2.91 mL||14.56 mL||29.13 mL|
|5 mM||0.58 mL||2.91 mL||5.83 mL|
|10 mM||0.29 mL||1.46 mL||2.91 mL|
|50 mM||0.06 mL||0.29 mL||0.58 mL|
References are publications that support the biological activity of the product.
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
Stichartz et al (1973) The inhibition of sodium currents in myelinated nerve by quaternary derivatives of lidocaine. J.Gen.Physiol. 62 37 PMID: 4541340
Perkins and Wong (1995) Intracellular QX-314 blocks the hyperpolarization activated inward current Iq in hippocampal CA1 pyramidal cells. J.Neurophysiol. 73 911 PMID: 7760149
Talbot and Sayer (1996) Intracellular QX-314 inhibits calcium currents in hippocampal CA1 pyramidal neurons. J.Neurophysiol. 76 2120 PMID: 8890325
If you know of a relevant reference for QX 314 bromide, please let us know.
Keywords: QX 314 bromide, QX 314 bromide supplier, Na+, channel, blockers, Sodium, NaV, Channels, voltage-gated, voltage-dependent, QX314, bromide, Voltage-gated, 1014, Tocris Bioscience
Citations are publications that use Tocris products. Selected citations for QX 314 bromide include:
Chuhma et al (2014) DA neurons control striatal cholinergic neurons via regionally heterogeneous DA and glutamate signaling. Proc Natl Acad Sci U S A 81 901 PMID: 24559678
Kuroyanagi et al (2009) Postsynaptic glutamate receptor δ family contributes to presynaptic terminal differentiation and establishment of synaptic transmission. J Neurophysiol 106 4912 PMID: 19258455
Purkey et al (2018) AKAP150 Palmitoylation Regulates Synaptic Incorporation of Ca2+-Permeable AMPA Receptors to Control LTP. Cell Rep 25 974 PMID: 30355502
Sametsky et al (2015) Enhanced GABAA-Mediated Tonic Inhibition in Auditory Thalamus of Rats with Behavioral Evidence of Tinnitus. J Neurosci 35 9369 PMID: 26109660
Xue et al (2015) Structural elements that underlie Doc2β function during asynchronous synaptic transmission. Proc Natl Acad Sci U S A 112 E4316 PMID: 26195798
McGee et al (2015) Auxiliary Subunit GSG1L Acts to Suppress Calcium-Permeable AMPA Receptor Function. J Neurosci 35 16171 PMID: 26658868
Dale et al (2014) Vort. disinhibits pyramidal cell function and enhances synaptic plasticity in the rat hippocampus. J Psychopharmacol 28 891 PMID: 25122043
Gaffaney et al (2014) Mutations that disrupt Ca2+-binding activity endow Doc2β with novel functional properties during synaptic transmission. Mol Biol Cell 25 481 PMID: 24356452
Hong et al (2008) Glutamatergic transmission is sustained at a later period of development of medial nucleus of the trapezoid body-lateral superior olive synapses in circling mice. J Neurosci 28 13003 PMID: 19036993
He et al (2020) Nucleus Accumbens Tac1-Expressing Neurons Mediate Stress-Induced Anhedonia-like Behavior in Mice Cell rep 33 PMID: 33147466
He et al (2013) Synaptic and extrasynaptic plasticity in glutamatergic circuits involving dentate granule cells following chronic N-MthD.-aspartate receptor inhibition. J Neurosci 109 1535 PMID: 23255721
Zhang et al (2008) Resveratrol attenuates early pyramidal neuron excitability impairment and death in acute rat hippocampal slices caused by oxygen-glucose deprivation. Exp Neurol 212 44 PMID: 18495119
Ferrarese et al (2018) Dendrite-Specific Amplification of Weak Synaptic Input during Network Activity In Vivo. Cell Rep 24 3455 PMID: 30257207
He and Bausch (2014) Synaptic plasticity in glutamatergic and GABAergic neurotransmission following chronic Mem. treatment in an in vitro model of limbic epileptogenesis. BMC Neurosci 77 379 PMID: 24184417
Toyoda et al (2007) Requirement of extracellular signal-regulated kinase/mitogen-activated protein kinase for long-term potentiation in adult mouse anterior cingulate cortex. Mol Pain 3 36 PMID: 18053155
Gipson and Yeckel (2007) Coincident glutamatergic and cholinergic inputs transiently depress glutamate release at rat schaffer collateral synapses. J Neurophysiol 97 4108 PMID: 17303811
Baldelli et al (2007) Lack of synapsin I reduces the readily releasable pool of synaptic vesicles at central inhibitory synapses. J Neurosci 27 13520 PMID: 18057210
Li et al (2019) TMEM16B regulates anxiety-related behavior and GABAergic neuronal signaling in the central lateral amygdala. Elife 8 PMID: 31482844
Acuña et al (2016) Phosphorylation state-dependent modulation of spinal glycine receptors alleviates inflammatory pain. J Clin Invest 126 2547 PMID: 27270175
Linnemann et al (2006) Transient change in GABA(A) receptor subunit mRNA expression in Lurcher cerebellar nuclei during Purkinje cell degeneration. Neuron 7 59 PMID: 16872511
Xu et al (2006) Presynaptic regulation of the inhibitory transmission by GluR5-containing kainate receptors in spinal substantia gelatinosa. Mol Pain 2 29 PMID: 16948848
Spoljaric et al (2019) KCC2-Mediated Cl- Extrusion Modulates Spontaneous Hippocampal Network Events in Perinatal Rats and Mice. Cell Rep 26 1073 PMID: 30699338
Puranam et al (2015) Disruption of Fgf13 causes synaptic excitatory-inhibitory imbalance and genetic epilepsy and febrile seizures plus. Korean J Physiol Pharmacol 35 8866 PMID: 26063919
Ahn et al (2015) Characteristics of K(+) Outward Currents in the Cochlear Outer Hair Cells of Circling Mice within the First Postnatal Week. PLoS One 19 383 PMID: 26170743
Lench et al (2015) Differential Effects of D-Cycloserine and ACBC at NMDA Receptors in the Rat Entorhinal Cortex Are Related to Efficacy at the Co-Agonist Binding Site. Toxins (Basel) 10 e0133548 PMID: 26193112
Egawa et al (2013) Optogenetic probing and manipulation of the calyx-type presynaptic terminal in the embryonic chick ciliary ganglion. PLoS One 8 e59179 PMID: 23555628
Wu et al (2013) Ovarian hormone loss impairs excitatory synaptic transmission at hippocampal CA3-CA1 synapses. J Neurosci 33 16158 PMID: 24107948
Lerner et al (2010) Endocannabinoid signaling mediates psychomotor activation by adenosine A2A antagonists. J Neurosci 30 2160 PMID: 20147543
Zhang et al (2009) Tamox. mediated estrogen receptor activation protects against early impairment of hippocampal neuron excitability in an oxygen/glucose deprivation brain slice ischemia model. Brain Res 1247 196 PMID: 18992727
Chen and Chesler (2015) Autocrine boost of NMDAR current in hippocampal CA1 pyramidal neurons by a PMCA-dependent, perisynaptic, extracellular pH shift. J Neurosci 35 873 PMID: 25609607
Toyoda et al (2009) Roles of the AMPA receptor subunit GluA1 but not GluA2 in synaptic potentiation and activation of ERK in the anterior cingulate cortex. Mol Pain 5 46 PMID: 19664265
Sur et al (2003) N-desmethylclozapine, an allosteric agonist at muscarinic 1 receptor, potentiates N-MthD.-aspartate receptor activity. Proc Natl Acad Sci U S A 100 13674 PMID: 14595031
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QX-314 was used to block voltage-gated sodium channels, i.e. prevent action potential propagation. The compound develops its effect in 1 microM concentration, in use-dependent mode. Figure: EPSC evoked by electrical stimulation in hippocampal pyramidal neuron at positive membrane potential (+40 mV); QX-314 is added to intracellular solution.
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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.