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Chemical Compound Review

Lopac-L-1788     (2,6-dimethylphenyl) carbamoylmethyl...

Synonyms: Tocris-1043, CCG-204792, Lopac0_000707, AC1Q5LWK, AR-1D5488, ...
 
 
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Disease relevance of QX-222

 

High impact information on QX-222

  • The binding site for an open-channel blocker, QX-222, at mouse muscle nicotinic acetylcholine receptors was probed using site-directed mutagenesis, oocyte expression, and electrophysiological analysis [2].
  • The proposed cytoplasmic end of the M2 transmembrane helix is termed position 1'. At position 10' (alpha S252, beta T263, gamma A261, delta A266), Ala residues yield stronger and longer binding of QX-222 than Ser or Thr residues [2].
  • Spontaneous and evoked action potentials were blocked by TTX or by intracellular injection of a local anesthetic, QX-222 [3].
  • We conclude that ether and QX-222 do not compete for a common binding site [4].
  • We report measurement of the gating currents of Na channels in canine cardiac Purkinje cells in the absence and presence of QX-222, a quaternary derivative of lidocaine, applied intracellularly, and benzocaine, a neutral local anesthetic [5].
 

Biological context of QX-222

  • 7. Raising QX-222 concentration, at any given membrane potential, augments I1(0) and I3(0) at the expense of I2(0) [6].
  • It is hypothesized that the second component in QX-222 represents currents of unaltered or normal conductance kinetics, and that the first and third components in QX-222, as well as the major component and tail in QX-314, represent current of "QX-altered conductance kinetics" [6].
  • Reversibility of Ia EPSP investigated with intracellularly iontophoresed QX-222 [7].
  • 2 QX-222 and procaine, applied to the extracellular surface, reversibly inhibited the peak amplitude of the whole-cell nicotinic ACh-evoked current in a concentration-dependent manner, with half-maximal inhibitory concentrations (IC50) of 28 microM and 2.8 microM, respectively, at -80 mV [8].
  • We have been examining the interaction of a local anesthetic derivative, QX-222, with the ion channel pore of the muscle AChR, using a combination of mutagenesis, oocyte expression, and electrophysiology [9].
 

Anatomical context of QX-222

  • For Xenopus myocyte cholinergic receptors, examples of the use of this method are given for several concentration-dependent reactions including blockade by the local anesthetic QX-222, activation by acetylcholine, and modulation of current amplitude by sodium ions [10].
 

Associations of QX-222 with other chemical compounds

 

Analytical, diagnostic and therapeutic context of QX-222

  • Both agents totally blocked AP generation without decreasing the magnitude of the Ia e.p.s.p. It is suggested that intracellularly iontophoresed QX-222 (on account of its low lipid solubility) could be used as a pharmacological tool to block specifically the active Na and channels in only the cell impaled by the microelectrodes [12].
  • 3. Intracellular iontophoresis of QX-222 (a trimethyl analogue of lignocaine) or methylxylocholine, prevented action-potential generation and reduced the GM increase during current depolarization so that positive levels of EM could be reached [7].

References

  1. Differential blockade of nerve injury-induced thermal and tactile hypersensitivity by systemically administered brain-penetrating and peripherally restricted local anesthetics. Chen, Q., King, T., Vanderah, T.W., Ossipov, M.H., Malan, T.P., Lai, J., Porreca, F. The journal of pain : official journal of the American Pain Society. (2004) [Pubmed]
  2. An open-channel blocker interacts with adjacent turns of alpha-helices in the nicotinic acetylcholine receptor. Charnet, P., Labarca, C., Leonard, R.J., Vogelaar, N.J., Czyzyk, L., Gouin, A., Davidson, N., Lester, H.A. Neuron (1990) [Pubmed]
  3. Electrophysiological properties of neuroendocrine cells of the intact rat pars intermedia: multiple calcium currents. Williams, P.J., MacVicar, B.A., Pittman, Q.J. J. Neurosci. (1990) [Pubmed]
  4. Cooperative interactions between general anesthetics and QX-222 within the pore of the acetylcholine receptor ion channel. Dilger, J.P., Vidal, A.M. Mol. Pharmacol. (1994) [Pubmed]
  5. Kinetic effects of quaternary lidocaine block of cardiac sodium channels: a gating current study. Hanck, D.A., Makielski, J.C., Sheets, M.F. J. Gen. Physiol. (1994) [Pubmed]
  6. A voltage-clamp study of the effect of two lidocaine derivatives on the time course of end-plate currents. Beam, K.G. J. Physiol. (Lond.) (1976) [Pubmed]
  7. Reversibility of Ia EPSP investigated with intracellularly iontophoresed QX-222. Flatman, J.A., Engberg, I., Lambert, J.D. J. Neurophysiol. (1982) [Pubmed]
  8. Local anaesthetic blockade of neuronal nicotinic ACh receptor-channels in rat parasympathetic ganglion cells. Cuevas, J., Adams, D.J. Br. J. Pharmacol. (1994) [Pubmed]
  9. Reverse pharmacology of the nicotinic acetylcholine receptor. Mapping the local anesthetic binding site. Leonard, R.J., Charnet, P., Labarca, C., Vogelaar, N.J., Czyzyk, L., Gouin, A., Davidson, N., Lester, H.A. Ann. N. Y. Acad. Sci. (1991) [Pubmed]
  10. Single-channel dose-response studies in single, cell-attached patches. Auerbach, A. Biophys. J. (1991) [Pubmed]
  11. Attenuation of glutamate-action, excitatory postsynaptic potentials, and spikes by intracellular QX 222 in hippocampal neurons. Puil, E., Carlen, P.L. Neuroscience (1984) [Pubmed]
  12. The response of cat spinal motoneurones to the intracellular application of agents with local anaesthetic action. Engberg, I., Flatman, J.A., Lambert, J.D. Br. J. Pharmacol. (1984) [Pubmed]
 
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