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MeSH Review

Action Potentials

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Disease relevance of Action Potentials

  • We propose that enhancement of BK channels in vivo leads to increased excitability by inducing rapid repolarization of action potentials, resulting in generalized epilepsy and paroxysmal dyskinesia by allowing neurons to fire at a faster rate [1].
  • Excessive prolongation of the action potential at low heart rates predisposes individuals with LQT3 to fatal arrhythmias, typically at rest or during sleep [2].
  • Our results suggest that Ca2+ entry into a ganglion cell during repeated action potentials initiates a long-lasting mechanism for the enhancement of a nicotinic ACh action on the subsynaptic membrane [3].
  • Our results suggest that intracellular lactate may play a significant role in activating cardiac ATP-sensitive potassium channels and shortening action potential duration even at ATP levels similar to those resulting from moderate to severe myocardial ischemia [4].
  • To investigate the potential action of antacids on prednisone absorption and on prednisolone serum levels, we studied 5 healthy volunteers and 12 patients with chronic active liver disease [5].

Psychiatry related information on Action Potentials

  • Trimebutine, given during phases I and II of the migratory motor complex, was followed by a period of regular spike potentials and contractions; the increased motor activity was significantly greater when the drug was given during phase II [6].
  • Additional experiments were done in which we superfused PF from adult and old animals with O for long periods to determine the time-response relationships for ouabain effects on maximum diastolic potential, action potential amplitude, Vmax and APD50 [7].
  • The PSNs recorded in this study exhibited: (1) progressive decrease in discharge rate from waking to NREM to REM sleep; (2) long action potential duration, and (3) reduction of discharge rate after systemic administration of a selective 5-HT(1A) agonist, (+/-)-8-hydroxy-2-(di-n-propylamino) tetralin hydrobromide (8-OH-DPAT) [8].

High impact information on Action Potentials

  • In different regions of the heart, action potential waveforms are distinct, owing to differences in Na(+), Ca(2+), and K(+) channel expression, and these differences contribute to the normal, unidirectional propagation of activity and to the generation of normal cardiac rhythms [9].
  • An electrophysiological classification of the AV nodal area, based on transmembrane action potential characteristics during various imposed atrial rhythms (rapid pacing, trains of premature impulses), into AN (including ANCO and ANL), N, and NH zones has been described by various authors for the rabbit heart [10].
  • An agrin fragment that acts as a competitive antagonist depresses action potential frequency, showing that endogenous agrin regulates native alpha3NKA function [11].
  • Thus, MiRP2-Kv3.4 channels set resting membrane potential (RMP) and do not produce afterhyperpolarization or cumulative inactivation to limit action potential frequency [12].
  • napts is a recessive mutation that affects the level of sodium channel activity and, at high temperature, causes paralysis associated with a loss of action potentials [13].

Chemical compound and disease context of Action Potentials

  • The present study was performed to examine the influence of isoproterenol on the genesis of EADs and on the action potential durations and QTU intervals in patients with congenital long QT syndrome [14].
  • A highly significant correlation was demonstrated between the amplitude of the epicardial action potential notch and the amplitude of the J wave recorded during interventions that alter the appearance of the electrocardiographic J wave, including hypothermia, premature stimulation, and block of the transient outward current by 4-aminopyridine [15].
  • The study suggests that sotalol can provide effective prophylaxis against sustained ventricular tachycardia; this prophylactic efficacy is not typical for pure beta-adrenergic antagonism but may at least partly result from experimentally observed prolongation of the ventricular action potential duration [16].
  • BACKGROUND: The activation of ATP-sensitive K+ (K+ ATP) channels by K+ ATP openers, eg, pinacidil, hypoxia, and ischemia, is known to shorten the ventricular action potential [17].
  • Hyperkalemia produced a bradycardia-dependent and slight reduction in action potential duration and antagonized the action potential-prolonging effect of procainamide, particularly at shorter cycle lengths [18].

Biological context of Action Potentials


Anatomical context of Action Potentials


Associations of Action Potentials with chemical compounds

  • Broadening the presynaptic action potential with the potassium-channel blocker tetraethylammonium, which increases Ca2+ entry, further enhances the rate of replenishment [29].
  • Leptin increases the frequency of action potentials in the anorexigenic POMC neurons by two mechanisms: depolarization through a nonspecific cation channel; and reduced inhibition by local orexigenic neuropeptide-Y/GABA (gamma-aminobutyric acid) neurons [30].
  • Like 5-HT, dopamine causes a reduction of the afterhyperpolarization, but in this case it is due to a reduction of calcium entry during the action potential, which results in a reduced activation of KCa [31].
  • The amplitude of spine NMDA-receptor-mediated [Ca2+] transients (and the synaptic plasticity which depends on this) may thus be sensitive to the number of quanta released by a burst of action potentials and to changes in the concentration profile of glutamate in the synaptic cleft [32].
  • Glucose competence allows membrane depolarization, the generation of action potentials, and Ca2+ influx, events that are known to trigger insulin secretion [33].

Gene context of Action Potentials

  • Sodium currents and action potentials were characterized in Purkinje neurons from ataxic mice lacking expression of the sodium channel Scn8a [34].
  • We found that Hcrt cells have broad action potentials with elongated later positive deflections that distinguish them from adjacent antidromically identified cells [35].
  • The mle(napts) mutation causes temperature-dependent blockade of action potentials resulting from decreased abundance of para-encoded Na+ channels [36].
  • I propose a new hypothesis for the potential action or function of the NPC1 protein in the endosome [37].
  • Semi-dominant, gain-of-function mutations in egl-19 cause myotonia: mutant muscle action potentials are prolonged and the relaxation delayed [38].

Analytical, diagnostic and therapeutic context of Action Potentials


  1. Calcium-sensitive potassium channelopathy in human epilepsy and paroxysmal movement disorder. Du, W., Bautista, J.F., Yang, H., Diez-Sampedro, A., You, S.A., Wang, L., Kotagal, P., Lüders, H.O., Shi, J., Cui, J., Richerson, G.B., Wang, Q.K. Nat. Genet. (2005) [Pubmed]
  2. Abrupt rate accelerations or premature beats cause life-threatening arrhythmias in mice with long-QT3 syndrome. Nuyens, D., Stengl, M., Dugarmaa, S., Rossenbacker, T., Compernolle, V., Rudy, Y., Smits, J.F., Flameng, W., Clancy, C.E., Moons, L., Vos, M.A., Dewerchin, M., Benndorf, K., Collen, D., Carmeliet, E., Carmeliet, P. Nat. Med. (2001) [Pubmed]
  3. Sustained rise in ACh sensitivity of a sympathetic ganglion cell induced by postsynaptic electrical activities. Kumamoto, E., Kuba, K. Nature (1983) [Pubmed]
  4. Lactate activates ATP-sensitive potassium channels in guinea pig ventricular myocytes. Keung, E.C., Li, Q. J. Clin. Invest. (1991) [Pubmed]
  5. Decreased bioavailability of prednisone due to antacids in patients with chronic active liver disease and in healthy volunteers. Uribe, M., Casian, C., Rojas, S., Sierra, J.G., Go, V.L. Gastroenterology (1981) [Pubmed]
  6. Short report: effect of two prokinetic drugs on the electrical and motor activity of the small bowel in dogs. Defilippi, C., Gomez, E. Aliment. Pharmacol. Ther. (1993) [Pubmed]
  7. Senescence-related changes in the responsiveness to ouabain of canine Purkinje fibers. Hewett, K., Vulliemoz, Y., Rosen, M.R. J. Pharmacol. Exp. Ther. (1982) [Pubmed]
  8. Discharge modulation of rat dorsal raphe neurons during sleep and waking: effects of preoptic/basal forebrain warming. Guzmán-Marín, R., Alam, M.N., Szymusiak, R., Drucker-Colín, R., Gong, H., McGinty, D. Brain Res. (2000) [Pubmed]
  9. Molecular physiology of cardiac repolarization. Nerbonne, J.M., Kass, R.S. Physiol. Rev. (2005) [Pubmed]
  10. Morphology and electrophysiology of the mammalian atrioventricular node. Meijler, F.L., Janse, M.J. Physiol. Rev. (1988) [Pubmed]
  11. Alpha3Na+/K+-ATPase is a neuronal receptor for agrin. Hilgenberg, L.G., Su, H., Gu, H., O'Dowd, D.K., Smith, M.A. Cell (2006) [Pubmed]
  12. MiRP2 forms potassium channels in skeletal muscle with Kv3.4 and is associated with periodic paralysis. Abbott, G.W., Butler, M.H., Bendahhou, S., Dalakas, M.C., Ptacek, L.J., Goldstein, S.A. Cell (2001) [Pubmed]
  13. napts, a mutation affecting sodium channel activity in Drosophila, is an allele of mle, a regulator of X chromosome transcription. Kernan, M.J., Kuroda, M.I., Kreber, R., Baker, B.S., Ganetzky, B. Cell (1991) [Pubmed]
  14. Early afterdepolarizations induced by isoproterenol in patients with congenital long QT syndrome. Shimizu, W., Ohe, T., Kurita, T., Takaki, H., Aihara, N., Kamakura, S., Matsuhisa, M., Shimomura, K. Circulation (1991) [Pubmed]
  15. Cellular basis for the electrocardiographic J wave. Yan, G.X., Antzelevitch, C. Circulation (1996) [Pubmed]
  16. Electrophysiologic testing in assessment of therapy with sotalol for sustained ventricular tachycardia. Senges, J., Lengfelder, W., Jauernig, R., Czygan, E., Brachmann, J., Rizos, I., Cobbe, S., Kübler, W. Circulation (1984) [Pubmed]
  17. Endogenous adenosine does not activate ATP-sensitive potassium channels in the hypoxic guinea pig ventricle in vivo. Xu, J., Wang, L., Hurt, C.M., Pelleg, A. Circulation (1994) [Pubmed]
  18. Modulation of procainamide's effect on cardiac conduction in dogs by extracellular potassium concentration. A quantitative analysis. Villemaire, C., Nattel, S. Circulation (1994) [Pubmed]
  19. NMDA receptors regulate developmental gap junction uncoupling via CREB signaling. Arumugam, H., Liu, X., Colombo, P.J., Corriveau, R.A., Belousov, A.B. Nat. Neurosci. (2005) [Pubmed]
  20. The actions of synaptically released zinc at hippocampal mossy fiber synapses. Vogt, K., Mellor, J., Tong, G., Nicoll, R. Neuron (2000) [Pubmed]
  21. Effect of angiotensin-converting-enzyme (ACE) inhibitor trandolapril on human diabetic neuropathy: randomised double-blind controlled trial. Malik, R.A., Williamson, S., Abbott, C., Carrington, A.L., Iqbal, J., Schady, W., Boulton, A.J. Lancet (1998) [Pubmed]
  22. Dendritic K+ channels contribute to spike-timing dependent long-term potentiation in hippocampal pyramidal neurons. Watanabe, S., Hoffman, D.A., Migliore, M., Johnston, D. Proc. Natl. Acad. Sci. U.S.A. (2002) [Pubmed]
  23. Role of the conserved WHXL motif in the C terminus of synaptotagmin in synaptic vesicle docking. Fukuda, M., Moreira, J.E., Liu, V., Sugimori, M., Mikoshiba, K., Llinás, R.R. Proc. Natl. Acad. Sci. U.S.A. (2000) [Pubmed]
  24. Injection of subunits of cyclic AMP-dependent protein kinase into cardiac myocytes modulates Ca2+ current. Osterrieder, W., Brum, G., Hescheler, J., Trautwein, W., Flockerzi, V., Hofmann, F. Nature (1982) [Pubmed]
  25. Glutamate locally activates dendritic outputs of thalamic interneurons. Cox, C.L., Zhou, Q., Sherman, S.M. Nature (1998) [Pubmed]
  26. Imidazole inhibits a temperature-dependent component of mammalial skeletal muscle action potential. Cheung, D.W., Daniel, E.E. Nature (1980) [Pubmed]
  27. RNA synthesis dependence of action potential development in spinal cord neurones. O'Dowd, D.K. Nature (1983) [Pubmed]
  28. Dopamine inhibition of action potentials in a prolactin secreting cell line is modulated by oestrogen. Dufy, B., Vincent, J.D., Fleury, H., Du Pasquier, P., Gourdji, D., Tixier-Vidal, A. Nature (1979) [Pubmed]
  29. High-frequency firing helps replenish the readily releasable pool of synaptic vesicles. Wang, L.Y., Kaczmarek, L.K. Nature (1998) [Pubmed]
  30. Leptin activates anorexigenic POMC neurons through a neural network in the arcuate nucleus. Cowley, M.A., Smart, J.L., Rubinstein, M., Cerdán, M.G., Diano, S., Horvath, T.L., Cone, R.D., Low, M.J. Nature (2001) [Pubmed]
  31. Control of lamprey locomotor neurons by colocalized monoamine transmitters. Schotland, J., Shupliakov, O., Wikström, M., Brodin, L., Srinivasan, M., You, Z.B., Herrera-Marschitz, M., Zhang, W., Hökfelt, T., Grillner, S. Nature (1995) [Pubmed]
  32. Synaptic calcium transients in single spines indicate that NMDA receptors are not saturated. Mainen, Z.F., Malinow, R., Svoboda, K. Nature (1999) [Pubmed]
  33. Pancreatic beta-cells are rendered glucose-competent by the insulinotropic hormone glucagon-like peptide-1(7-37). Holz, G.G., Kühtreiber, W.M., Habener, J.F. Nature (1993) [Pubmed]
  34. Altered subthreshold sodium currents and disrupted firing patterns in Purkinje neurons of Scn8a mutant mice. Raman, I.M., Sprunger, L.K., Meisler, M.H., Bean, B.P. Neuron (1997) [Pubmed]
  35. Behavioral correlates of activity in identified hypocretin/orexin neurons. Mileykovskiy, B.Y., Kiyashchenko, L.I., Siegel, J.M. Neuron (2005) [Pubmed]
  36. The mle(napts) RNA helicase mutation in drosophila results in a splicing catastrophe of the para Na+ channel transcript in a region of RNA editing. Reenan, R.A., Hanrahan, C.J., Barry, G. Neuron (2000) [Pubmed]
  37. Guilty until proven innocent: the case of NPC1 and cholesterol. Ioannou, Y.A. Trends Biochem. Sci. (2005) [Pubmed]
  38. Mutations in the alpha1 subunit of an L-type voltage-activated Ca2+ channel cause myotonia in Caenorhabditis elegans. Lee, R.Y., Lobel, L., Hengartner, M., Horvitz, H.R., Avery, L. EMBO J. (1997) [Pubmed]
  39. GluR5 kainate receptor activation in interneurons increases tonic inhibition of pyramidal cells. Cossart, R., Esclapez, M., Hirsch, J.C., Bernard, C., Ben-Ari, Y. Nat. Neurosci. (1998) [Pubmed]
  40. Neural regulation of acetylcholinesterase mRNAs at mammalian neuromuscular synapses. Michel, R.N., Vu, C.Q., Tetzlaff, W., Jasmin, B.J. J. Cell Biol. (1994) [Pubmed]
  41. Primary T wave abnormalities caused by uniform and regional shortening of ventricular monophasic action potential in dog. Autenrieth, G., Surawicz, B., Kuo, C.S., Arita, M. Circulation (1975) [Pubmed]
  42. Microinjection of catalytic subunit of cyclic AMP-dependent protein kinase enhances calcium action potentials of bag cell neurons in cell culture. Kaczmarek, L.K., Jennings, K.R., Strumwasser, F., Nairn, A.C., Walter, U., Wilson, F.D., Greengard, P. Proc. Natl. Acad. Sci. U.S.A. (1980) [Pubmed]
  43. Cellular basis for the negative dromotropic effect of adenosine on rabbit single atrioventricular nodal cells. Wang, D., Shryock, J.C., Belardinelli, L. Circ. Res. (1996) [Pubmed]
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