Neurophysiology

, Volume 39, Issue 3, pp 237–241

Sucrose-gap technique: Advantages and limitations

Article

Abstract

The sucrose-gap technique has been widely used as a convenient tool for recording of the membrane activities from myelinated or unmyelinated nerves and muscle preparations (such as smooth and cardiac muscles). The quantitative measurements of membrane and action potentials in preparations with electrical coupling between their compartments are made much easier by this technique; the recorded potentials are rather similar to those recorded with a microelectrode. Recording of the membrane activities is of great value to experimenters studying the nervous system due to the simplicity and ease of use of this technique and the broad spectrum of sensitivity to agents influencing the electrical activity. This paper is focused on the set-up procedure and operation of the sucrose-gap technique, which provides an inexpensive, practical, and effective method for the investigation of the effects of drugs on the membrane activities of nerves and muscles in vitro.

Keywords

action potentials membrane potential sucrose-gap technique nerves muscles 

Preview

Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.

References

  1. 1.
    B. Hille, Ionic Channels of Excitable Membranes, Sinauer Associates, Inc., Sunderland, Mass. (2001).Google Scholar
  2. 2.
    S. G. Waxman and J. M. Ritchie, “Molecular dissection of the myelinated axon,” Ann. Neurol., 33, 121–136 (1993).PubMedCrossRefGoogle Scholar
  3. 3.
    P. Jirounek, E. Chardonnens, and P. C. Brunet, “Afterpotentials in non-myelinated nerve fibers,” J. Neurophysiol., 65, 860–873 (1991).PubMedGoogle Scholar
  4. 4.
    P. K. Stys and J. D. Kocsis, “Electrophysiological approaches to the study of axons,” in: The Axon: Structure, Function and Pathophysiology, S. G. Waxman, J. D. Kocsis, and P. R. Stys (eds.), Oxford Univ. Press, New York (1995), pp. 328–340.Google Scholar
  5. 5.
    T. Mert, Y. Gunes, M. Guven, et al., “Comparison of nerve conduction blocks by an opioid and a local anesthetic,” Eur. J. Pharmacol., 439, 77–81 (2002).PubMedCrossRefGoogle Scholar
  6. 6.
    J. Sakai, O. Honmou, J. D. Kocsis, and K. Hashi, “The delayed depolarization in rat cutaneous afferent axons is reduced following nerve transection and ligation, but not crush: implications for injury-induced axonal Na channel reorganization,” Muscle Nerve, 21, 1040–1047 (1998).PubMedCrossRefGoogle Scholar
  7. 7.
    S. L. Son, K. Wong, and G. Strichartz, “Antagonism by local anesthetics of sodium channel activators in the presence of scorpion toxins: Two mechanisms for competitive inhibition,” Cell Mol. Neurobiol., 24, 565–577 (2004).PubMedCrossRefGoogle Scholar
  8. 8.
    R. Shi, T. Asano, C. N. Vining, and A. R. Blight, “Control of membrane sealing in injured mammalian spinal cord axons,” J. Neurophysiol., 84, 1763–1769 (2000).PubMedGoogle Scholar
  9. 9.
    F. J. Julian, J. W. Moore, and D. E. Goldman, “Membrane potentials of the lobster giant axon obtained by use of the sucrose-gap technique,” J. Gen. Physiol., 45, 1195–1216 (1962).PubMedCrossRefGoogle Scholar
  10. 10.
    P. N. Strong, J. T. Smith, and J. T. W. Keana, “A convenient bioassay for detecting nanomolar concentration of lidokaine,” Toxicon, 11, 433–438 (1973).PubMedCrossRefGoogle Scholar
  11. 11.
    E. F. Barrett and J. N. Barrett, “Intracellular recording from vertebrate myelinated axons: mechanism of the depolarizing afterpotential,” J. Physiol., 323, 117–144 (1982).PubMedGoogle Scholar
  12. 12.
    D. L. Eng, T. R. Gordon, J. D. Kocsis, and S. G. Waxman, “Current-clamp analysis of a time-dependent rectification in rat optic nerve,” J. Physiol., 421, 185–202 (1990).PubMedGoogle Scholar
  13. 13.
    J. D. Kocsis, T. R. Gordon, and S. G. Waxman, “Mammalian optic nerve fibers display two pharmacologically distinct potassium channels,” Brain Res., 383, 357–361 (1986).PubMedCrossRefGoogle Scholar
  14. 14.
    F. Erne-Brand, P. Jirounek, J. Drewe, et al., “Mechanism of antinociceptive action of clonidine in nonmyelinated nerve fibers,” Eur. J. Pharmacol., 383, 1–8 (1999).PubMedCrossRefGoogle Scholar
  15. 15.
    M. A. Rizzo, J. D. Kocsis, and S. G. Waxman, “Slow Na+ conductance of dorsal root ganglion neurons: intraneuronal homogeneity and inter neuronal heterogeneity,” J. Neurophysiol., 72, 2796–2815 (1994).PubMedGoogle Scholar
  16. 16.
    C. Dalle, M. Schneider, F. O. Clergue, et al., “Inhibition of the Ih current in isolated peripheral nerve: A novel mode of peripheral antinociception,” Muscle Nerve, 24, 254–261 (2001).PubMedCrossRefGoogle Scholar
  17. 17.
    S. Marsh, “An extracellular recording technique for monitoring drug-induced changes in membrane polarization and evoked potential amplitudes from whole nerve bundles and ganglia,” in: FFB4, Electrodes for Stimulation and Bioelectric Potential Recording, Biomesstechnik-Verlag March, Germany (1988), pp. 232–235.Google Scholar
  18. 18.
    R. Stämpfli, “A new method for measuring membrane potentials with external electrodes,” Experientia, 10, 508–509 (1954).PubMedCrossRefGoogle Scholar
  19. 19.
    C. G. Oxford and J. P. Pooler, “Selective modification of sodium channel gating in lobster axons by 2,4,6-trinitrophenol. Evidence for two inactivation mechanisms,” J. Gen. Physiol., 66, 765–779 (1975).PubMedCrossRefGoogle Scholar
  20. 20.
    L. Leppanen and P. K. Stys, “Ion transport and membrane potential in CNS myelinated axons: I. Normoxic conditions,” J. Neurophysiol., 78, 2086–2094 (1997).PubMedGoogle Scholar
  21. 21.
    N. Persaud and G. R. Strichartz, “Micromolar lidocaine selectively blocks propagating ectopic impulses at a distance from their site of origin,” Pain, 99, 333–340 (2002).PubMedCrossRefGoogle Scholar
  22. 22.
    B. D. Brich, J. D. Kocsis, F. D. Gregorio, et al., “A voltage-and time-dependent rectification in rat spinal root axons,” J. Neurophysiol., 66, 719–728 (1991).Google Scholar
  23. 23.
    A. H. Tokuno, C. W. Bradberry, B. Everill, et al., “Local anesthetic effects of cocaethylene and isopropylcocaine on rat peripheral nerves,” Brain Res., 996, 159–167 (2004).PubMedCrossRefGoogle Scholar
  24. 24.
    M. A. Peasley and R. Shi, “Ischemic insult exacerbates acrolein-induced conduction loss and axonal membrane disruption in guinea pig spinal cord white matter,” J. Neurol. Sci., 216, 23–32 (2003).PubMedCrossRefGoogle Scholar
  25. 25.
    A. H. Tokuno, J. D. Kocsis, and S. G. Waxman, “Noninactivating, tetrodotoxin-sensitive Na conductance in peripheral axons,” Muscle Nerve, 28, 212–217 (2003).PubMedCrossRefGoogle Scholar
  26. 26.
    R. Hahin and G. R. Strichartz, “Effects of deuterium oxide on the rate and dissociation constants for saxitoxin and tetrodotoxin action,” J. Gen. Physiol., 78, 113–139 (1981).PubMedCrossRefGoogle Scholar
  27. 27.
    M. P. Blaustein and D. E. Goldman, “Origin of axon membrane hyperpolarization under sucrose-gap,” Biophys. J., 6, 453–470 (1966).PubMedGoogle Scholar
  28. 28.
    P. Jirounek and R. W. Straub, “The potential distribution and the short-circuiting factor in the sucrose gap,” Biophys. J., 11, 1–10 (1971).PubMedGoogle Scholar
  29. 29.
    P. Jirounek, G. J. Jones, C. W. Burckhardt, and R. W. Straub, “The correction factors for sucrose gap measurements and their practical application,” Biophys. J., 33, 107–120 (1981).PubMedCrossRefGoogle Scholar

Copyright information

© Springer Science+Business Media, Inc. 2007

Authors and Affiliations

  1. 1.Cukurova UniversityAdanaTurkey

Personalised recommendations