Display options
Share it on

Front Comput Neurosci. 2015 Apr 28;9:44. doi: 10.3389/fncom.2015.00044. eCollection 2015.

The CNP signal is able to silence a supra threshold neuronal model.

Frontiers in computational neuroscience

Francesca Camera, Alessandra Paffi, Alex W Thomas, Francesca Apollonio, Guglielmo D'Inzeo, Frank S Prato, Micaela Liberti

Affiliations

  1. Department of Information Engineering, Electronics and Telecommunications, "Sapienza" University of Rome Rome, Italy.
  2. Bioelectromagnetics Group, Imaging Program, Lawson Health Research Institute London, ON, Canada.

PMID: 25972807 PMCID: PMC4412122 DOI: 10.3389/fncom.2015.00044

Abstract

Several experimental results published in the literature showed that weak pulsed magnetic fields affected the response of the central nervous system. However, the specific biological mechanisms that regulate the observed behaviors are still unclear and further scientific investigation is required. In this work we performed simulations on a neuronal network model exposed to a specific pulsed magnetic field signal that seems to be very effective in modulating the brain activity: the Complex Neuroelectromagnetic Pulse (CNP). Results show that CNP can silence the neurons of a feed-forward network for signal intensities that depend on the strength of the bias current, the endogenous noise level and the specific waveforms of the pulses. Therefore, it is conceivable that a neuronal network model responds to the CNP signal with an inhibition of its activity. Further studies on more realistic neuronal networks are needed to clarify if such an inhibitory effect on neuronal tissue may be the basis of the induced analgesia seen in humans and the antinociceptive effects seen in animals when exposed to the CNP.

Keywords: CNP signal; Hodgkin and Huxley neuron model; feed-forward neuron network; magnetic stimulation of the brain; pulsed magnetic fields

References

  1. IEEE Trans Biomed Eng. 2011 May;58(5):1294-302 - PubMed
  2. PLoS Comput Biol. 2012;8(10):e1002615 - PubMed
  3. Brain Stimul. 2013 Jul;6(4):469-76 - PubMed
  4. Biochim Biophys Acta. 2006 May;1758(5):597-605 - PubMed
  5. Cell. 2009 Oct 16;139(2):267-84 - PubMed
  6. Conf Proc IEEE Eng Med Biol Soc. 2007;2007:2404-7 - PubMed
  7. Bioelectromagnetics. 2006 Jul;27(5):414-22 - PubMed
  8. Bioelectromagnetics. 2005 Jul;26(5):367-76 - PubMed
  9. Biol Cybern. 2008 Nov;99(4-5):427-41 - PubMed
  10. Neurosci Lett. 2004 Jun 10;363(2):157-62 - PubMed
  11. Pain Res Manag. 2006 Summer;11(2):85-90 - PubMed
  12. Bioelectromagnetics. 2004 Apr;25(3):196-203 - PubMed
  13. Neurosci Lett. 1997 Jan 31;222(2):107-10 - PubMed
  14. Pain Res Manag. 2007 Winter;12(4):249-58 - PubMed
  15. Conf Proc IEEE Eng Med Biol Soc. 2006;1:4183-6 - PubMed
  16. J Physiol. 1952 Aug;117(4):500-44 - PubMed
  17. Conf Proc IEEE Eng Med Biol Soc. 2009;2009:1525-8 - PubMed
  18. Network. 2013;24(3):99-113 - PubMed
  19. Neurosci Lett. 2004 Jan 2;354(1):30-3 - PubMed
  20. Bioelectromagnetics. 2007 Dec;28(8):599-607 - PubMed
  21. Neurosci Lett. 2001 Jan 12;297(2):121-4 - PubMed
  22. J Membr Biol. 2013 Oct;246(10):761-7 - PubMed
  23. J R Soc Interface. 2010 Mar 6;7(44):467-73 - PubMed
  24. Peptides. 1998;19(2):333-42 - PubMed
  25. Bioelectromagnetics. 2009 Jan;30(1):9-20 - PubMed
  26. Proc Natl Acad Sci U S A. 2001 Jun 19;98(13):7253-8 - PubMed
  27. IEEE Trans Neural Netw. 2003;14(6):1569-72 - PubMed
  28. IEEE Trans Biomed Eng. 2012 Aug;59(8):2302-11 - PubMed
  29. Biol Cybern. 2006 Feb;94(2):118-27 - PubMed
  30. J Theor Biol. 1978 Apr 6;71(3):401-20 - PubMed

Publication Types