Literature DB >> 15826857

Differences in potentials and excitability properties in simulated cases of demyelinating neuropathies. Part II. Paranodal demyelination.

D I Stephanova1, M Daskalova.   

Abstract

OBJECTIVE: The purpose of the present investigation is to study the potentials and axonal excitability properties in progressively greater degrees of uniform paranodal demyelination of human motor nerve fibres.
METHODS: Using our previous double cable model of human motor nerve fibre, 3 paranodally systematically demyelinated cases (termed as PSD1, PSD2 and PSD3) are simulated by an uniform paranodal resistance reduction (20, 50 and 77%) along the fibre length.
RESULTS: Considerably reduced amplitudes, prolonged durations and slowed conduction velocities are obtained for the intracellular potentials of the PSD2 and PSD3 cases. In contrast, the electrotonic potentials show abnormally greater increase in the early part of the hyperpolarizing responses. The extracellular potentials indicate increased polyphasia in the PSD3 case. The strength-duration time constants are shorter and the rheobases higher in the demyelinated cases. In the recovery cycles, the demyelinated cases have less refractoriness, greater supernormality and less late subnormality than the normal case.
CONCLUSIONS: The reduction of the paranodal seal resistance has significant effects on the potentials and axonal excitability properties of the simulated demyelinated human motor fibres. The obtained abnormalities in the potentials and excitability properties can be observed in vivo in patients with chronic inflammatory demyelinating polyneuropathy. SIGNIFICANCE: The study provides important information about the pathology of human demyelinating neuropathies.

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Year:  2005        PMID: 15826857     DOI: 10.1016/j.clinph.2005.01.005

Source DB:  PubMed          Journal:  Clin Neurophysiol        ISSN: 1388-2457            Impact factor:   3.708


  8 in total

1.  Excitation block in a nerve fibre model owing to potassium-dependent changes in myelin resistance.

Authors:  A R Brazhe; G V Maksimov; E Mosekilde; O V Sosnovtseva
Journal:  Interface Focus       Date:  2010-12-01       Impact factor: 3.906

2.  Primary paranode demyelination modulates slowly developing axonal depolarization in a model of axonal injury.

Authors:  Vladislav Volman; Laurel J Ng
Journal:  J Comput Neurosci       Date:  2014-07-03       Impact factor: 1.621

3.  Early identification of 'acute-onset' chronic inflammatory demyelinating polyneuropathy.

Authors:  Jia-Ying Sung; Jowy Tani; Susanna B Park; Matthew C Kiernan; Cindy Shin-Yi Lin
Journal:  Brain       Date:  2014-06-19       Impact factor: 13.501

4.  Differences in membrane properties in simulated cases of demyelinating neuropathies: internodal focal demyelinations without conduction block.

Authors:  D I Stephanova; M S Daskalova; A S Alexandrov
Journal:  J Biol Phys       Date:  2006-04-20       Impact factor: 1.365

5.  Differences in membrane properties in simulated cases of demyelinating neuropathies: internodal focal demyelinations with conduction block.

Authors:  D I Stephanova; M S Daskalova; A S Alexandrov
Journal:  J Biol Phys       Date:  2006-06-14       Impact factor: 1.365

6.  Excitability and the safety margin in human axons during hyperthermia.

Authors:  James Howells; Dirk Czesnik; Louise Trevillion; David Burke
Journal:  J Physiol       Date:  2013-04-22       Impact factor: 5.182

7.  Differences between the channels, currents and mechanisms of conduction slowing/block and accommodative processes in simulated cases of focal demyelinating neuropathies.

Authors:  Diana I Stephanova; Mariya S Daskalova
Journal:  Eur Biophys J       Date:  2008-02-20       Impact factor: 1.733

8.  Membrane property abnormalities in simulated cases of mild systematic and severe focal demyelinating neuropathies.

Authors:  Diana Stephanova; Mariya Daskalova
Journal:  Eur Biophys J       Date:  2007-09-05       Impact factor: 1.733

  8 in total

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