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Sökning: onr:"swepub:oai:DiVA.org:kth-93681" > Modeling activity-d...

LIBRIS Formathandbok  (Information om MARC21)
FältnamnIndikatorerMetadata
00004377naa a2200445 4500
001oai:DiVA.org:kth-93681
003SwePub
008120423s2014 | |||||||||||000 ||eng|
0247 a https://urn.kb.se/resolve?urn=urn:nbn:se:kth:diva-936812 URI
0247 a https://doi.org/10.1152/jn.00777.20122 DOI
040 a (SwePub)kth
041 a engb eng
042 9 SwePub
072 7a ref2 swepub-contenttype
072 7a art2 swepub-publicationtype
1001 a Tigerholm, Jennyu KTH,Beräkningsbiologi, CB,Stockholm Brain Institute, Stockholm, Sweden4 aut0 (Swepub:kth)u1k1jm7d
2451 0a Modeling activity-dependent changes of axonal spike conduction in primary afferent C-nociceptors
264 1b American Physiological Society,c 2014
338 a print2 rdacarrier
500 a QC 20140602. Updated from manuscript to article in journal.
520 a Action potential initiation and conduction along peripheral axons is a dynamic process that displays pronounced activity dependence. In patients with neuropathic pain, differences in the modulation of axonal conduction velocity by activity suggest that this property may provide insight into some of the pathomechanisms. To date, direct recordings of axonal membrane potential have been hampered by the small diameter of the fibers. We have therefore adopted an alternative approach to examine the basis of activity-dependent changes in axonal conduction by constructing a comprehensive mathematical model of human cutaneous C-fibers. Our model reproduced axonal spike propagation at a velocity of 0.69 m/s commensurate with recordings from human C-nociceptors. Activity-dependent slowing (ADS) of axonal propagation velocity was adequately simulated by the model. Interestingly, the property most readily associated with ADS was an increase in the concentration of intra-axonal sodium. This affected the driving potential of sodium currents, thereby producing latency changes comparable to those observed for experimental ADS. The model also adequately reproduced post-action potential excitability changes (i.e., recovery cycles) observed in vivo. We performed a series of control experiments replicating blockade of particular ion channels as well as changing temperature and extracellular ion concentrations. In the absence of direct experimental approaches, the model allows specific hypotheses to be formulated regarding the mechanisms underlying activity-dependent changes in C-fiber conduction. Because ADS might functionally act as a negative feedback to limit trains of nociceptor activity, we envisage that identifying its mechanisms may also direct efforts aimed at alleviating neuronal hyperexcitability in pain patients.
650 7a MEDICIN OCH HÄLSOVETENSKAPx Medicinska och farmaceutiska grundvetenskaperx Neurovetenskaper0 (SwePub)301052 hsv//swe
650 7a MEDICAL AND HEALTH SCIENCESx Basic Medicinex Neurosciences0 (SwePub)301052 hsv//eng
650 7a NATURVETENSKAPx Data- och informationsvetenskapx Bioinformatik0 (SwePub)102032 hsv//swe
650 7a NATURAL SCIENCESx Computer and Information Sciencesx Bioinformatics0 (SwePub)102032 hsv//eng
653 a activity-dependent slowing
653 a recovery cycles
653 a mechano-insensitive nociceptor
653 a computer modeling
7001 a Petersson, Marcusu KTH,Beräkningsbiologi, CB,Stockholm Brain Institute, Stockholm, Sweden4 aut0 (Swepub:kth)u14bsy5t
7001 a Obreja, Otiliau Anaesthesiology, Universitaetsmedizin Mannheim, Univ. of Heidelberg4 aut
7001 a Lampert, Angelikau Inst. of Physiol. and Pathophysiology, Friedrich-Alexander-Uni versität Erlangen-Nürnberg4 aut
7001 a Carr, Richardu Anaesthesiology, Universitaetsmedizin Mannheim, Univ. of Heidelberg4 aut
7001 a Schmelz, Martinu Anaesthesiology, Universitaetsmedizin Mannheim, Univ. of Heidelberg,4 aut
7001 a Fransén, Eriku KTH,Beräkningsbiologi, CB,Stockholm Brain Institute, Stockholm, Sweden4 aut0 (Swepub:kth)u14yg0os
7102 a KTHb Beräkningsbiologi, CB4 org
7730 t Journal of Neurophysiologyd : American Physiological Societyg 111:9, s. 1721-1735q 111:9<1721-1735x 0022-3077x 1522-1598
8564 u https://europepmc.org/articles/pmc4044369
8564 8u https://urn.kb.se/resolve?urn=urn:nbn:se:kth:diva-93681
8564 8u https://doi.org/10.1152/jn.00777.2012

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